The Encyclopedia of ADDICTIVE DRUGS



The Encyclopedia of


The Encyclopedia of



GREENWOOD PRESS Westport, Connecticut London

Library of Congress Cataloging-in-Publication Data

Miller, Richard Lawrence.
The encyclopedia of addictive drugs / Richard Lawrence Miller.

p. cm.
Includes bibliographical references and index. ISBN 0–313–31807–7 (alk. paper)
1. Drugs of abuse—Handbooks, manuals, etc.

RM316.M555 2002 615′.78—dc21 2002075332

I. Title.

British Library Cataloguing in Publication Data is available. Copyright 2002 by Richard Lawrence Miller

All rights reserved. No portion of this book may be reproduced, by any process or technique, without the express written consent of the publisher.

Library of Congress Catalog Card Number: 2002075332 ISBN: 0–313–31807–7

First published in 2002

Greenwood Press, 88 Post Road West, Westport, CT 06881 An imprint of Greenwood Publishing Group, Inc.

Printed in the United States of America


The paper used in this book complies with the Permanent Paper Standard issued by the National Information Standards Organization (Z39.48–1984).

10 9 8 7 6 5 4 3 2 1


Introduction 1 Drug Types 11 Alphabetical Listings of Drugs 31 Sources for More Information 445 Drug Name Index 453 Subject Index 489


The Encyclopedia of Addictive Drugs will save readers many hours of time that would otherwise be spent tracking down basic facts in science journals and libraries. This book is useful to a wide variety of persons—from a student doing a term paper to reporters preparing a story, from parents reading that story to a narcotics law enforcement officer needing extra information for a public presentation.

In writing this book the approach has been multidisciplinary, meaning that perspectives from several fields of research have been pulled together. The same substance may mean different things to a chemist, a biologist, a physi- cian, or an anthropologist. Thousands of scientific reports were sifted for in- formation and concepts that will be meaningful to readers seeking basic information about specific substances and about drugs in general.

The core of this book is an alphabetical listing of substances. Some are not ordinarily thought of as drugs, but all have been misused in ways indistin- guishable from drug abuse. While information in the individual listings and elsewhere may refer to various physical effects, such information does not constitute medical advice. Anyone with a medical difficulty needs to consult a medical practitioner, not this book.

In addition to meaty information about what drugs do, this book includes trivia that might interest, for example, a student preparing a report or a home- work assignment. For instance, some individual listings of drugs mention little-known military usage that might intrigue teens interested in the armed forces. Some experiments are mentioned not because they are necessary to know about, but because they might add depth to a term paper or inspire a student to pursue a new angle. Material about effects on pregnancy is inher- ently important but might also have special interest for female readers.

In addition to alphabetical listings of substances, this book includes a section about drug types in which substances are arranged in general categories, such

2 The Encyclopedia of Addictive Drugs

as stimulants, with further grouping by classes of stimulants (amphetamine, anorectic, cocaine, pyridine alkaloid). Such an arranging of drugs puts them in a broader context of information. A chemist knows that a certain element has particular characteristics because of its place in the periodic table, and a biologist knows that a certain organism will have particular characteristics because of its species classification. A reader of this book can automatically glean information about an individual substance because of the way it is clas- sified. For example, everything said in this book about stimulants applies to the class of stimulants known as amphetamines; everything said about am- phetamines applies to the particular drug methamphetamine. (Substances printed in bold have main entries in this book’s alphabetical section.) A reader familiar with basics about stimulants and who only needs a few specifics about methamphetamine can quickly find those details. A reader who needs to un- derstand more about the general nature of stimulants can find that back- ground information as well. Persons desiring to go deeper than the summaries of scientific information in alphabetical entries can consult reliable sources listed at the end of each entry. Many of those sources list still more references.

This book concludes with a guide to finding general information about drugs. Here readers are directed not only to ostensibly neutral sources of information but also to sources taking explicit and differing stances on various aspects of drug use.

The index lists street names and other alternate names (used in various communities at various times), giving page numbers where information can be found about those drugs.

Descriptions of individual drugs in the alphabetical section of this book present the scientific consensus about those substances, based mainly upon reports from refereed science journals. A refereed journal is one that does not merely accept an author’s word but instead has the articles critiqued and approved by assorted experts prior to publication. Articles in such journals are fundamental sources of scientific information. Although findings reported in this book come from scientific investigations around the world, not every- one agrees with what scientists discover about drugs. Sometimes scientists themselves disagree with one another. The history of science is filled with detection of errors, and future research will no doubt provide new under- standings of these drugs. This book, however, presents scientific consensus concerning these drugs as the twenty-first century begins.


Drug abuse is an emotionally charged topic involving more than facts about pharmaceuticals. Personal and moral values are involved, as are fears that sometimes transform into anger. The author of this book has studied drug abuse questions since the 1980s; visited with prosecutors, judges, and health care givers, along with drug abusers and their families; drafted drug control legislation introduced by Republican and Democratic legislators; testified be- fore legislative committees; and given public presentations. In all settings, facts have rapidly disappeared in discussion of the topic.

For most of the twentieth century, addiction was considered a physical ef-

Introduction 3

fect of some drugs. If a drug failed to produce physical symptoms associated with addiction, the substance was classified as nonaddictive. In the 1980s, however, some researchers began arguing that addiction could exist without associated physical symptoms, that mental craving alone was enough to power addiction.1 An important boost to acceptance of that concept came in 1987 when the American Psychiatric Association declared that “cocaine de- pendence” did not require physical dependence for diagnosis.2 The APA stated, “Continuing use of cocaine appears to be driven by persistent craving and urges for the substance rather than attempts to avoid or alleviate with- drawal symptoms.”3 That approach yielded a broader understanding: that people could be addicted to things other than drugs, a new and controversial concept but one that was becoming more accepted as the twenty-first century began.

Regardless of whether addiction can be more of a mental process than a physical one, the likelihood of a user developing a harmful relationship with drugs is greater with some substances than with others. The harm may be physical. The harm may be disruption of a user’s life. Experience shows, for example, that cocaine is far more risky to use than caffeine.

Some drugs can be used so much that they and a person’s body develop what may be called a physical resonance. That is not a standard drug abuse term, but it communicates the concept more vividly than other terminology. Resonance means that an individual’s body has adapted to the drug in such a way that stopping use of the drug makes a person feel ill. Symptoms depend on the drug and can range from a runny nose to convulsions. Not all drugs can produce such a state, but those that can are traditionally called addictive. Indeed, appearance or nonappearance of an “abstinence” or “withdrawal” syndrome of illness upon sudden end to drug dosage used to be considered a definitive test of whether a drug is addictive and whether a user is an addict. Some specialists might use the term neuroadaptation for the mechanism that creates resonance, but here more conservative language that asserts less about roles of the brain and nervous system will be used.

Resonance is typically, and somewhat misleadingly, called “dependence” by many persons. An addict who temporarily feels sick upon stopping a drug but who later feels better is not really “dependent” on it, in the ordinary dictionary sense of that word’s meaning. Granted, physical dependence upon a drug is possible, in the dictionary sense, regardless of whether the under- lying mechanism is neuroadaptation. An example is a diabetic who needs insulin. Cutting off insulin supply would make the diabetic sicker and sicker, so the person truly is dependent on the drug. Its presence is necessary for good health. Normally, however, that is not what is meant by saying a drug abuser is dependent on a substance; rather, one means the abuser will feel temporarily ill if dosage suddenly stops. Nonetheless, some drug addictions can involve the dictionary meaning of dependence. For example, persons ex- tremely addicted to alcohol or barbiturates can die if cut off from their supply. Death typically comes from cascading problems culminating in convulsions. That dismal outcome is uncommon but possible. In addition, dependence is sometimes used in contexts making it synonymous with addiction, perhaps referring to persons undergoing treatment to break dependence on some drug

4 The Encyclopedia of Addictive Drugs

they crave and are unable to stop taking. Because dependence has multiple meanings, the term is not ideal. However, this book uses the term because of its familiarity to specialists, despite its potential for causing confusion among general readers.

The concepts of addiction and dependence differ. Someone who takes a lot of barbiturates may experience both states. Someone who uses a lot of mari- juana may experience neither. Knowing the differences between those two concepts can help a person spot confusion in rhetoric about drug abuse.

A person who has dependence on a drug may experience an abstinence or withdrawal syndrome if the supply runs out. The syndrome may begin several hours or several days after drug use stops, depending on how long a drug and its by-products last in the human body. Different drugs have different withdrawal symptoms, and they are specified in this book’s alphabetical list- ings. Often a withdrawal symptom is the opposite of what a drug does. For example, if a drug constipates a person, withdrawal from that drug may in- clude diarrhea. If a drug makes a person sleepy, withdrawal may include insomnia. Sometimes the withdrawal syndrome can be avoided if dosage is gradually reduced rather than stopped suddenly. At times the syndrome is avoided by substituting another drug that has “cross-tolerance” with the first one. Cross-tolerance means that one drug can substitute for another in some ways, typically in ways that prevent a withdrawal syndrome from emerging. A classic example allows methadone to be substituted for heroin. This book’s alphabetical section notes cross-tolerance among assorted drugs. Cross- tolerance is a concept that differs from tolerance described below.

Tolerance means that as time passes, a person must use more and more of a drug to get the same effect. Such an outcome is a traditional sign of addic- tion. Tolerance can develop to some effects of a drug and not to others. For example, an amphetamine addict may become tolerant to euphoric properties of the drug, but not to its poisonous qualities. A cocaine addict may build tolerance to appetite-loss properties of the drug but not to other actions. The opposite may also happen, in which a person becomes sensitized to a drug and needs less and less. Evidence for such a development has been seen in humans with DOM and benzodiazepines and in animals with cocaine and DMT. Such a development, however, would not be considered evidence of addiction. Tolerance can have a strong mental component; the same phenom- enon can be seen in reduced pleasure gained from continual indulgence in wild music events or a particular food or shopping. Recreational and medical users can take the same drug, often with medical users never developing tol- erance—perhaps because of the purpose for which they take the drug and not because of its chemistry, although that possible explanation is not yet con- firmed. Some experts argue that tolerance is indeed a physical effect, caused by organic brain changes induced by a drug. Ultimately those experts are correct: All mental feelings and processes result from changes in the brain’s electrochemical activity. Some of these changes can even be measured and correlated with broad psychological characteristics. For example, changes in brain waves and emotions can be seen after some drugs are administered. Our understanding of such things remains crude, however. We don’t know how brain chemicals and electricity induce a person to love someone or hate an

Introduction 5

idea. Ultimately some still unknown physical process may explain why people who take a drug for pleasure develop a tolerance to its effects, while people who take the same substance for medical purposes never experience a change in what the drug does.

From a purely physical standpoint, someone who has recreationally abused a drug for years may indeed be able to tolerate a stronger dose than someone who takes the same drug for the first time. The abuser’s body may develop physical adaptations permitting high doses. For instance, body chemistry can change in ways that counteract a drug, requiring more and more of the sub- stance to overcome the change. Nonetheless, for many practical purposes we can say the cause of tolerance is psychological. This was implied in medical research comparing the amount of meperidine required to relieve pain in appendectomy patients.4 The study was conducted in Beirut and examined records of patients who underwent surgery before, during, and after a brutal civil war that destroyed much of that city. For pain relief, prewar patients needed more of the drug than wartime or postwar patients did. Researchers concluded that part of the reason was a psychological change in how pain was evaluated during those years of brutality. The study did not directly in- vestigate tolerance, but it did demonstrate that a change in attitude can change the amount of drug effect perceived by users.

Change in attitude illustrates the influence of set and setting on drug effects. Set describes someone’s basic personality and expectations about what a drug does. Setting is the environment in which drug use occurs. Rat experimenta- tion5 demonstrated that the setting in which a drug is administered can alter the amount of tolerance, with those conditions demonstrating a psychological component in physical tolerance. Countless human examples demonstrate that set and setting can determine how much effect a given drug dose produces, whether it is pleasant or unpleasant, even whether a dose is tolerable or fatal.

Dosage affects a drug’s impact. Overdose of most drugs can produce serious unwanted effects, including death. In addition to the amount of drug, the method of dosage (injection, oral, smoking, or other routes) can make a huge difference in effects. The same amount of drug can have a much different impact depending on route of administration. A “safe” dose by one route can be fatal by another. An effect at one dosage level may be the opposite of what happens at a different dosage level. Sometimes a drug can cause a condition that it is supposed to prevent. Such paradoxical actions illustrate hazards in- volved in reckless drug use.

Taking more than one drug of a given type can be expected to increase effects typical of that type. For example, a person who ingests the depressant alcohol simultaneously with an opiate depressant will normally experience deeper depressant effects than if just one of the drugs was used. Taking a normal dose of several drugs from one type can be the practical equivalent of overdosing on any one of them. Taking drugs of different types can also be hazardous. For example, the stimulant cocaine and the depressant heroin do not cancel each other’s effects if taken together; instead, the body may be assaulted from different directions simultaneously and break down under the attack.

6 The Encyclopedia of Addictive Drugs


Historical experience shows addiction to be more likely with some drugs than with others, just as some road intersections are more hazardous than others even though anyone might drive through them safely at a given time. Whether the subject be drugs or intersections, persons concerned about dan- gers attempt to discover if similarities exist. Do certain characteristics of in- tersections (speed limits, stop signs, obscured vision) indicate whether danger is more likely? Characteristics of drugs, particularly their chemical formulas, are examined to determine similarities that might indicate whether particular drugs have more addictive or abuse potential than others. For example, the shape of a drug’s molecule may determine how a user’s body reacts, so drugs with molecules of a similar shape might be expected to have similar effects. Also, new substances derived from an old drug may be assumed to have similarities to the old drug.


In the United States the result has been a blend of science and law called “scheduling,” set up in 1970 by the federal Comprehensive Drug Abuse Pre- vention and Control Act, which replaced all previous federal narcotics laws. (The legal definition of “narcotics” includes stimulants such as cocaine and hallucinogens such as LSD.) Scheduling is an ongoing process affected by the same influences that shape other laws. Sometimes Congress or a state legis- lature puts a drug in a particular schedule. Sometimes a federal or state official does so. Like all law, scheduling has an element of arbitrariness, enhanced as federal statutes interact with state laws and local ordinances. Nonetheless, even though results can be puzzling, basic principles in scheduling are clear.

In the United States drugs are either scheduled or unscheduled. Unsched- uled drugs may be benign or highly dangerous, available over the counter or by prescription only, perhaps even available to children through a plant grow- ing wild in the woods. A hospital emergency room may deal with someone who uses an unscheduled drug, but the U.S. Drug Enforcement Administra- tion probably will not. Almost all drugs are unscheduled, whether they be pharmaceutical creations from a laboratory or natural products harvested from the soil.

Scheduled drugs are theoretically ranked by their potential for abuse. Not all abuse is addictive, but the rankings imply that some drugs are more of an addiction hazard than others. At the time this book was written, five schedules existed. Generally drugs in a lower-numbered schedule are considered more prone to abuse than those in higher-numbered schedules. Heroin is a Schedule I drug. A cough medicine available without prescription might be in Schedule V. Schedule I is also used for abused drugs having no medical use approved by regulatory agencies in the United States. Thus Schedule I includes mari- juana even though decades of research have shown it to be more benign than most drugs listed in other schedules. Schedule I also includes some drugs (dextromoramide, dipipanone, phenoperidine, and others) used routinely by doctors in other countries but that lack approval from U.S. authorities. So

Introduction 7

although Schedule I is often viewed as a list of the most dangerous drugs, relatively harmless ones are listed if they are unapproved for medical use in the United States, while drugs that can easily kill even when administered in a hospital setting are listed in schedules indicating less danger of abuse. Still, the general rule is that drugs are scheduled according to their abuse potential, with drugs in lower-numbered schedules having more abuse potential than drugs in higher-numbered schedules. Some illicit drug makers try to avoid scheduling regulations altogether by tweaking the chemical composition of a substance just enough that it is no longer the molecule defined in a schedule. Such “designer drugs” remain legal until schedules are updated again.

Schedule I is for drugs ruled as being most prone to abuse, lacking generally accepted use in the American health care system, and being so dangerous that health practitioners cannot safely administer these drugs to patients. Except for specially authorized scientific studies, possession of a Schedule I substance is illegal under any circumstance. No physician can authorize a patient to use a Schedule I item. Schedule II is for drugs ruled as being most prone to abuse but in use in the American health care system and carrying the potential to cause major physical or mental dependence upon continued usage. Schedule III is for drugs ruled as being less prone to abuse; these are generally accepted by the American health care system but pose risks of “moderate or low” phys- ical dependence or “high” psychological dependence. Schedule IV is for drugs ruled as being still less prone to abuse; these are generally accepted by the American health care system and are less likely to result in physical or psy- chological dependence than Schedule III substances. Schedule V is for drugs least prone to abuse; they are generally accepted by the American health care system and are less likely to result in physical or psychological dependence than Schedule IV compounds.

This book’s alphabetical listings give each drug’s federal schedule status. States also have schedules. At times, state and federal schedules may not “match” for a particular drug. For example, under international treaty the U.S. government put flunitrazepam in Schedule IV, but federal authorities believed it should be Schedule I. So states have been encouraged to put the substance in Schedule I. Sometimes federal authorities change a drug’s sched- ule, and states may lag behind in conforming. For practical purposes, federal and state schedules have equal legal standing. A drug user who runs afoul of a state schedule can be punished as severely as a person who runs afoul of a federal schedule. A further complication is that although a drug that is un- listed in any schedule is presumed to be unscheduled, official pages of sched- ules do not necessarily specify all scheduled substances. Sometimes the official pages have not caught up with official decisions; sometimes a chemical is covered if it is derived from a scheduled substance, without a separate listing for the chemical being required. The list of sources at the end of this book tells how to find the official pages of schedules.

For many years, stimulants, depressants, and hallucinogens basically com- prised the entire contents of schedules. In the 1990s another type of drug was added, anabolic steroids. Various types of steroids exist. The anabolics can be used to build muscle mass and have long been popular among athletes seek- ing an edge in competitions. Anabolic steroids can have other effects as well,

8 The Encyclopedia of Addictive Drugs

effects particularly harmful to young persons whose bodies are still devel- oping. Attainment of adult height can be thwarted, and sexual organs can be damaged. Rising concern about injury to younger athletes caused the strict regulations of scheduling to be applied to these drugs, although other types of control (requiring prescriptions and suppressing nonmedical sales) had long been in place.

Scheduling is an element of law enforcement. Penalties for illegal use or possession of a drug depend partly upon its schedule. A related purpose of scheduling involves control of scheduled substances through tracking pre- scriptions written by health care practitioners and by tracking inventory rec- ords of pharmacies.

Pregnancy Categories

Legal drugs are placed in a Pregnancy Category, a system used to classify the risk of birth defects if the substance is used by a pregnant woman. Dif- ferent countries have different systems of categories. The alphabetical entries in this book use the U.S. Food and Drug Administration system that was in place as the twenty-first century began.

Pregnancy Category A. Studies using pregnant women do not show birth defects caused by the drug in the first trimester, and evidence has not emerged show- ing risk later in pregnancy.

Pregnancy Category B. Studies using pregnant women have not been conducted, but experiments with pregnant animals fail to demonstrate birth defects. Al- ternatively, animal experiments have produced birth defects, but studies using pregnant women have not.

Pregnancy Category C. Animal experiments have produced birth defects, but no studies have used pregnant women to examine the potential for human birth defects. Alternatively, no animal or human studies have been conducted to determine the drug’s potential for causing birth defects.

Pregnancy Category D. Studies or reports of clinical experience indicate that the drug causes human birth defects, but using the drug during pregnancy may be so important to the woman’s health that fetal risk is justified (for example, no acceptable alternative therapy is available to deal with the woman’s illness).

Pregnancy Category X. Animal or human studies or clinical reports indicate the drug causes birth defects, and the drug’s potential benefits for a pregnant woman’s health do not justify risk to fetal development (for example, accept- able therapies are available that do not involve the drug).

Often a birth defect is thought of as something apparent upon birth, but scientists have found that some problems from fetal drug exposure such as cancer do not become evident until adulthood. And even though problems might not be observed among infants of women who used a certain drug during pregnancy, that fact does not necessarily mean the drug has no impact on fetal development. Drugs discussed in this book typically affect a user’s brain, suggesting that they may be particularly prone to harming fetal brain and nervous system development. Due to the course of fetal development,

Introduction 9

those effects may occur in a later stage of pregnancy than types of harm in- volving bones or other organs. In addition to matters affecting fetal devel- opment, pregnancy can alter a drug’s effect on the woman, for example, causing a dose to last longer than in a nonpregnant woman. That, in turn, could cause a pregnant woman to receive a cumulative overdose if she uses an amount suitable for a nonpregnant woman.


Numbers are a common element in articles and speeches about drugs. Num- bers can seem to provide precise information. Occasionally, however, the pre- cision is illusory. For example, a study6 of drug deaths in major U.S. cities during the early 1970s found that 60% of deaths in New York involved meth- adone, but it was involved in under 1% of deaths in Los Angeles and 0% in Chicago. Depending on which city’s experience someone was inclined to cite, methadone could be made to appear as a major or as an insignificant problem. Statistics may lump substances together, perhaps saying that a particular per- centage of persons who died had marijuana or cocaine in their blood. Those are two very different drugs. What percentage was marijuana and what per- centage was cocaine? What percentages were at a level of intoxication? Would intoxication have had anything to do with the cause of death? If so, was the death due to a poisonous effect of the drug, or was it due to a poor decision while intoxicated? Many statistics offer no answers to such questions. Even when statistics are both reliable and meaningful, often they are rapidly out- dated.

For all those reasons, The Encyclopedia of Addictive Drugs offers few statistics. Numbers found in this book are solid and should still have meaning years from now. The list of general sources at the end of this book includes Internet Web sites that can provide the latest statistics. They may be accurate, but (as indicated above) their meaning may be uncertain.


1. For an overview see J. Orford, “Addiction as Excessive Appetite,” Addiction 96 (2001): 15–31. For example, cocaine was long considered non-addictive because usage did not produce physical symptoms of addiction. In the 1980s this traditional under- standing was challenged by research reports such as F.H. Gawin and H.D. Kleber, “Abstinence Symptomatology and Psychiatric Diagnosis in Cocaine Abusers: Clinical Observations,” Archives of General Psychiatry 43 (1986): 107–13; H.D. Kleber and F.H. Gawin, “In Reply,” Archives of General Psychiatry 44 (1987): 298; H.D. Kleber, “Epidemic Cocaine Abuse: America’s Present, Britain’s Future?” British Journal of Addiction 83 (1988): 1364. Those challenges met skepticism or even outright rejection from A.E. Skodol, “Diagnostic Issues in Cocaine Abuse,” in H.I. Spitz and J.S. Rosecan, eds., Cocaine Abuse: New Directions in Treatment and Research (New York: Brunner/Mazel, 1987), 120; D.W. Teller and P. Devenyi, “Bromocriptine in Cocaine Withdrawal—Does It Work?” International Journal of the Addictions 23 (1988): 1197–1205; A.S.V. Burgen and J.F. Mitchell, Gaddum’s Pharmacology, 9th ed. (Oxford: Oxford University Press, 1985), 76; J.E.F. Reynolds. Martindale: The Extra Pharmacopoeia, 28th ed. (London: The Phar- maceutical Press, 1982), 914; J.M. Arena, ed., Poisoning: Toxicology, Symptoms, Treat-

10 The Encyclopedia of Addictive Drugs

ments, 5th ed. (Springfield, IL: Charles C. Thomas, 1986), 557; Drug Facts and Comparisons, 1990 ed. (St. Louis: Facts and Comparisons, 1989), 2078; A. Goth, Medical Pharmacology: Principles and Conduct, 11th ed. (St. Louis: C.V. Mosby Company, 1984), 350; B.K. Colasanti, “Contemporary Drug Abuse,” in C.R. Craig and R.E. Stitzel, eds., Modern Pharmacology, 2d ed. (Boston: Little, Brown and Company, 1986), 620; F.J. Gold- stein and G.V. Rossi, “Pharmacological Aspects of Drug Abuse,” in A.R. Gennaro, ed., Remington’s Pharmaceutical Sciences, 17th ed. (Easton, PA: Mack Publishing, 1985), 1351; G.K. McEvoy, ed., American Hospital Formulary Drug Service Information (Bethesda, MD: American Society of Hospital Pharmacists, 1989), 1508; Sidney Kaye, Handbook of Emergency Toxicology: A Guide for the Identification, Diagnosis, and Treatment of Poisoning, 5th ed. (Springfield, IL: Charles C. Thomas, 1988), 272; R.E. Gosselin, R.P. Smith, and H.C. Hodge, Clinical Toxicology of Commercial Products, 5th ed. (Baltimore: Williams & Wilkins, 1984), III–117.

2. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed., rev. (Washington, DC: American Psychiatric Association, 1987), 166–68.

3. Ibid., 179.

4. H.K. Armenian, M.A. Chamieh, and A. Baraka, “Influence of Wartime Stress and Psychosocial Factors in Lebanon on Analgesic Requirements for Postoperative Pain,” Social Science and Medicine 15E (February 1981): 63–66.

5. J. Vila, “Protection from Pentobarbital Lethality Mediated by Pavlovian Condi- tioning,” Pharmacology, Biochemistry, and Behavior 32 (1989): 365–66; R.E. Hinson and S. Siegel, “Pavlovian Inhibitory Conditioning and Tolerance to Pentobarbital-Induced Hy- pothermia in Rats,” Journal of Experimental Psychology: Animal Behavior Processes 12 (1986): 363–70.

6. E.C. Dinovo et al., “Analysis of Results of Toxicological Examinations Performed by Coroners’ or Medical Examiners’ Laboratories in 2000 Drug-Involved Deaths in Nine Major U.S. Cities,” Clinical Chemistry 22 (1976): 847–50.

Drug Types

This section of the book groups drugs in common ways that help readers make basic distinctions among them. For example, a drug grouped here among stim- ulants has basic differences from one grouped with depressants. Likewise, all drugs in the same classification share common attributes. Many details about drugs in the following classes are in the alphabetical listings of specific sub- stances, in addition to the general overview below.


As the name implies, these drugs stimulate the user. A trucker might use stimulants to drive a cargo cross country without rest. A soldier might use them to perform strenuous action that would otherwise be impossible. Stim- ulants frequently achieve such ends by drawing upon a person’s reserves of stamina and energy. Occasional use in that way can help accomplish tasks, and if a person is able to rest and recuperate afterward, perhaps no harm is done. Abusing powerful stimulants, however, is like burning a candle at both ends to produce more light. The quick burst of energy may be followed by collapse.

Not all stimulants are powerful. Some are so mild that they are readily available in certain foods such as caffeine in coffee, tea, and soda. A person taking a few ounces of such a beverage will likely need no recuperation at all from the stimulative action. Nonetheless, multiple doses of caffeine can pro- duce a strong effect, and some natural products can be massaged to increase the dose. Caffeine is far less powerful than cocaine, but a person using a lot of caffeine can become as jittery and hyperactive as a person using a little cocaine. A mild drug can be abused.

Using potent pharmaceutical stimulants is a way to improve feelings of well-being because increased energy can improve self-confidence regardless

12 The Encyclopedia of Addictive Drugs

of any other effects on body chemistry. Such a mental state can make current problems seem less troublesome. They may not go away, but worries about them can decline. That effect of stimulants can be seductive. Moreover, if that is the reason someone uses stimulants, stopping the drug can be doubly dif- ficult. Not only are feelings of self-confidence and energy replaced by self- doubt and exhaustion, but problems that never went away will probably seem all the worse. And indeed they may really be worse if the stimulant user has taken no effective action to deal with them.

For information about specific stimulants not otherwise classified below, see the entries on: caffeine, modafinil, pemoline, and yohimbe.

Amphetamine Class

Amphetamine stimulants are pharmaceutical products created in laborato- ries, not harvested or refined from natural products. When amphetamines debuted under the brand name Benzedrine during the Great Depression of the 1930s, they were an ingredient used for inhalers that people would sniff to relieve stopped-up noses. Another effect was a burst of energy and alert- ness, sometimes accompanied by a brightening of mood into euphoria, and people began using the nonprescription inhalers for recreational purposes. Such drugs were called Cartwheel, Euphodine, and Halloo-wach. Ampheta- mines became accepted therapeutically as a treatment for depression and worked best if a person simply had difficulty coping with stress during part of a day, as a dose wears off quickly and can leave a person feeling lower if nothing has changed in the situation causing the stress. For example, a dose might deal effectively with occasional aggravation in the workplace but not work so well for a person who stayed at home all the time with continual depression. In the 1930s oral tablets of Benzedrine (“Bennies”) became avail- able. Both inhalers and tablets tended to promote insomnia, and that effect was soon used medically to fight narcolepsy, an affliction in which a person suddenly falls asleep numerous times throughout the day. The drug was also used to treat Parkinson’s disease, epilepsy, and alcoholism and to help persons suffering from attention deficit hyperactivity disorder (ADHD). ADHD begins in childhood and involves difficulty in paying proper attention to surround- ings while also acting restless. Usually the condition goes away as children grow older, but it can continue into adult life. Treating the condition with a stimulant may sound counterproductive, but experience shows that low doses of amphetamine class stimulants can ease ADHD. Practitioners had to learn caution in prescribing to children, however, as occasionally this treatment could intensify rather than diminish the undesired conduct.

World War II brought wide use of amphetamines as military forces on all sides issued “pep pills” to give personnel an edge in combat. The most prom- inent combat pills were Benzedrine (amphetamine sulfate), Dexedrine (dex- troamphetamine), and Methedrine (methamphetamine). Combining such drugs with hard physical labor can be risky, with a user crumpling from overexerting the heart and overheating the whole body, an additional combat hazard for users. In contrast to some other military forces, the United States did not routinely issue the pills except to bomber crews. Nonetheless, the drug

Drug Types 13

was freely available to U.S. personnel who wanted it and was a standard item in survival packs. To improve alertness, national leaders such as British Prime Minister Winston Churchill and, later on, President John F. Kennedy freely used amphetamines as well.1 Kennedy’s New Frontier rhetoric was character- ized by his frequent call for “vigor,” a prime effect of amphetamines, and a state of being that was important to him.

In athletic events, long-standing records fell after amphetamines became available; speculation exists about whether diet and training were solely re- sponsible for a sudden burst of feats that no human had ever been able to perform. We know for sure that racehorses were doped with amphetamines in that era.

The wartime habit of using amphetamines to increase worker productivity made a peacetime transition in Japan and Sweden, where amphetamine abuse became a major concern in the 1950s. In the United States concern also grew with publicity about dangerous ingestion of these tablets by exhausted long- haul truckers. Even though federal officials had cracked down on “upper” sales at truck stops and gas stations, in 1965 the Interstate Commerce Com- mission (ICC) described amphetamines as a serious threat to motorists sharing the road with trucks, a claim disputed by the American Trucking Association.2

Reports that a drug is used for recreation traditionally raise suspicions about it in America, and an undercurrent of such reports about amphetamines picked up strength in the 1950s. Members of New York’s fashionable “beau- tiful people” who used the drug were called the Benzedrine Set, and in Hol- lywood the tablets were called “Dolls.” Connoisseurs began dosing themselves simultaneously with barbiturate depressants for what was called “a bolt and a jolt.” At the social scale’s other end, investigators confirmed a brisk business at various prisons where guards were illicitly selling inhalers to prisoners. Outside the jails, crimes against property and persons were attributed to in- halers.

Although restrictions governed sales of inhalers, they were officially non- prescription and priced under a dollar. One inhaler would yield the equivalent of 25 Benzedrine tablets. The original manufacturer of amphetamine sulfate, along with competitors who produced the drug, tried to mix substances into inhalers that would thwart misuse. Abusers found ways to overcome those deterrents, however.

Hearing about alleged results of amphetamine abuse may have been exotic entertainment for most Americans, but they became alarmed by stories of pleasure usage by youths. Inhaler parties by teenagers became so notorious around Kansas City, Missouri, that a U.S. senator introduced federal legisla- tion to curb inhaler sales (Kansas City merchants were retailing hundreds more a week than would be expected in a medicinal context).3 Pharmaceutical companies began withdrawing brands from the market, and in 1959 the U.S. Food and Drug Administration (FDA) announced that the product would henceforth be available by prescription only.

In the 1960s amphetamines received publicity as an element of the hippie pharmacopeia, with that association promoting disdain for a type of drug that had originally been welcomed by ordinary people. Illicit usage of injectable amphetamines became known as “speeding,” a reference to hyperactivity re-

14 The Encyclopedia of Addictive Drugs

sulting from such needle work. Federal authorities placed new restrictions on these stimulants during the 1960s. Varieties available from drugstores de- clined, as did physicians’ ability to prescribe them. The 31 million prescrip- tions made in 1967 comprise a number never equaled since.

Amphetamines stimulate the central nervous system (the brain and associ- ated anatomy). At one time evidence of damage to nerve cells was not clear enough to satisfy some credible researchers that such a hazard exists, despite any theoretical reasons for concern, but in the 1990s evidence was becoming persuasive. Among other things, researchers have found that persons who continually abuse amphetamines and persons with a certain type of organic brain injury (“focal damage to orbitofrontal PFC [prefrontal cortex]”) have similar problems in making decisions.4 Severity correlates to length of am- phetamine abuse. Nonprescription sales have long been banned in Sweden due to kidney system damage, and amphetamines are suspects in liver dam- age involving hepatitis. Amphetamines also excite the heart, increasing pulse rate and blood pressure. Normally cardiac effects are unharmful but can be risky at high doses. To a lesser extent, amphetamines help to open air path- ways in the lungs while stimulating breathing. A less welcome action can be promotion of muscle and vocal tics, causing users to jerk or cry out uncon- trollably. This problem, however, applies more to persons already troubled by tic afflictions than to persons having no such disability. Amphetamines can also cause rashes or hives. Libido can also change, perhaps involving a stronger sex drive, perhaps involving impotence.

Various foods and drugs can interact with amphetamines. Vitamin C and fruit juices lessen amphetamine effects, while common stomach antacid prep- arations increase them. Amphetamines can boost actions of widely prescribed psychological medicines called tricyclic antidepressants, an interaction also affecting heart action. Amphetamines can counteract medicines intended to control high blood pressure and can also release extra noradrenaline hormone that is stored in the bodies of people taking monoamine oxidase inhibitors (MAOIs, found in some antidepressants and some Parkinson’s disease medi- cation). That release can raise blood pressure enough to create headaches while simultaneously raising body temperature enough to kill a person. The danger of MAOI interaction is far less with oral amphetamine dosage than with intravenous injection, and some medical practitioners have simultane- ously prescribed oral forms of amphetamine and MAOI drugs, believing that probable benefits outweigh possible risks. Lithium carbonate, a medicine used to control manic behavior, can reduce central nervous stimulation caused by amphetamines.

Psychological effects vary. In addition to results that many persons would find attractive (noted above), users can also become grouchy, jittery, unable to sleep, and suspicious of other persons. Someone highly intoxicated on am- phetamines can act mixed up and pugnacious, be frightened, and have hal- lucinations. This type of drug promotes impulsive actions—not a good consequence if a user is angry and afraid. Overindulgence can leave a person tired, peevish, confused, and depressed when the drug session ends. A serious abuser can develop symptoms duplicating schizophrenia.

Over time some abusers feel a need to increase dosages in order to get the

Drug Types 15

same effects that lower doses once provided. That suggests an abuser has developed “tolerance” to the drug, a classic component of addiction. In con- trast to abusers of other drugs, amphetamine abusers commonly fight toler- ance not by gradually increasing their dose but by alternating between periods of little use and binges of massive use, a practice promoting inconsistent be- havior that can bewilder acquaintances. Despite all of this, into the 1980s am- phetamines were described as not addictive.

Although amphetamines have a long history and widespread usage, their potential for causing cancer is unknown; necessary animal experiments had not been conducted as the twentieth century closed. Abnormal fetal devel- opment has occurred in mice receiving over 40 times the maximum safe hu- man dose, but normal development of offspring has occurred despite administration of 12.5 times the maximum human dose to rats and 7 times the maximum to rabbits.5 One human study noted a tendency for more cleft palates than usual if mothers used amphetamines during the first two months of pregnancy.6 Amphetamines easily pass from a pregnant woman into the fetal blood supply. Standard medical advice cautions pregnant women against using the drug without first discussing the issue with a physician. Some stud- ies claim to find that children born of women who abused amphetamines during pregnancy will have long-term problems with personality and intelli- gence—but these same women abused other drugs as well; some were dis- pleased about their pregnancies; and about 80% of children in one study had been taken away from the mothers and put into foster homes.7 Problems faced by such youngsters may well originate outside amphetamines. Tracking am- phetamines’ physical effect on offspring is easier. Babies from women who abused amphetamines during pregnancy can exhibit anxiety and physical dis- comfort suggesting dependence and withdrawal. We know that excessive use by a pregnant woman can promote premature birth and reduce a newborn’s weight. Genetic predisposition appears to influence how much this type of drug will affect fetal development.

Amphetamines enter human milk and can reach levels three to seven times higher than shown in maternal blood, so nursing mothers can be dosing their infants. Because this kind of drug can act as an appetite suppressant, causing a person to take in inadequate nutrition, that effect is still another concern if infants receive amphetamines through a mother’s milk.

For information about specific amphetamine class stimulants, see alphabet- ical listings for: dextroamphetamine, ephedrine, khat, ma huang, metham- phetamine, methcathinone, and methylphenidate.

Anorectic Class

Many persons in the United States consider themselves overweight. That self-perception may be more prevalent than obesity itself, but even so, by medical standards a good 33% to 50% of Americans are overweight.8 That condition can aggravate or even cause serious physical afflictions such as di- abetes, high blood pressure, and heart disease. Persons seeking slimness and who are dissatisfied with results from changes in diet and exercise may seek pharmacological help.

16 The Encyclopedia of Addictive Drugs

The first diet drug to receive scientific endorsement was thyroid hormone. Its use for this purpose began in the 1890s on the theory that it would boost a person’s metabolism and thereby promote faster use of calories. The same theory made dinitrophenol a standard diet drug before World War II. Al- though it boosted metabolic rate, it also boosted rates of cataracts and of harm to the peripheral nervous system (which involves the functioning of various organs and muscles). For those reasons the drug was abandoned. In the 1930s amphetamines became available and quickly became a popular diet aid de- spite their potential for abuse.

Many stimulants suppress appetite, and some are used as medicines to help people lose weight. Those medicines are called “anorectics.” Their stimulant effects may be lower than drugs in other classes but can still have potential for abuse and addiction. For that reason, many anorectics are scheduled sub- stances.

Such drugs are casually described as appetite suppressants, but not all pro- mote weight loss in that way. For instance, some may affect the way food is absorbed in the body; some increase a person’s rate of metabolism so the person burns more calories; some make a person more physically energetic. Question has even been raised about whether a stimulant’s anorectic action simply comes from elevating the mood of depressed people and thereby re- ducing their need to gain comfort from eating. Mechanisms by which anorec- tics work are poorly understood.

Indeed, whether they work at all is uncertain. Compared to placebos, most studies show additional weight loss among persons taking anorectics to be measurable but barely noticeable; some studies show anorectics to be no more effective than placebos. In experiments where anorectics work well, skeptics wonder if results come from factors other than the drug, such as rapport between physician and patient, belief that the substance would work, or even from basics such as controls on food intake during the experiment. Scientists directing one study of anorectics concluded that sensations of appetite sup- pression were so subtle that a user could miss them unless the person was trying to be aware of them.9 The effectiveness of an anorectic declines as weeks go by, through development of tolerance. A telling exception to development of tolerance is methylcellulose, an unscheduled substance used to increase bulk of consumed food and thereby increase the physical feeling of fullness. The substance has no psychological effect, and no tolerance develops. Meth- ylcellulose is also among the least effective dieting aids.

Abusers of stimulant anorectics exhibit symptoms similar to those found among abusers of amphetamines, from skin rash to psychosis. Some persons using anorectics properly under medical supervision experience muscle pain and cramps, weariness, peevishness, depression, difficulty in thinking. That group of symptoms is the same as those undergone by persons trying to cope with lack of food regardless of drug use, a coincidence raising question about whether some undesired effects attributed to anorectics are simply undesired effects of being hungry.

A harsh fact about anorectics is that weight lost while using them tends to return if a person stops taking the drugs (and generally they are intended for short-term use only). Behavioral therapy teaches people how to change their

Drug Types 17

eating and exercise habits. A comparison study10 not only found behavioral therapy superior to anorectic therapy in preventing regain of lost pounds but also found behavioral therapy to be more effective alone than when using anorectics along with it—a troubling result for advocates of anorectics. Skep- tics ask whether drugs that produce only mild temporary improvement in a chronic condition are worth anything.

For information about specific anorectic class stimulants, see alphabetical listings for: benzphetamine, diethylpropion, fenfluramine, mazindol, phen- dimetrazine, phenmetrazine, phentermine, and sibutramine.

Cocaine Class

As decades change, so do attitudes toward cocaine. In the latter 1800s it was widely used by ordinary middle-class Americans and had a reputation no worse than alcohol or tobacco. In the years before World War I, news media stories tied the drug to African Americans and crime, and public opin- ion transformed the substance from a commonplace item into a substance used mainly by social deviants. Cocaine received little attention from the 1960s illicit drug culture, which seemingly considered cocaine an archaic item no longer of interest. In the 1970s cocaine was portrayed as a drug used by wealthy “beautiful people,” and in the 1980s it was portrayed as a poor ghetto dweller’s drug. In the 1800s cocaine was considered highly addictive, but from the 1950s into the 1980s it was described as nonaddictive. By the 1990s cocaine was called the most addictive drug known, and demand for the product re- sulted in accessibility likened to fast-food hamburgers. Although tolerance develops with abuse of most stimulants and was reported with cocaine in the 1800s, in the 1970s and 1980s a scientific consensus held that tolerance did not develop among cocaine abusers. On the contrary, abuse was believed to sen- sitize people taking the drug, allowing them to achieve the same effects with smaller and smaller doses. Yet by the 1990s cocaine addicts were believed to have a compulsive desire to take more and more of the drug. They were seen to engage in the same kind of binge habit exhibited by amphetamine abusers.

Although a chemical formula stays unaltered as decades pass, ways of using a substance can change. Long ago cocaine was used to make mildly stimulat- ing drinks. Velo-Coca and Vin Mariani were popular cocaine beverages of the nineteenth century, the latter endorsed by notables such as Thomas Edison, Jules Verne, and Pope Leo XIII. The soft drink Coca-Cola originally contained cocaine, but the drug was dropped from the soda early in the twentieth cen- tury. These old beverages, however, had about the same relation to cocaine as beer has to white lightning moonshine. A pint of beer and a pint of white lightning may both contain alcohol, but their impact on a user will likely differ. Compared to full-strength pharmaceutical cocaine, old cocaine bever- ages were relatively weak concoctions.

Some notables are famed for their use of the full-strength product, the most famous example being that of the pioneering psychiatrist Sigmund Freud. When he no longer found the drug useful, he tapered off and eventually quit with no particular difficulty. His example has been duplicated by many other users. He and they were persons enjoying lives of fulfillment in which cocaine

18 The Encyclopedia of Addictive Drugs

was simply one part. In contrast, persons who are dissatisfied with their lives, for whom cocaine brings relief of unhappiness, may face a harder struggle in giving up the drug if it begins degrading the quality of their lives. The more needs a drug satisfies for a person, the stronger its appeal. Some needs may be biological; a study of identical twins finds their cocaine usage patterns to be remarkably similar.11 Some needs may derive from a person’s life situation.

Cocaine abuse is normally part of a multiproblem lifestyle. A study of homeless cocaine abusers found that achieving abstinence was easier for them if they obtained shelter and employment.12 Compared to the whole popula- tion, cocaine addicts are much likelier to be addicted to gambling as well.13 Alcoholism and suicidal thoughts increase the likelihood that a person who uses cocaine will become addicted.14 One study of persons being treated for cocaine abuse found over one half to be jobless and over one third to have jail records.15 A survey of crack smokers found that over one third had been physically attacked over a one-year period.16 Five years of records at one hos- pital showed the following primary reasons for admission of cocaine-using patients: assaults, stabbings, and bullet wounds.17 Such persons obviously face serious challenges other than cocaine; any inability to cope with the drug is but a single element in a general inability to cope with life.

For information about specific cocaine class stimulants, see alphabetical list- ings for: coca and cocaine.

Pyridine Alkaloids Class

Tobacco and areca nut are the most widely used substances containing drugs from this class. Although most Americans think of tobacco’s nicotine as a recreational drug, it has had agricultural functions as a pesticide and for ridding farm animals of worms. Nicotine is readily absorbed through the skin and causes “green tobacco sickness” among farmworkers who handle leaves, a poisoning sometimes severe enough to require hospitalization. The tobacco plant has been known to kill livestock that eat it. Humans have also been poisoned when attempting to use tobacco as food, such as by boiling greens.

Tobacco apparently originated in the Americas, where native peoples did not seem to regard it as a recreational substance. Their uses were spiritual and medical. Even in the twentieth century some native peoples used tobacco to treat conditions ranging from chills to infections and snake bites. When Europeans discovered tobacco in the New World, they removed it from the cultural context in which its primary uses had been medical and spiritual. Used without those restrictions, hazards became obvious soon enough. Lack- ing the shared social values that had long limited tobacco’s use in the New World, Europeans attempted to control the substance by law. Property of cul- tivators and traffickers became subject to forfeiture in Hungary and Russia and even Japan. In the 1600s smoking was condemned by the pope and by King James of England, and smokers were condemned to death in Turkey, Iran, Russia, and some German states. Legal harshness, however, was unable to substitute for the social values that had limited consumption in lands where tobacco originated.

We often measure drug addiction by the amount of drug used, assuming

Drug Types 19

that the more a person uses, the stronger the drug’s hold. Researchers have found this assumption to be incorrect for nicotine. Measured by strength of dependence symptoms, a person who smokes more than a half pack of tobacco cigarettes each day may be no more addicted than a person who smokes just half a pack,18 meaning the lighter smoker may have just as much trouble quitting as the heavier smoker.

Among cigarette users, the amount of smoking depends in part on the to- bacco’s nicotine content, but other factors are also involved. During the 1990s in the United States female smokers tended to have a higher degree of tobacco addiction than male smokers did (measured not in number of cigarettes smoked but in strength of addiction symptoms such as tolerance, withdrawal, and difficulty in reducing consumption).19 Whites had stronger levels of ad- diction than did members of other races.20 Adolescents tended to smoke fewer cigarettes than middle-aged persons, but despite adolescents’ lower usage, their addiction symptoms were just as strong as those found in heavier- smoking middle-aged persons.21 Older smokers were the least addicted even though they were the heaviest users.22 Researchers are unsure whether such differences are caused by biology or culture or a combination.

In the United States tobacco smoking is associated with being an adult, and adolescents may take up the practice partly as a symbol of their passage into adulthood. Role models are also important; a prominent person who smokes may inspire admirers to do so. Celebrity endorsements of cigarettes were once routine in advertising, but the admired person can also be a personal acquain- tance. A survey in Spain revealed that the role model of teachers who smoke seems to be a major factor in starting the habit among students there.23

The popularity of smoking among American teenagers declined in the 1970s and 1980s but increased in the 1990s. A cancer statistics authority reported that by 1997 over 33% of American high schoolers were using cigarettes.24 A study of Taiwanese high school students published in 1999 found a much lower usage rate, more like 10%.25 In 1999 a survey of over 14,000 young adult American college students found about 33% using some sort of tobacco prod- uct, mostly cigarettes.26 The latest statistics can be found through the “Sources for More Information” at the end of this book.

For information about specific pyridine alkaloids class stimulants, see al- phabetical listings for: areca nut and nicotine.


Depressants generally have the opposite effect of stimulants. Many depres- sants are used as sedatives or tranquilizers, terms often used as if they mean the same thing even though some experts would dispute such interchangeable usage of the terms sedative and tranquilizer. Depressant drugs slow a person down, and one result can be reduction of tension, which in turn can improve a mentally depressed mood. Depressant withdrawal symptoms typically in- clude uneasiness and sleeping difficulty. If dependence is strong enough, withdrawal may also involve tremors, loss of strength, delirium, and seizures. Gradual reduction in dosage may help avoid withdrawal symptoms, but much depends on the particular drug and the strength of dependence.

20 The Encyclopedia of Addictive Drugs

For information about specific depressants not listed among the following classes, see alphabetical listings for: alcohol, chloral hydrate, ethchlorvynol, GHB, glutethimide, ketamine, mandrake, meprobamate, methaqualone, PCP, pentazocine, zaleplon, and zolpidem.

Barbiturate Class

Barbiturates were introduced into medical practice during the early 1900s, for combating insomnia, anxiety, and seizures. Despite occasional flurries of concern, not until the 1960s did much alarm grow about barbiturates in the United States. Members of a U.S. Senate subcommittee began portraying the drug class as a menace in the 1970s, and afterward stricter controls were put on use.

Barbiturates and alcohol have similar effects. If someone intoxicated by al- cohol takes barbiturates, the drunkenness will deepen as if more alcohol had been swallowed. Pharmaceutical effects of alcohol alone can kill a person who overdoses, and adding barbiturates can transform a session of social drinking into a fatal one. More than one person has died by taking barbiturate sleeping pills with alcohol instead of water.

The similarity of alcohol and barbiturates is also shown by the appearance of a serious withdrawal syndrome called delirium tremens in alcohol and barbiturate abusers who are cut off from their drug. Lesser withdrawal symp- toms for both drugs may include perspiring and vomiting. Barbiturate with- drawal may involve dizziness, tremors, fidgety behavior, edgy feelings, and insomnia. Even with strict medical supervision, withdrawal can be fatal. Tol- erance can develop. More details can be found in alphabetical entries for spe- cific barbiturates.

A person using barbiturates should take the same precautions as a person using alcohol, for example, using care about running dangerous machinery such as automobiles.

Barbiturates can cause reflex sympathetic dystrophy of the arm, a disease in which a hand loses bone density and becomes painful and difficult to move. This class of drugs may also cause a syndrome that produces pain in the shoulder and hand, interfering with their movement. Extended dosage with barbiturates may cause rickets, a disease in which bones soften. One of the most dangerous effects of barbiturate overdose is temporary stoppage of elec- trical activity in the brain, which could lead to premature declaration of a patient’s death, particularly if the patient is being treated for some injury without caregivers knowing about the person’s barbiturate usage.

This class of substances may interfere with blood thinner medicine, with birth control pills, and with other female hormone medications. Barbiturates may extend the time that an MAOI dose lasts.

In animal experiments barbiturates have encouraged the development of cancer.

When used by pregnant women, barbiturates can cause birth defects rang- ing from internal organ deformities to malformations of the face. If a pregnant woman uses barbiturates regularly, her offspring may be born resonant with

Drug Types 21

them. This class of drugs passes into the milk of nursing mothers and may depress consciousness, pulse rate, and respiration of nursing infants.

For information about specific barbiturate class depressants, see alphabetical listings for: butalbital, mephobarbital, pentobarbital, and phenobarbital.

Benzodiazepine Class

Benzodiazepines became widely available for medical purposes in the 1960s and replaced barbiturates in treatments of many conditions. Benzodiazepines proved themselves less prone to abuse than barbiturates, in addition to being safer—accidental overdose is unlikely because the amount needed for a med- ical effect is so much smaller than a poisonous amount. In addition to reducing anxiety, benzodiazepines may improve quality of sleep—from fighting insom- nia to eliminating sleepwalking. This class of drugs is also used to calm people and to treat convulsions. Some users experience mild euphoria.

As might be expected with drugs that promote sleep, benzodiazepines can worsen reaction time, vigilance, and thinking abilities and therefore should be used cautiously if a person is operating dangerous machinery such as an au- tomobile. Problems may also develop for persons who are already unsteady on their feet, such as elderly persons prone to falling. The substances can also cause memory trouble, typically difficulty in recalling recent experiences. Headache, peevishness, confusion, and tremors may occur. In unusual cases rageful outbursts may occur. These are “paradoxical reactions,” meaning they are the opposite of what would be expected from the drug. Expressions of rage possibly emerge because the drug reduces anxiety in a person who is angry about something, and less anxiety can lead to less inhibition against doing something.

Over a 12-year span a practitioner observed patients taking benzodiazepines to treat serious sleep problems such as night terrors and sleepwalking. The practitioner found that 2% of this population (not 2% of all patients but just those using benzodiazepines against these sleep disorders) occasionally abused them,27 and this population base included persons with a previous history of drug abuse; thus we can expect benzodiazepine abuse to be even lower in a general population. Among persons treated for drug abuse, ben- zodiazepines are among the least-abused substances. Experiments giving free access to benzodiazepines to persons undergoing treatment for drug abuse revealed little interest in those compounds.28 This class of depressants can be highly popular among special populations, however. One study noted that 30% of alcoholics were using benzodiazepines.29 When benzodiazepines were given to rats in experiments, the animals’ consumption of alcohol increased,30 suggesting that human benzodiazepine usage might increase alcohol’s appeal. Although benzodiazepines are administered to treat alcohol withdrawal, com- bining the two substances recreationally is a dangerous mix that can prove fatal.

Different benzodiazepines have differing attractiveness to abusers. Mea- sured by amount of misuse, claims made by misusers about drug effects, men- tal and physical effects verified in scientific experiments, and impressions reported by medical caregivers, diazepam is considered to have one of the

22 The Encyclopedia of Addictive Drugs

greatest potentials for abuse. Alprazolam and lorazepam have similar, but lower, risk. Halazepam and oxazepam seem to be among the least risky for abuse.

Tolerance to some benzodiazepine effects can develop (many details are in this book’s alphabetical section). Dependence can also emerge, with a with- drawal syndrome similar to those of alcohol and barbiturates. Often the syn- drome may be avoided by gradual reduction of dosage.

Small studies have found that women who use benzodiazepines during pregnancy produce infants who are smaller than normal.31 Children in one of these studies32 rapidly caught up in some growth perimeters, but at the age of 18 months head size still remained smaller than normal. Facial deformities were common. The children had persistent trouble with muscle control. Sim- ilar findings in another small study33 included mental retardation, but still another study34 noted that such children also had heavy fetal exposure to alcohol, exposure that is known to produce mental retardation. Thus the actual role of benzodiazepines was unclear.

Some of these reports did not track outcomes past infancy. Research track- ing children up to four years of age found that early problems attributed to benzodiazepines cleared up in most of them.35 When teachers were asked to evaluate schoolchildren who had fetal exposure, the instructors found no dif- ference between them and classmates.36

Researchers who investigated the outcome of thousands of pregnancies found no evidence that benzodiazepines cause cleft palate.37 A large study involving hundreds of pregnancies found birth defects to be no more likely among women who used benzodiazepines than among women who did not use them; and even when malformations occurred, no particular kind of birth defect tended to appear in benzodiazepine offspring.38 Drugs that cause fetal harm generally cause particular types of damage; lack of a particular type with benzodiazepines suggests that the drug was not the cause of observed malformations. Some investigators believe they have detected a particular birth defect pattern, but such findings have been questioned.39 As the twenty- first century began, a research team reported evidence that benzodiazepines may damage fetal brain development.40 Science has not yet rendered a verdict on the safety of benzodiazepines during pregnancy. Infants with fetal expo- sure can be born dependent on this type of drug. It passes into breast milk, but the amount from lower-dosage levels probably has no effect on nursing infants.

For information about specific benzodiazepine class depressants, see alpha- betical listings for: alprazolam, chlordiazepoxide, clonazepam, clorazepate, diazepam, estazolam, flunitrazepam, flurazepam, halazepam, lorazepam, midazolam, oxazepam, prazepam, quazepam, temazepam, and triazolam.

Opiate Class

Along with alcohol, opiates are the oldest known depressants. At one time the term narcotic referred specifically and only to opiates, but when drug con- trol laws were strengthened in the early twentieth century the language of

Drug Types 23

those laws expanded the dictionary definition of narcotic and made it a syn- onym for all controlled drugs.

Although opiates have various medical uses, the main therapeutic appli- cation is pain control. Other common uses are for fighting coughs and reduc- ing diarrhea. Some other therapeutic uses of specific opiates are given in this book’s alphabetical listings of drugs.

The chance of medical opiate usage turning a person into an addict is slim. Very few persons receiving medical opiates find them attractive, and almost all patients who enjoy opiates already have a drug abuse problem. Researchers examined records of 11,882 patients who received narcotics and found 4 with a subsequent addiction problem who lacked a prior drug addiction history.41 The chance of developing dependence is higher, but a patient can be weaned off opiates in ways that avoid withdrawal symptoms.

Illicit users of opiates generally seek to achieve a mental state of indifference in which problems and frustrations no longer feel bothersome. A person high on opiates is oblivious to the world and unlikely to bother anyone. Some users experience euphoria.

Classic unwanted actions from opiates are constipation, urinary difficulty, low blood pressure, and breathing trouble. MAOI drugs, described earlier, may interact dangerously with opiates. In contrast to such problems, a desir- able drug interaction is that opiates may boost pain relief from aspirin.

Originally the phrase “being hooked on a drug” referred to being so reso- nant with (that is, dependent on) an opiate that a withdrawal syndrome oc- curred if dosage stopped. Symptoms of opiate withdrawal are similar to those of influenza: sweats, goose bumps, muscle aches, cramps, runny nose, diar- rhea, and sleep difficulties. Although conscienceless and irresponsible addicts may be particularly short-tempered and dangerous if undergoing withdrawal, for other persons the experience is miserable, but not horrible, and usually lasts only a few days. Traditionally those few days are the extent of with- drawal, but some authorities believe a subsequent stage of withdrawal occurs in which a person experiences aches, insomnia, and grouchiness for several months. Such symptoms, however, may simply be signs that the psychological buffer provided by opiate use is no longer available.

Drug addiction “maintenance” programs are designed to supply enough drug to hold off withdrawal but not enough to produce recreational sensa- tions. Unless participants supplement the legal dosage with illicit supplies, such persons will not experience opiate effects enjoyed by addicts. Someone on a maintenance dose can adequately perform job duties and safely operate a motor vehicle. Performance may not be as sharp as in a drug-free state, but performance is in the normal range.

Opiates have a wide range of effects on fetal behavior. If a pregnant woman uses opiates regularly the fetus soon adapts to the presence of the drug and seems to develop normally, although an infant can be born resonant with (that is, dependent on) the drug and undergo withdrawal. Intermittent use of opi- ates is more damaging to a fetus than regular use, with the changing drug environment causing extra stress as a fetus copes with one condition and then another. Opiates cause fetal metabolism to increase, diverting energy away from body development. Infants born to opiate users are commonly smaller

24 The Encyclopedia of Addictive Drugs

than normal, and early slowness of brain development has been observed. Evidence exists that fetal exposure causes long-lasting problems in children, involving impulsiveness and inattention, but some researchers feel that home environment (often involving a single-parent opiate abuser with additional problems) is a better explanation for those difficulties.

For information about specific opiate class depressants, see alphabetical list- ings for: buprenorphine, codeine, dihydrocodeine, etorphine, heroin, hy- drocodone, hydromorphone, morphine, nalbuphine, opium, oxycodone, pholcodine, and thebaine.

Opioid Class

Opioids are often called opiates, which is satisfactory for practical purposes because the two classes of drugs basically produce the same effects in the same way. A technical difference exists between the two classes, however. If the history of a product were traced backward through its manufacturing processes, opiates generally would begin with the opium plant, but opioids would generally begin in a laboratory. Despite this technical distinction, the terms opiates and opioids are often used synonymously. Some of these sub- stances are called “semisynthetic” and are referred to as “opiate/opioid.” Some opiates, such as morphine, can even be manufactured wholly in a lab- oratory without starting from the natural product opium; thus the same chem- ical can be either an opiate or an opioid.

For information about specific opioid class depressants, see alphabetical list- ings for: butorphanol, dextromethorphan, dextromoramide, dextrorphan, di- phenoxylate, dipipanone, fentanyl, ketobemidone, LAAM, levorphanol, meperidine, methadone, oxymorphone, phenoperidine, piritramide, propox- yphene, remifentanil, and trimeperidine.


The steroids governed by schedules of controlled substances are anabolic steroids. Anabolic substances build up parts of living organisms, as opposed to catabolic substances, which decompose those parts. Anabolic steroids are abused mainly by persons desiring to increase muscle mass, such as compet- itive athletes and body builders. Steroids can improve muscle strength in fe- males and in castrated males, but scientific evidence is weaker for intact males. Still, steroids do seem to promote muscle mass, endurance, and overall athletic performance while dosage continues. Some scientists suspect that any perfor- mance enhancement experienced from anabolic steroids comes not from mus- cle power but from psychological effects, with the drugs increasing a user’s aggressiveness. Anabolic steroids can produce mania, anger, impulsiveness, euphoria, and feelings of invincibility—a combination that may lead some users into harmful social interactions. The combination can produce other types of unwise behavior as well, such as extravagant expenditures of money and taking reckless physical risks. Reports exist of paranoia and hallucinations developing while using steroids and disappearing when steroid usage is stopped.

Drug Types 25

Sports governing authorities banned the use of anabolic steroids by com- petitors. Some athletes ignore the ban in hopes of avoiding detection. Various other drugs are prohibited as well, but in 1988 most of the failed drug tests ordered by the International Olympic Committee revealed anabolic steroids, the most common one being nandrolone.42 Below that elite level, athletic use of steroids seems uncommon. In the 1990s a study involving 58,625 college students found only 175 steroid takers to study.43 That small group also had a much higher consumption of other drugs, legal and illegal, than the average student—suggesting that the steroid abusers were predisposed to use drugs for coping with all sorts of life situations, not just sports. Similar association of steroids with other illicit drug usage is found at the high school level.44 High school steroid statistics are often based on the concept of “lifetime use.” Lifetime use means a person has taken a steroid at least once, which is not the same as regularly taking them. The number of regular users will be much smaller than the number of “lifetime” users.

Anabolic steroids are related to testosterone. Most, if not all, are androgens, substances promoting male characteristics. A female who uses those drugs may develop facial hair and a deeper voice, along with unwanted changes in sexual organs. In a young person who is still growing, androgens can pre- maturely halt further growth and thereby cause a smaller adult stature. Among persons of either gender and any age, androgens may alter blood composition and increase the body’s retention of various minerals. That re- tention is not necessarily good. For example, sodium retention promotes bloat- ing and can be inadvisable for persons with heart trouble. Liver damage and reduction of male fertility may occur due to anabolic steroids. Extended use of the substance may worsen cholesterol levels, thereby narrowing blood ves- sels, and such narrowing promotes heart attack and stroke years later. Steroid abusers tend to take far higher doses than are considered medically safe, thus further increasing the risks. Oral and slow-release under-the-skin implant for- mats of anabolic steroids can be processed in ways that will physically permit them to be injected. Such a practice is highly dangerous, as noninjectable for- mats of drugs have components that are not designed for direct introduction into the bloodstream.

Anabolic steroid dependence is reported with withdrawal symptoms that can include weariness and depression. Use by a pregnant woman can per- manently masculinize a female fetus.

For information about specific anabolic steroids, see alphabetical listings for: boldenone, ethylestrenol, fluoxymesterone, methandriol, methandrosteno- lone, methyltestosterone, nandrolone, oxandrolone, oxymetholone, stano- zolol, testolactone, testosterone, and trenbolone.


Although various drugs cause hallucinations, some drugs are so notable for such an effect that they are classified as hallucinogens. Controversy exists about what a hallucination is. Is it a bluish tint to colors in a normal scene? Is it wavy motions in a solid and stationary object? Is it shapes in fireplace flames transforming into animal heads? Is it something that goes away if

26 The Encyclopedia of Addictive Drugs

someone’s eyes open? Is it a creature that appears out of nowhere and pro- vides mystical insights? Is it sensations of floating? Is it a different flow of time? Is it cross-wiring of senses, where colors are heard and smells are seen? Specialists may quibble, but this book classifies all such experiences as hal- lucinations.

Many people dislike hallucinatory experiences, especially people who like to be in control of themselves and of situations around them. Such people often find hallucinations not only unpleasant but downright frightening. Other people find the sensations intriguing and pleasurable.

Scientific interest in hallucinogens began to emerge in the 1800s, blossoming in the 1950s and 1960s. In those latter times hallucinogens were popularly identified with beatniks and hippies, and social disapproval of those lifestyles promoted legal restrictions on hallucinogens that terminated almost all sci- entific research regarding these substances. Thus much of the scientific data is old.

For information about specific hallucinogens, see alphabetical listings for: AET, amanita, belladonna, bufotenine, DET, DMT, DOB, DOM, dronabi- nol, ergot, ibogaine, jimson weed, LSD, marijuana, MDA, MDEA, MDMA, mescaline, morning glory, nutmeg, peyote, psilocybin, 2C-B, and yage.


Although some authorities consider inhalants to be depressants, and inha- lants have hallucinogenic qualities, for several reasons this book lists inhalants as a substance type in their own right. First, despite easy availability, inhalants are among the most dangerous of abused substances. There is no range of inhalants, some of which are benign and some of which are risky, as there is with stimulants or depressants. All inhalants are dangerous despite wide var- iations in their chemistry, and this sets them apart from other types of drugs. Second, inhalants are generally used by inhaling them in their gaseous state (which is not the same as smoking and also differs from eating a solid or drinking a liquid). That dosage format sets them apart from other drugs. Third, inhalants are used mainly by younger persons (typically teenage males), a usage pattern that also sets inhalants apart from other drugs.

With some inhalants the amount needed to produce a recreational effect is close to a fatal dose, and deadly outcomes demonstrate that the difference was too close for some deceased users to handle. In addition, strenuous exercise seems related to inhalant death, troublesome for users at dance clubs. The products are often flammable, sometimes producing serious physical injury unrelated to pharmacology. Some users act as if they do not realize they need a continual supply of oxygen, and they administer inhalants in ways that cause suffocation. In addition to all these acute dangers, long-term use of many inhalants can produce nerve damage, impairing the ability to use arms and legs and hands and feet, damage verified scientifically. Another type of long-term damage appears to be assorted types of psychoses. This conse- quence is harder to verify because inhalant users often take other potent drugs, so proving which mind-altering drug affected the mind can be very difficult. Unquestionably, however, inhalant users can develop states of mind interfer-

Drug Types 27

ing with—or even preventing—their ability to function in society. Admittedly, some users avoid serious outcomes, just as some car drivers run red lights without harm. Escape, however, does not mean that danger should be disre- garded.

Generally, adult drug users shun most inhalants except as a choice of des- peration if nothing else is available. Inhalant users tend to be teenagers or younger, perhaps because other drugs of abuse (even alcohol and tobacco) are harder for some young persons to obtain. Sniffing is often a social event with acquaintances rather than a solitary pastime. As the 1960s began, the average age among 130 glue sniffers in Denver was 13.45 In this group 124 were male; most were lower-class Hispanics in trouble with school or law enforcement authorities; many had emotional problems. Another study found glue sniffers to have personalities matching those of alcoholics.46 Gasoline sniffers are often emotionally deprived teens from troubled families, typically living lower-class lives in rural areas, often members of native populations whose cultures have been devastated (American Indians in the United States, aborigines in Aus- tralia, Island peoples in the Pacific). Case studies of butane sniffers tell of lonely persons with difficulties at school or at home. A psychological test of 59 inhalant abusers47 found them to be impulsive persons with little respect for authority. Most research finds inhalant users to be unhappy persons mar- ginalized by society. Yet not all researchers find that inhalant users are social misfits from dysfunctional families; some appear to be ordinary persons, though still youthful.

That difference in findings—most researchers saying inhalant abusers are social misfits, with some researchers contending inhalant abusers are normal— deserves an attempt at explanation. Many inhalant researchers work where inhalant abuse has been publicized as a major community problem, and those places tend to have populations of socially marginalized people. Researchers commonly study persons receiving medical attention for inhalant abuse, and sometimes the medical attention is received involuntarily by court order. Such persons may be no more typical of inhalant users than hospitalized alcoholics receiving court-ordered treatment are typical of most alcohol users. And the definition of “user” may influence understanding. A user who sniffs several times a day is not the same kind of user who sniffed with some friends once or twice over a period of several years. Although most research finds inhalant abusers to be troubled outcasts, it is possible that such typical findings are due to the demographics of the population being studied.

For information about specific inhalants, see alphabetical listings for: bu- tane, ether, freon, gasoline, mothballs, nitrite, nitrous oxide, TCE, and tol- uene.


1. W.P. Czerwinski, “Amphetamine-Related Disorders,” Journal of the Louisiana State Medical Society 150 (1998): 491; R. Reeves, “President’s Health the Great Coverup of JFK Years,” Kansas City Star, Oct. 11, 1992, K4; R. Reeves, President Kennedy: Profile of Power (New York: Simon & Schuster, 1993), 178, 243, 648n. 146; T.C. Reeves, A Question

28 The Encyclopedia of Addictive Drugs

of Character: A Life of John F. Kennedy (New York: The Free Press, 1991), 295–96; C.D. Heymann, A Woman Named Jackie (New York: Lyle Stuart, 1989), 296–319.

2. R. King, The Drug Hang-up (New York: W.W. Norton, 1972), 271, 283–85.

3. C.O. Jackson, “The Amphetamine Inhaler: A Case Study of Medical Abuse,” Journal of the History of Medicine and Allied Sciences 26 (1971): 187–96. The author is also indebted to Jackson’s article for other colorful examples of amphetamine’s history.

4. R.D. Rogers et al., “Dissociable Deficits in the Decision-making Cognition of Chronic Amphetamine Abusers, Opiate Abusers, Patients with Focal Damage to Pre- frontal Cortex, and Tryptophan-Depleted Normal Volunteers: Evidence for Monoam- inergic Mechanisms,” Neuropsychopharmacology 20 (1999): 322–39.

5. “Adderall,” “Dextrostat,” and “Dexedrine,” in Physicians’ Desk Reference, 56th ed. (Montvale, NJ: Medical Economics Company, 2002), 1513, 3231, 3237.

6. L. Milkovich and B.J. van den Berg, “Effects of Antenatal Exposure to Anorectic Drugs,” American Journal of Obstetrics and Gynecology 129 (1977): 637. See also M.A. Plessinger, “Prenatal Exposure to Amphetamines: Risks and Adverse Outcomes in Pregnancy,” Obstetrics and Gynecology Clinics of North America 25 (1998): 119–38.

7. L. Cernerud et al., “Amphetamine Addiction during Pregnancy: 14-Year Follow- up of Growth and School Performance,” Acta Paediatrica 85 (1996): 204–8; L. Billing et al., “The Influence of Environmental Factors on Behavioural Problems in 8-Year-Old Children Exposed to Amphetamine during Fetal Life,” Child Abuse and Neglect 18 (1994): 3–9. See also M. Eriksson et al., “Cross-sectional Growth of Children Whose Mothers Abused Amphetamines during Pregnancy,” Acta Paediatrica 83 (1994): 612–17.

8. C.M. Apovian, “The Use of Pharmacologic Agents in the Treatment of the Obese Patient,” Journal of the American Osteopathic Association, pt.2, 99 (1999, Suppl.): S2–S7; W.S. Poston II et al., “Challenges in Obesity Management,” Southern Medical Journal 91 (1998): 710–20.

9. S.B. Penick and J.R. Hinkle, “The Effect of Expectation on Response to Phen- metrazine,” Psychosomatic Medicine 26 (1964): 369–73.

10. J. Mellar and L.E. Hollister, “Phenmetrazine: An Obsolete Problem Drug,” Clin- ical Pharmacology and Therapeutics 32 (1982): 672.

11. K.S. Kendler et al., “Illicit Psychoactive Substance Use, Heavy Use, Abuse, and Dependence in a U.S. Population–Based Sample of Male Twins,” Archives of General Psychiatry 57 (2000): 261–69.

12. J.B. Milby et al., “Initiating Abstinence in Cocaine Abusing Dually Diagnosed Homeless Persons,” Drug and Alcohol Dependence 60 (2000): 55–67.

13. G.W. Hall et al., “Pathological Gambling among Cocaine-Dependent Outpa- tients,” American Journal of Psychiatry 157 (2000): 1127–33.

14. C.S. Lopes and E.S. Coutinho, “Transtornos mentais como fatores de risco para o desenvolvimento de abuso/dependeˆncia de coca ́ına: Estudo caso-controle” (Mental disorders as risk factors for the development of cocaine abuse/dependence: Case- control study), Revista de Saude Publica 33 (1999): 477–86 (abstract in English).

15. Hall et al., “Pathological Gambling among Cocaine-Dependent Outpatients.”

16. H.A. Siegal et al., “Crack-Cocaine Users as Victims of Physical Attack,” Journal of the National Medical Association 92 (2000): 76–82.

17. C.R. Schermer and D.H. Wisner, “Methamphetamine Use in Trauma Patients: A Population-Based Study,” Journal of the American College of Surgeons 189 (1999): 442–49. 18. D.B. Kandel and K. Chen, “Extent of Smoking and Nicotine Dependence in the

United States: 1991–1993,” Nicotine and Tobacco Research 2 (2000): 263–74. 19. Ibid.

20. Ibid. 21. Ibid. 22. Ibid.

Drug Types 29

23. M.A. Herna ́ndez-Mezquita et al., “Opinio ́n de los directores escolares sobre la influencia de factores del medio escolar en la actitud de nin ̃ os y jovenes ante el tabaco” (Influence of school environment on student’s attitudes about tobacco consumption in the opinion of the headmasters), Anales Espan ̃oles de Pediatr ́ıa 52 (2000): 132–37 (abstract in English).

24. G.A. Giovino, “Epidemiology of Tobacco Use among U.S. Adolescents,” Nicotine and Tobacco Research 1 (1999, Suppl. 1): S31–S40.

25. M.Y. Chong, K.W. Chan, and A.T. Cheng, “Substance Use Disorders among Ad- olescents in Taiwan: Prevalence, Sociodemographic Correlates and Psychiatric Comor- bidity,” Psychological Medicine 29 (1999): 1387–96.

26. N.A. Rigotti, J.E. Lee, and H. Wechsler, “U.S. College Students’ Use of Tobacco Products: Results of a National Survey,” Journal of the American Medical Association 284 (2000): 699–705.

27. C.H. Schenck and M.W. Mahowald, “Long-Term, Nightly Benzodiazepine Treat- ment of Injurious Parasomnias and Other Disorders of Disrupted Nocturnal Sleep in 170 Adults,” American Journal of Medicine 100 (1996): 333–37.

28. D.A. Ciraulo, “Abuse Potential of Benzodiazepines,” Bulletin of the New York Academy of Medicine 61 (1985): 728–41.

29. L. Walters and P. Nel, “Die Afhanklikheidspotensiaal van die Bensodiasepiene: Toepassing van die Resultate van die Behandeling van die Alkoholonttrekkingsind- room” (The addiction potential of benzodiazepines. Application of the results of treat- ment of alcohol withdrawal syndrome), South African Medical Journal 59 (1981): 115–16 (abstract in English). See also L. Walters and P. Nel, “Pharmacological Requirements of Patients during Alcohol Withdrawal,” South African Medical Journal 59 (1981): 114.

30. A.H. Soderpalm and S. Hansen, “Benzodiazepines Enhance the Consumption and Palatability of Alcohol in the Rat,” Psychopharmacology 137 (1998): 215–22.

31. In addition to other studies cited in this paragraph, see L. Laegreid, G. Hagberg, and A. Lundberg, “The Effect of Benzodiazepines on the Fetus and the Newborn,” Neuropediatrics 23 (1992): 18–23.

32. L. Laegreid, G. Hagberg, and A. Lundberg, “Neurodevelopment in Late Infancy after Prenatal Exposure to Benzodiazepines—A Prospective Study,” Neuropediatrics 23 (1992): 60–67.

33. L. Laegreid, “Clinical Observations in Children after Prenatal Benzodiazepine Exposure,” Developmental Pharmacology and Therapeutics 15 (1990): 186–88. See also G. Viggedal, “Mental Development in Late Infancy after Prenatal Exposure to Benzodi- azepines—A Prospective Study,” Journal of Child Psychology and Psychiatry, and Allied Disciplines 34 (1993): 295–305.

34. U. Bergman et al., “Effects of Exposure to Benzodiazepine during Fetal Life,” Lancet 340 (1992): 694–96. See also J.A. Kuller et al., “Pharmacologic Treatment of Psy- chiatric Disease in Pregnancy and Lactation: Fetal and Neonatal Effects,” Obstetrics and Gynecology 87 (1996): 789–94; S.D. Silberstein, “Headaches and Women: Treatment of the Pregnant and Lactating Migraineur,” Headache 33 (1993): 536.

35. P.R. McElhatton, “The Effects of Benzodiazepine Use during Pregnancy and Lac- tation,” Reproductive Toxicology 8 (1994): 461–75.

36. L. Stika et al., “Effects of Drug Administration in Pregnancy on Children’s School Behaviour,” Pharmaceutisch Weekblad: Scientific Edition 12 (1990): 252–55 (abstract in En- glish).

37. A. Czeizel, “Lack of Evidence of Teratogenicity of Benzodiazepine Drugs in Hun- gary,” Reproductive Toxicology 1 (1987–1988): 183–88. See also Kuller et al., “Pharma- cologic Treatment of Psychiatric Disease in Pregnancy and Lactation: Fetal and Neonatal Effects.”

38. A. Ornoy et al., “Is Benzodiazepine Use during Pregnancy Really Teratogenic?”

30 The Encyclopedia of Addictive Drugs

Reproductive Toxicology 12 (1998): 511–15. See also P.R. McElhatton et al., “The Outcome of Pregnancy in 689 Women Exposed to Therapeutic Doses of Antidepressants: A Col- laborative Study of the European Network of Teratology Information Services (EN- TIS),” Reproductive Toxicology 10 (1996): 285–94.

39. L. Laegreid et al., “Congenital Malformations and Maternal Consumption of Ben- zodiazepines: A Case-Control Study,” Developmental Medicine and Child Neurology 32 (1990): 432–41; P.R. McElhatton, “The Effects of Benzodiazepine Use during Pregnancy and Lactation,” Reproductive Toxicology 8 (1994): 461–75; U. Bergman, “Pharmacoepi- demiological Perspectives on the Suspected Teratogenic Effects of Benzodiazepines,” Bratislavske Lekarske Listy 92 (1991): 560–63 (abstract in English).

40. J.W. Olney et al., “Environmental Agents That Have the Potential to Trigger Massive Apoptotic Neurodegeneration in the Developing Brain,” Environmental Health Perspectives 108 (2000, Suppl. 3): 383–88.

41. J. Porter and H. Jick, “Addiction Rare in Patients Treated with Narcotics,” New England Journal of Medicine 302 (1980): 123.

42. “Nandrolone decanoate,” in Therapeutic Drugs, ed. C. Dollery, 2d ed. (New York: Churchill Livingstone, 1999), N29.

43. P.W. Meilman et al., “Beyond Performance Enhancement: Polypharmacy among Collegiate Users of Steroids,” Journal of American College Health 44 (1995): 98–104.

44. R.H. du Rant, L.G. Escobedo, and G.W. Heath, “Anabolic-Steroid Use, Strength Training, and Multiple Drug Use among Adolescents in the United States,” Pediatrics 96 (1995, pt. 1): 23–28.

45. H.H. Glaser and O.N. Massengale, “Glue-Sniffing in Children: Deliberate Inha- lation of Vaporized Plastic Cements,” Journal of the American Medical Association 181 (1962): 300–304.

46. P.W. Lewis and D.W. Patterson, “Acute and Chronic Effects of the Voluntary Inhalation of Certain Commercial Volatile Solvents by Juveniles,” Journal of Drug Issues 4 (1974): 167.

47. R.J. Goldsmith, “Death by Freon,” Journal of Clinical Psychiatry 50 (1989): 36–37.

Alphabetical Listings of Drugs

All substances listed here have been declared a public concern by government officials, medical caregivers, or news media. If a listing mentions another drug’s name in bold type, that drug has an entry of its own in this section of the book.

Some drugs have similar effects. For example, most anabolic steroids pro- mote development of male characteristics when used by females. If an indi- vidual anabolic steroid is known to have that effect, that information is given in the individual listing. Such a style might make some entries seem repetitive if someone is looking up one anabolic steroid after another, but this approach improves the odds of important information being communicated. A cross- reference style that expects readers to flip back and forth among pages to “see this” or “see that” in order to avoid repetition might work for scientists, but for readers of this book, ease of usage is more important.

Although many drugs of abuse are described in this section, many others exist that are not included here. The choice of which to include and which to leave out was based on several factors. The first was whether a drug is listed in the U.S. government schedule of controlled substances. Another factor was whether a drug is abused even though it is not a controlled substance. Still another factor was whether enough data exist in the scientific literature to provide solid information. With some drugs described here, scientific infor- mation is scanty concerning particular aspects of a given drug, such as poten- tial for causing cancer; that lack is specifically noted where relevant in drug descriptions.

Drugs are alphabetized by common name. Listings are arranged in the fol- lowing manner:

Pronunciation: The proper way to pronounce a substance’s name is given here. Sometimes alternative pronunciations are included.

32 The Encyclopedia of Addictive Drugs

Chemical Abstracts Service Registry Number: This number (CAS RN) is unique to every chemical, just like a fingerprint or a U.S. Social Security number is unique to each person. Drugs, like people, may go by different names, but different-sounding drugs having the same CAS RN are identical—that is, chemically and structurally the same. The CAS RN can be used to search var- ious databases for more information about a drug and can also be used to confirm that a scientific report is indeed about the drug in question.

Formal Names: Entries in this section are a partial list of brand names and ge- neric names. Some are for combination products including the drug. These names are used by scientists and health care providers.

Informal Names: These are casual and slang terms for the drug. The lists are not necessarily complete, but they do include typical informal names. Some nicknames are used for more than one drug.

Type: The type of drug and its class are given so a reader can refer to pages elsewhere in this book having background information about that substance.

Federal Schedule Listing: The status line gives the drug’s legal standing (see page 6 for explanations of “schedules”) and the U.S. Drug Enforcement Ad- ministration Controlled Substances Code Number if the drug is a controlled substance.

USA Availability: The availability line tells what must normally be done to ob- tain the substance legally in the United States. Normally Schedule V substances are prescription, but can be nonprescription in some state jurisdictions. A non- prescription item may still have other regulations limiting its availability, such as requiring a purchaser to be an adult or to register the purchase, as with over-the-counter (OTC) codeine-containing cough medicines. A substance may be legally available but may become illegal if used in prohibited ways.

Pregnancy Category: Not all drugs have an official pregnancy category desig- nation. For example, such a rating does not exist for substances lacking official approval for therapeutic use. See page 8 for an explanation of categories.

Occasionally information in one of the above listings could not be verified despite diligent search. In such cases the topic is omitted.

The detailed descriptions of each drug are arranged to cover:

• uses
• drawbacks
• abuse factors
• (some but not all) drug interactions
• cancer (risks)
• pregnancy (effects)
• (in some cases) additional information

Reliable sources of additional scientific information are suggested at the end of each individual substance entry. At the back of this book is a list of general information sources, some of which may have additional data about the sub- stance covered in the alphabetical entry. Many drugs have been studied for decades, and some references reflect the venerable history of such studies.

Alphabetical Listings of Drugs 33

Drug descriptions occasionally mention the following concepts:

One drug may be stronger than another, but such a comparison depends not only on the effect being measured but on the animal species being tested. Frogs, chickens, and rats may react very differently than humans would to an equivalent dose of various drugs. For example, bufotenine and LSD effects are thousands of times stronger in humans than in monkeys; a dose that leaves a small monkey unfazed might devastate a human. Animal experiments are useful to know about, but the results do not necessarily extrapolate to humans. When this book compares strengths of drugs, the comparison simply gives a rough idea of strengths and has no bearing on determining what size dose of one drug would be equivalent to another size dose of a different substance.

When one drug is said to “boost” the effect of another, this means the increase is more than would be expected from simply adding the effect of one drug to the other (1 1 2) but instead involves synergistic chemical and biological processes yielding a total that is more than the combination of parts (1 1 3).

“Flashback” is an ability (voluntary or involuntary) to reexperience a drug state without taking the substance. Some details about flashback are given in this book’s description of LSD, although the phenomenon is not limited to that drug (see also, for example, this book’s listings about methamphetamine and psilocybin).

“Polydrug” abuse is a typical element of setting. For example, heroin ad- dicts normally abuse other drugs as well. Someone who takes MDMA at a dance club may well take cocaine at the same time, just as some persons simultaneously smoke tobacco and drink alcohol. Even if all the compounds inside an illicit user can be verified, determining which is responsible for which effect can be challenging. This book’s alphabetical section presents both the conclusions and doubts that scientists express about polydrug use, along with some classic interactions that occur when more than one drug is taken at the same time. Individuals who get into a medical emergency after drug use should bring samples of substances to health care providers; an item may not be what a user thinks it is, and effective treatment must be based on chemical reality rather than consumer belief.

Animal experiments may show that a drug can cause cancer or birth defects. The practical meaning of such results is sometimes clouded because the same drug may affect different species in different ways. Also animal tests some- times involve many times the recommended human dose, perhaps levels high enough to poison the animals. These kinds of tests are not meaningless but may involve levels of risk unlikely to be experienced by humans. And yet large doses having no effect on animals do not guarantee a drug’s safety for pregnant women. In some countries a compound called thalidomide was ap- proved for human use after animal tests revealed no potential for causing birth defects, but in humans the substance produced severe congenital malforma- tions such as missing or highly deformed limbs.

Experiments testing a drug occasionally produce conflicting results—some may say a drug does something; some may indicate the drug will not do it. These kinds of uncertainties are unsatisfying, but that is the way scientific research operates. Perhaps conflicting results come from differences in dosage

34 The Encyclopedia of Addictive Drugs

size, or the manner in which a dose is given, or diet, or living conditions, or any number of other causes. Perhaps the conflict is due to researcher errors—a classic error being failure to run adequate controls (for example, failing to give the drug and a placebo in the same manner to a large number of the same kind of experimental subjects). The size of a drug experiment can also be a problem. Many involve a handful of volunteers. Conclusions from small stud- ies (that is, studies involving a small number of test subjects) are not as sig- nificant as conclusions from studies measuring thousands of persons. Sometimes drug effect information is based on medical case reports, in which something has happened to one person but has not been experimentally tested to determine how typical the effect is. Malnourishment and physical afflictions can affect drug actions. Another tricky angle occurs when reports say a drug is “associated” with an effect, meaning the drug is administered and an effect follows. “Before and after” time sequence is not the same as “cause and effect” (chanting may be associated with the subsequent end of a solar eclipse, but it does not cause the termination). In scientific drug reports what scientists say about drugs can be less certain than what public policymakers say.

This section of the book strives to present the consensus of mainstream scientific thought. However, sometimes the only available information comes from observations lacking experimental confirmation, at the present time; the reader should keep in mind that by definition such observations are not yet part of a consensus even if they are reported in scientific journals.


Pronunciation: a ̄-ee-tee
Chemical Abstracts Service Registry Number: 2235-90-7
Formal Names: Alpha-Ethyltryptamine, Etryptamine, Monase
Informal Names: Alpha-ET, Alpha-Ethyl, ET, Love Pearls, Love Pills, Trips Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7249)
USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This substance has been used for decades. It has similarities to DMT in chemistry and actions and was made a Schedule I substance partly because some AET effects are reminiscent of MDMA. As a Schedule I substance AET has no approved medical use in the United States but has been used elsewhere (in Europe, for example) as an antidepressant.

Intoxication symptoms can resemble those of amphetamine, and urine tests for amphetamine can also pick up AET. When AET was given to rats, in some ways they responded as if they had received either amphetamine or MDMA.

A researcher who used AET reported enjoyable sensations of energy and contentment. As dosage increased, so did euphoria and enjoyment of sensual activity such as eating, music, and sex. In several accounts of effects halluci- nations were not reported.

Drawbacks. AET has been associated with agranulocytosis, a blood disease involving development of sores in various places throughout the body.

Abuse factors. Tolerance is reported. Some opiate abusers trying to break their addiction have used AET to ease opiate withdrawal symptoms.

Drug interactions. AET is a monoamine oxidase inhibitor (MAOI), a type of drug that can interact dangerously with some of the other drugs described in this book.

Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

Daldrup, T., et al. “Etryptamine, a New Designer Drug with a Fatal Effect.” Zeitschrift fu ̈r Rechtsmedizin 97 (1986): 61–68 (article in German, but summary available in English).

36 AET

Huang, X.M., M.P. Johnson, and D.E. Nichols. “Reduction in Brain Serotonin Markers by Alpha-Ethyltryptamine (Monase).” European Journal of Pharmacology 200 (1991): 187–90.

Krebs, K.M., and M.A. Geyer. “Behavioral Characterization of Alpha-Ethyltryptamine, a Tryptamine Derivative with MDMA-Like Properties in Rats.” Psychopharma- cology (Berlin) 113 (1993): 284–87.

Morano, R.A., et al. “Fatal Intoxication Involving Etryptamine.” Journal of Forensic Sci- ences 38 (1993): 721–25.


Pronunciation: AL-kuh-hall
Chemical Abstracts Service Registry Number: 64-17-5 Formal Names: Ethanol, Ethyl Alcohol, Hydroxy Ethane Informal Names: Liquor
Type: Depressant. See p. 19
Federal Schedule Listing: Unlisted

USA Availability: Freely available to adults; various jurisdictions limit access to minors; some pharmaceutical preparations are prescription

Uses. Various kinds of alcohol exist; many are poisonous, such as wood alcohol, and are not intended for drinking. Those types are not substances of abuse and are not discussed in this book.

In former times physicians prescribed alcohol as a treatment for assorted afflictions. That usage is largely outmoded, but alcohol is still a common in- gredient in cough remedies, is applied to skin as a disinfectant, and is a com- ponent of some injectable solutions. Alcohol is used as a partial antidote for methanol poisoning associated with inhalant abuse, and it is used to combat glycol poisoning. In some medical procedures alcohol is administered to create a form of anesthesia called a nerve block. Around 1970 at one hospital a com- bination of alcohol and chloral hydrate was routinely given to make pregnant women unconscious during labor, although alcohol is also a treatment for stopping premature labor. The substance can be a sleep aid (a “nightcap” drink), but researchers have found that it interferes with dreaming, which is an important component of sleep. Tolerance can develop to sleep-inducing actions, and dream content can become disturbing for awhile after usage stops. Some persons drink alcohol to cope with stress. Evidence exists that moderate consumption of wine may help people live longer by reducing risk of heart disease and cancer.

Drawbacks. As with many other drugs, moderate recreational use can be pleasurable while causing little harm. In contrast, excessive use can not only have psychological effects harmful to family and social functioning but also injure the stomach, liver, kidneys, heart, and brain. Rat experiments have dem- onstrated damage to the pancreas, damage that is boosted by cigarette smoke. A study found that men with spinal osteoporosis, a disease increasing the likelihood of broken bones, drink more alcohol than persons without the dis-

38 Alcohol

ease; this finding does not mean that alcohol causes the affliction, but it does indicate the need for further research. Alcohol does not make peaceful indi- viduals rageful, but it can lower inhibitions while leaving a person able to act out urges. Thus violent and criminal acts are commonly associated with al- cohol intoxication. Impairment of mental and physical activity can occur dur- ing acute intoxication, making operation of dangerous machinery (such as automobiles) hazardous. During intoxication sensory perceptions are blunted, reducing awareness of tastes, smells, sounds, and pain.

Lesser known problems are associated with alcohol. Male users experience a decline in testosterone levels, and females may experience menstrual diffi- culties. The nerve inflammation disease beriberi has been linked with alco- holism, and research has raised the possibility that alcoholism can worsen Alzheimer’s disease. Some studies report that drinkers have a slightly higher chance of developing cataracts, but a very large study involving 77,466 women found little, if any, relationship between the substance and cataracts. Experi- ments show that a drink of alcohol encourages more cigarette consumption and that persons who use both alcohol and nicotine tend to drink more when cigarettes are unavailable. Although alcohol can make a person feel hotter, that effect is superficial; the substance actually lowers body temperature, mak- ing alcohol counterproductive if a chilled person is trying to warm up; the substance should not be given to persons injured by exposure to cold tem- peratures. Alcoholics commonly have memory trouble, and small studies find that heavy-drinking nonalcoholics have impaired thinking skills even while sober.

Abuse factors. In addition to being a potent intoxicant, alcohol is one of the most addictive substances. Tolerance (“holding your liquor”) and dependence may occur. Withdrawal can be dangerous, with death occurring (typically from difficulties leading to convulsions) despite intense medical supervision. The withdrawal syndrome is called delirium tremens. Its symptoms are sim- ilar to those of barbiturate withdrawal: weariness, nervousness, perspiration, tremors, vomiting, cramps, high blood pressure, accelerated heartbeat, con- vulsions, and hallucinations. Symptoms may be worse in elderly persons.

Women tend to be more affected by alcohol than men are because, among other reasons, the drug has more bioavailability in females (more of a given dose is used in females, so they need less quantity than men do in order to reach the same level of effect).

Drug interactions. Alcohol lengthens the duration of effects from chlordi- azepoxide, diazepam, and lorazepam. Cocaine worsens liver damage caused by alcohol. When rats receiving morphine or methadone drink alcohol, the alcohol blood level takes longer to increase but then lasts longer, a result suggesting that a human opiate user might have to drink more in order to get an alcohol effect and would then stay intoxicated longer than someone who does not use opiates. Rat studies indicate that steady opiate consumption may intensify alcohol dependence. In rats, alcohol, chlordiazepoxide, and pen- tobarbital all have cross-tolerance with one another, meaning that one will substitute for the other to some extent. So many drugs interact dangerously with alcohol that a person should always check information labels on drug containers before using the substances simultaneously with alcohol.

Alcohol 39

Cancer. Most laboratory tests give no indication that alcohol has a potential for causing cancer. Nonetheless, mice experimentation indicates that long-term use of alcohol can cause liver cancer. Human reports indicate an increased risk for prostate cancer. Women who take more than two drinks a day have an increased risk of breast cancer. A study of 8,006 Japanese men in Hawaii found an association between alcohol and cancer of the lungs and rectum, but “association” is not the same as cause and effect. Evidence indicates that saliva might transform alcohol in ways that promote oral cancer.

Pregnancy. A study of 430 couples in Denmark found fertility to decline among women as their alcohol consumption increased, but no effect was ob- served on male fertility. In contrast, a study of farm couples in Canada found no difference in fertility between women who did or did not drink alcohol. Still another study, in the Netherlands, found male alcohol consumers to have higher fertility as consumption increased, with no difference in fertility rate between women who drank different amounts. Such findings of sometimes yes, sometimes no, are a classic sign of an “invalid variable,” which in this case would mean that no difference in fertility can be attributed to alcohol (although more studies would be needed to reach a firm conclusion, and some authorities say the trend of research indicates that alcohol does reduce female fertility).

A study found that premature infants were more likely among pregnant teenagers who drank alcohol than among those who did not. That effect was not seen among older pregnant women who drank. Other research has noted lower birthweights among children delivered by pregnant alcohol consumers.

A human experiment documented fetal response to two glasses of wine drunk by women whose pregnancies were close to time of delivery: In that experiment fetal respiration and sleep were disturbed—which did not surprise researchers because heavy consumers of alcohol frequently give birth to in- fants having sleep difficulties. Such newborns may also have tremors and poor reflexes and cry more than normal. Children can be born dependent on the drug.

Alcohol is a well-known cause of birth defects. In mice the substance is known to cause a facial deformity called holoprosencephaly, and a human case report suggests that heavy dosage can do the same in humans. Less dra- matic facial characteristics are common after substantial prenatal exposure to alcohol. Other human birth defects attributed to alcohol include kidney, heart, and brain trouble. More subtle damage has been measured as a slight decline in IQ among schoolchildren of mothers who took two or more drinks a day during pregnancy. Male exposure to some drugs can produce birth defects, and researchers have found problems in behavior and thinking skills among children of alcoholic fathers as well as among offspring of pregnant alcoholics. Fetal alcohol syndrome (FAS) is a collection of afflictions observed in children typically born to women who had six or more drinks a day while pregnant. The syndrome may include low birthweight, defective vision, delayed devel- opment, specific facial characteristics, trouble with muscles and joints, heart abnormality, and mental retardation. Problems can be long-lasting and even permanent. Prenatal exposure to alcohol can delay motor skill development in children, cause difficulties in maintaining balance, and limit growth in

40 Alcohol

height. Such children may be more impulsive and aggressive. A study of ad- olescents compared two groups, one born with FAS and another whose moth- ers drank little or no alcohol during pregnancy. The FAS group showed impairment in some types of memory, attention, thinking, and learning—find- ings supported by other research as well. Some researchers believe that fetal exposure to alcohol has more to do with teenage drinking than family envi- ronment does. Comparing adults with heavy prenatal alcohol exposure to those without such exposure, a small study measured significant psychiatric differences, particularly with the alcohol subjects being more depressed and fearful.

Fetal damage from maternal alcohol use is unquestionable, but the amount of use necessary to cause damage is less certain and can be affected by a woman’s general physical condition and lifestyle (including nutrition and other drug usage). Occasional binge drinking and routine heavy drinking are certainly hazardous to fetal development, but for many years pregnant women have used alcohol in moderation without apparent effect on offspring. None- theless, in general, women are now advised to avoid any alcohol consumption during pregnancy.

Experimenters note that alcohol consumption reduces mothers’ milk pro- duction but does not affect energy provided by the milk. Alcohol levels in milk are similar to a mother’s blood levels. A nursing infant may be sickened by milk from a mother who abuses alcohol—an infant has not yet developed the proper body chemistry to break down alcohol, so a dose lasts longer in an infant than in an older child or adult.

Additional information. Beverage alcohol is a powerful intoxicant. Alcohol is also probably the most familiar drug, used so freely that many persons regard it solely as a beverage rather than as a drug. Indeed, for many years excessive drunkenness was considered a moral failing rather than a disease, and not until the 1950s was alcoholism officially recognized as an affliction appropriate for medical treatment.

By the 1800s drunkenness had become a major public concern in the United States. Temperance societies, organizations whose members pledged to avoid beverage alcohol and to discourage consumption by other persons, became politically powerful. Before the Civil War such groups had been able to get laws passed outlawing the sale of beverage alcohol in various communities and sometimes throughout entire states. Shortly after World War I this agi- tation culminated in the Eighteenth Amendment to the Constitution of the United States, giving the federal government power to ban manufacture and sale of beverage alcohol. Although purchase and consumption remained legal, the majority of Americans became so displeased with Prohibition that the Twenty-first Amendment to the Constitution was passed in the 1930s repeal- ing the earlier one.

Additional scientific information may be found in:

Chasan-Taber, L. et al. “A Prospective Study of Alcohol Consumption and Cataract Extraction among U.S. Women.” Annals of Epidemiology 10 (2000): 347–53. Curtis, K.M, D.A. Savitz, and T.E. Arbuckle. “Effects of Cigarette Smoking, Caffeine

Alcohol 41

Consumption, and Alcohol Intake on Fecundability.” American Journal of Epide-

miology 146 (1997): 32–41.
Florack, E.I., G.A. Zielhuis, and R. Rolland. “Cigarette Smoking, Alcohol Consumption,

and Caffeine Intake and Fecundability.” Preventive Medicine 23 (1994): 175–80. Gronbaek, M., et al. “Type of Alcohol Consumed and Mortality from All Causes, Coronary Heart Disease, and Cancer.” Annals of Internal Medicine 133 (2000):

Jensen, T.K. “Does Moderate Alcohol Consumption Affect Fertility? Follow up Study

among Couples Planning First Pregnancy.” BMJ 317 (1998): 505–10.
Kraus, L., et al. “Prevalence of Alcohol Use and the Association between Onset of Use and Alcohol-Related Problems in a General Population Sample in Germany.”

Addiction 95 (2000): 1389–1401.
Moore, M.H., and D.R. Gerstein, eds. Alcohol and Public Policy: Beyond the Shadow of

Prohibition. Washington, DC: National Academy Press, 1981.
Phillips, B.J., and P. Jenkinson. “Is Ethanol Genotoxic? A Review of the Published

Data.” Mutagenesis 16 (2001): 91–101.
Pihl, R.O., M. Smith, and B. Farrell. “Individual Characteristics of Aggressive Beer

and Distilled Beverage Drinkers.” International Journal of the Addictions 19 (1984):

Pollack, E.S. “Prospective Study of Alcohol Consumption and Cancer.” New England

Journal of Medicine 310 (1984): 617–21.
Weinberg, N.Z. “Cognitive and Behavioral Deficits Associated with Parental Alcohol

Use.” Journal of the American Academy of Child and Adolescent Psychiatry 36 (1997): 1177–86.


Pronunciation: al-PRAY-zoh-lam (also pronounced al-PRAZ-oh-lam)
Chemical Abstracts Service Registry Number: 28981-97-7
Formal Names: Alplax, Frontal, Solanax, Tafil, Trankimazin, Xanax, Xanor, Zotran Type: Depressant (benzodiazepine class). See page 21
Federal Schedule Listing: Schedule IV (DEA no. 2882)
USA Availability: Prescription
Pregnancy Category: D

Uses. This calming and sleep-inducing substance is probably the most fre- quently prescribed drug in the benzodiazepine class. Alprazolam is used mainly to help persons suffering from panic attacks and other anxiety disor- ders, but it is not recommended for posttraumatic stress disorder. The com- pound can dramatically lessen premenstrual syndrome (PMS) and is routinely given to women of child-bearing age. Improvement of PMS is not invariable, however, and two careful experiments yielded results showing little benefit. Theoretical reasons and results from a rat experiment suggest that alprazolam may help maintain bone mass. That action may be especially important to athletes and elderly women, who commonly suffer loss of bone mass—an affliction making breakage easier. The drug has been tested as an asthma treatment with encouraging results, though reasons for success are unclear. Some researchers believe the drug has potential in diabetes control. In an experiment measuring alprazolam’s pain-relieving properties, the drug re- duced the severity but not the frequency of chronic tension headaches. The compound has antidepressant and anticonvulsant properties, has been used to treat ringing in the ears and to alleviate tremors and catatonia, and has been found useful in easing alcohol withdrawal symptoms in alcoholics. A rat study suggests that alprazolam may also have a place in treating cocaine addiction. Measurements find the drug worsens snoring but improves quality of sleep (at least for the snorers).

Drawbacks. Motorists have suffered accidents attributed to drowsiness from alprazolam. Experiments show that the drug reduces startle response in hu- mans, which may mean drivers are less alert or respond less vigorously to situations. Case reports tell of alprazolam (alone and in combination with other medicine) causing the skin to become extra sensitive to sunlight. The compound may produce jaundice.

Alprazolam 43

Although the drug normally encourages eating, about 20% of persons in one study experienced weight loss, along with unwanted effects such as dif- ficulty in controlling muscles (including urinary incontinence), peevishness, bellicosity, and lowering of inhibitions. Researchers generally believe the drug interferes with sexual function in men and women. A case report tells of the drug causing mania with euphoria, high self-confidence, increased energy, and trouble with getting proper sleep—all rather untypical effects. Despite such possibilities, one team reviewing scientific literature found reports of unwanted actions to be uncommon for alprazolam, and another team con- cluded that alprazolam generally has fewer such reports than other benzodi- azepine class drugs. Analysts who examined medical records of 10,895 alprazolam patients found little mention of unwanted effects. In evaluating the infrequent accounts of mania, aggression, hallucinations, or other unex- pected psychological reactions to alprazolam, we should remember that many such cases involve persons already exhibiting psychiatric disturbances for which they are receiving the drug. Such reactions may be far less likely in a psychiatrically normal person.

Abuse factors. An experiment showed no tendency for abuse of alprazolam among users even though it is a controlled substance. A 1993 review of human and animal studies of the drug concluded that scientific experimental evidence failed to support a popular belief that abuse of alprazolam was more likely than abuse of other benzodiazepine class drugs. Another 1993 report dis- agreed but described alprazolam abuse as minuscule and limited to persons already misusing other drugs, particularly opiates and alcohol. Brainwave and other measurements imply that alprazolam has more appeal to alcoholic men than it does to nonalcoholics. Experiments show that persons with a family history of alcoholism tend to experience more pleasure (even euphoria) when taking alprazolam than do persons lacking such a history. Tests find the drug to have stronger effects (positive and negative) on women whose fathers were alcoholics, compared to women whose immediate family background does not include alcoholism. When experiments gave drug abusers a choice between diazepam or alprazolam, the abusers tried both but found alprazolam more pleasant.

Craving and tolerance do not seem to develop, but alprazolam can produce bodily dependence, which is a traditional sign of addictive potential. Sudden stoppage can cause seizures or delirium, so practitioners customarily wean their patients with tapering dosages. Withdrawal symptoms may include per- spiration, tremors, cramps, vomiting, diarrhea, cloudy eyesight, prickling sen- sations on the skin, and general befuddlement. Convulsions and seizures are reported. One experiment noted that withdrawal signs cleared up in a week.

Drug interactions. Kava is an intoxicating drink prepared from the kava plant, suspected of interacting so seriously with alprazolam that a coma may result. Persons taking antifungus drugs such as itraconazole or ketoconazole are supposed to avoid alprazolam, as those two drugs increase the power and prolong the effect of an alprazolam dose. The heartburn medicine cimetidine (Tagamet), the antidepressant fluoxetine (Prozac), and the pain-relieving opioid propoxyphene each lengthen the time an alprazolam dose lasts, and ritonavir (used against the human immunodeficiency virus in AIDS [acquired

44 Alprazolam

immunodeficiency syndrome]) can drastically boost the potency of alprazo- lam. In contrast, alprazolam’s effects are reduced by the epilepsy drugs phe- nytoin and carbamazepine, by the tuberculosis medicine rifampin, and by the asthma medication theophylline. A case of glaucoma resulting in blindness is attributed to a multidrug regimen of antidepressants and antianxiety medi- cines including alprazolam. Some tests find that the substance worsens reac- tion time and memory. Taking alprazolam with diazepam can cause persons to forget what happened while they were under the drugs’ influence. In one experiment alprazolam by itself seemed to interfere with memory even weeks after taking it, but deeper analysis of the results caused investigators to ques- tion any long-lasting effect. Persons functioning adequately while drinking alcohol decline in performance when a dose of alprazolam is added, and the combination may increase hostile attitudes and actions. Findings in a mice experiment showed alprazolam boosting pain relief provided by morphine, but a human experiment found no such increase (although alprazolam re- duced the typical nausea effect of morphine—a benefit that has also been demonstrated in cancer chemotherapy patients). Alprazolam has cross- tolerance with chlordiazepoxide.

Cancer. A two-year rat experiment found no evidence that alprazolam causes cancer. Measurements of persons receiving alprazolam for panic dis- order indicated the substance does not reduce levels of tumor necrosis factor- alpha, a protein that helps the body fight off cancer.

Pregnancy. Alprazolam experimentation with mice yielded no birth defects. Examination of pregnancies in which women used the drug during the first trimester found no more birth defects than would be expected if the drug were not taken at all, but researchers cautioned that the sample sizes (411 in one study and about 200 in another) were too small to reach firm conclusions about the drug’s effect on fetal development. A study of 88 infants born to women who used alprazolam during pregnancy found 10 born with “major” deformities. Mice having prenatal exposure to the drug show reduced social interaction, and males are more aggressive than normal. Such mice also exhibit subtle trouble with hind legs.

Clinicians have observed alprazolam to increase the hormone that prepares female breasts for milk production. When combined with the pain reliever tramadol and the antidepressant citalopram, alprazolam has been known to cause excessive milk flow. Alprazolam passes into milk, and nursing is not recommended for mothers taking the drug. In one case an infant even exhib- ited drug withdrawal symptoms when a nursing mother who was receiving alprazolam ceased nursing.

Additional scientific information may be found in:

Edwards, J.G. “Prescription-Event Monitoring of 10,895 Patients Treated with Alpra- zolam.” British Journal of Psychiatry 158 (1991): 387–92.

Jonas, J.M., and M.S. Cohon. “A Comparison of the Safety and Efficacy of Alprazolam versus Other Agents in the Treatment of Anxiety, Panic, and Depression: A Review of the Literature.” Journal of Clinical Psychiatry 54 (1993, Suppl.): 25–45.

Nishith, P., et al. “Brief Hypnosis Substitutes for Alprazolam Use in College Students:

Alprazolam 45

Transient Experiences and Quantitative EEG Responses.” American Journal of

Clinical Hypnosis 41 (1999): 262–68.
Romach, M.K. et al. “Characteristics of Long-Term Alprazolam Users in the Commu-

nity.” Journal of Clinical Psychopharmacology 12 (1992): 316–21.
Rothschild, A.J. “Comparison of the Frequency of Behavorial Disinhibition on Alpra- zolam, Clonazepam, or No Benzodiazepine in Hospitalized Psychiatric Pa-

tients.” Journal of Clinical Psychopharmacology 20 (2000): 7–11.
Rush, C.R., et al. “Abuse Liability of Alprazolam Relative to Other Commonly Used Benzodiazepines: A Review.” Neuroscience and Biobehavorial Reviews 17 (1993):

Sellers, E.M., et al. “Alprazolam and Benzodiazepine Dependence.” Journal of Clinical

Psychiatry 54 (1993, Suppl.): 64–75.
Spiegel, D.A. “Efficacy Studies of Alprazolam in Panic Disorder.” Psychopharmacology

Bulletin 34 (1998): 191–95.


Pronunciation: am-uh-NEYE-tuh
Chemical Abstracts Service Registry Number: None Formal Names: Amanita muscaria
Informal Names: Aga, Fly Agaric
Type: Hallucinogen. See page 25
Federal Schedule Listing: Unlisted
USA Availability: Nonprescription natural product Pregnancy Category: None

Uses. These mushrooms are found in much of the Northern Hemisphere and are known to grow elsewhere. Due to the possibility that an effective dose is close to a poisonous dose, and because of variations in potency, these mush- rooms are easily poisonous and have even been mixed with milk as bait to kill flies. Persons seeking amanita sometimes accidentally ingest Amanita phal- loides, also called Death Cap and Death Cup, which can be deadly poisonous to the kidneys and liver. Confusion with other dangerous mushrooms has also harmed people seeking Amanita muscaria.

The Amanita muscaria mushroom has been used to treat alcohol overdose and to relieve nervousness, fever, and pain of sore throat, nerves, and joints. The natural product contains muscimol, a chemical that initially acts as a stim- ulant but that can later produce temporary loss of muscular control as the drug action proceeds. Muscarine chloride can be prepared from amanita. In various animal species muscarine chloride can cause spasms and constrictions and lower blood pressure. The relevance of those studies to humans is unclear; for example, a dose that would poison a human leaves a monkey unfazed. Bufotenine has been reported in amanita, but the report is disputed. The ibotenic acid in amanita can produce hallucinations; a case report mentions visual hallucinations lasting for days after ingesting the mushroom. The mush- room is said to produce euphoria and to cause changes in sensory perceptions. Some persons consume the fungus for spiritual purpose, a practice that some authorities date back to ancient Buddhist times, with the Buddhists perhaps learning the custom from still older examples among forest peoples in north- ern Europe and Asia. Usage by Siberian shamans has been documented in modern times. Drug-induced insight into personal psychological issues is re- ported.

Amanita 47

Drawbacks. One user describes the experience as lacking in feelings of hap- piness, or love, or sexual impulses—a lack that sets amanita apart from many drugs that are used recreationally. A scientist who engaged in self- experimentation had similar results of emptiness. Of 6 subjects who received the mushroom in an experiment, all were nauseated, 2 vomited, 1 had hal- lucinations, and several had sensory distortions. None cared to repeat the experience. The supervising researcher wondered if variations in supplies of the natural product explained why the experiment’s results differed so greatly from hallucinations and pleasures reported by other persons. Personality, ex- pectations, and surrounding environment can shape the experience. A re- searcher interviewed 18 persons who ate Amanita muscaria or Amanita pantherina; half had eaten the mushrooms deliberately, and half thought they were consuming something else. Every person who accidentally ate the sub- stance found its actions unpleasant. In contrast, the mushroom’s effects were enjoyed by every individual who deliberately ate it.

Because active chemicals from the natural product are excreted into urine, people can dose themselves again by drinking their own urine, a dosage method that may horrify Americans but that a few other cultures have ac- cepted calmly.

Unwanted amanita effects can include twitching, cramps, abdominal dis- comfort, sweating, nausea, vomiting, diarrhea, dizziness, confusion, rapid heartbeat, difficulty in moving around, high body temperature, and convul- sions. Users can become manic and then sleepy, with those conditions alter- nating back and forth until a person collapses. Scientific journals contain many articles about brain damage caused by ibotenic acid, although conditions of experiments do not necessarily duplicate what happens when mushrooms are eaten. A person who received a dose of ibotenic acid in an experiment de- veloped a headache for two weeks. Under laboratory conditions amanita ex- tracts cause red blood cells to clump together.

Abuse factors. Not enough scientific information to report.
Drug interactions. Not enough scientific information to report. Cancer. Not enough scientific information to report.
Pregnancy. The muscimol in amanita causes birth defects in rats. Additional scientific information may be found in:

Davis, D.P., and S.R. Williams. “Amanita Muscaria.” Journal of Emergency Medicine 17 (1999): 739.

Fabing, H.D. “On Going Berserk: A Neurochemical Inquiry.” Scientific Monthly 83 (1956): 232–37.

Horne, C.H.W., and J.A.W. McCluskie. “The Food of the Gods.” Scottish Medical Journal 8 (1963): 489–91.

McDonald, A. “The Present Status of Soma: The Effects of California Amanita muscaria on Normal Human Volunteers.” In Mushroom Poisoning: Diagnosis and Treatment, ed. B.H. Rumack and E. Salzman. West Palm Beach, FL: CRC Press, 1978. 215–23.

Ott, J. “Psycho-Mycological Studies of Amanita: From Ancient Sacrament to Modern Phobia.” Journal of Psychedelic Drugs 8 (January–March 1976): 27–35.

Areca Nut

Pronunciation: AR-i-kuh nut (also pronounced uh-REE-kuh nut) Chemical Abstracts Service Registry Number: None
Formal Names: Areca catechu
Informal Names: Betel Nut, Katha, Pinang, Pugua

Type: Stimulant (pyridine alkaloids class). See page 18

Federal Schedule Listing: Unlisted

USA Availability: Nonprescription natural product, but restrictions apply to inter- state commerce

Pregnancy Category: None

Uses. Accounts of areca nuts date back to at least 504 B.C. They are about the size of a cherry and come from palm trees in the Indian Ocean region, grown in countries such as India, China, and the Philippines. Trees reach up to 90 feet in height, and nuts are about an inch in diameter. The product is used not only as a drug but also as a dye and in the leather tanning industry. Drug use of areca nut is common in South Africa, India, Taiwan, and other areas of South Asia and the Pacific basin. The product has been unfamiliar in the United States, but is available and is used in some immigrant communities.

Areca nut is a popular recreational stimulant relieving tension and produc- ing euphoria, regularly used by perhaps 200 million to 600 million persons, making it one of the most popular substances in the world. Users commonly put the nuts in a quid (a chewable cut) as with coca or tobacco. Effects may be unpleasant for new chewers: nausea, dizziness, burning sensation in the mouth, a closing sensation in the throat. With perseverance, those unwanted effects are replaced by desired ones. As with alcohol, in lands ranging from India to New Guinea areca nut has a place in religious and other ceremonies (engagements to marry, offerings to spirits), but the product’s main use is secular. In some places, areca nut is a social lubricant, much as beer is used in the United States. Paraphernalia involved with consuming areca nut may be either utilitarian or highly decorated functional artwork. The product adds a smell to the breath that many people find appealing. As with tobacco quids, users typically spit out areca nut juice, staining walls or other targets. Because such a practice may potentially promote the spread of disease, in some places large cans are lined with plastic bags and used as spittoons.

Comments from one user make the substance sound like fast-acting caf-

Areca Nut 49

feine; another user talked of a mild background stimulation accompanied by pleasant enhancements of perception; still another user described a brighten- ing of colors, with motions around him becoming jerky, as in old-time silent movies or modern Internet videos, and said he felt relaxed. (Those descrip- tions are anecdotal, not from scientific journals.) Areca nut users generally explain the experience as reducing hunger, tiredness, anxiety, and peevishness while increasing contentment and alertness—effects reminiscent of coca chew- ing. Some people simply use the quids as a cheaper substitute for chewing gum. Areca nut usage is seen more often in older persons than in younger and may therefore be declining. Younger persons do indulge, however. One survey found up to 16% of high school students in Taiwan regularly using the substance. Areca nut and nicotine both influence some of the same parts of the central nervous system in similar ways.

Chewers widely believe areca nut aids digestion. Chewing the substance can slow or accelerate pulse rate, raise or lower blood pressure, promote sal- ivation and tremors, and increase body temperature and sweating. Outdoor workers use areca nut to combat cold weather. Areca nut is used to rid hu- mans of worms. The substance is also a treatment for worms and constipation in animals. Traditional healing applications include treatment of edema, hep- atitis, gum disease, inadequate urine output, and gastrointestinal complaints including both constipation and diarrhea. Investigators find that areca nut reduces schizophrenia symptoms in schizophrenic chewers. Nonetheless, the natural product has little place in modern medicine.

Some authorities describe areca nut’s actions as similar to amphetamine. Although areca nut is a stimulant, its ability to improve workplace perfor- mance is unproven. One laboratory study demonstrated that the substance is unlikely to worsen job performance; another laboratory study showed im- provement in some reaction time; still another showed longer reaction time. Tests of workers who operated heavy earth-moving equipment while using areca nut found evidence that the men were more alert, but otherwise they exhibited no effect that would influence job performance; measurements in- cluded short-term memory, reaction time, and eye-hand coordination.

A chemical refined from areca nut (Areca II-5-C) shows excellent potential as a medicine to reduce blood pressure, even though the natural product tends to raise blood pressure. Experiments with areca nut’s pyridine alkaloid are- coline indicate that the chemical can improve memory in mice, and arecoline produces the same benefit in persons suffering from Alzheimer’s disease (al- though improvement may be marginal). Still other chemicals isolated from areca nut seem to have potential for inhibiting formation of plaque on teeth, although in practice areca nut chewers have more plaque than nonchewers. Chewers, however, also seem to have less tooth decay than nonchewers, and areca nut toothpaste has been marketed. Areca nut chewing is linked to a lower prevalence of a bowel disease called ulcerative colitis, but the possible protective effect has not been differentiated yet from tobacco smoking of chewers (nicotine is known to improve ulcerative colitis). One alcohol extract of areca nut has been successfully tested as a treatment for skin wrinkles, making people look younger. Another alcohol extract shows promise in treat- ing inflammations, allergies, and cancer. Burning areca leaves at a campsite

50 Areca Nut

helps repel some types of mosquito, effectively enough that researchers say the practice can reduce spread of disease carried by mosquitoes.

Drawbacks. Overindulgence can produce hallucinations and delusions, but those effects are uncommon. Based on chemical properties, theoretical reason exists for expecting areca nut to promote diabetes; animal experiments ex- ploring that hypothesis have been suggestive but not conclusive. Chewing areca nut produces large amounts of blood-red saliva, which over the years can turn teeth brown or black. The physical action of continual chewing day after day appears to promote breakage of tooth roots, while ever-present draining of saliva across corners of the mouth can crack that skin. Areca nut harms the antimicrobial ability of white blood cells, thereby promoting gum disease, but saliva of chewers apparently inhibits bacterial growth. Areca nut inhibits the body’s access to vitamin B1 and reduces metabolism of carbohy- drates, a situation that may produce an exhausting disease called beriberi.

The arecoline drug in areca nut can cause asthma. Some researchers spec- ulate that areca nut chewing helps explain why Asians are the predominant ethnic group hospitalized for asthma in Great Britain. Areca nut is known to reduce the healing qualities of asthma medications. Heartbeat abnormalities serious enough to hospitalize people have followed their chewing of areca nut, but a cause-effect relationship has not been established even though are- coline is known to cause cardiac crisis in dogs.

Because of chemical transformations caused by heat, using roasted nut in- stead of unroasted may reduce short-term adverse effects.

Pan masala is a product including areca nut and other substances. Pan mas- ala interferes with liver activity in rats.

Abuse factors. Some researchers have concluded that areca nut is as addic- tive as tobacco cigarettes. Unquestionably some users feel a strong continual need for the product; one person spoke of arising in the middle of the night to dose herself. Mild withdrawal symptoms are common but can become strong enough that persons seek medical aid. Withdrawal symptoms can in- clude fatigue, nervousness, depression, trouble with memory and concentra- tion, and paranoia. Compared to nonchewers, generally areca nut chewers are more likely to smoke cigarettes and drink alcohol—although researchers studying schizophrenics find that, compared to nonchewers, schizophrenic areca nut chewers are less likely to use recreational substances causing more damage to themselves than areca nut does.

Drug interactions. Areca nut is believed to interact with psychiatric medi- cines that can produce tremors and spasms reminiscent of Parkinson’s disease, worsening such adverse effects of the medicines. People using a preparation of areca nut and pumpkin seed have experienced dizziness and stomach upset. Animal experiments have identified a chemical in areca nut as an antidepres- sant operating as a monoamine oxidase inhibitor (MAOI), and various drugs described in this book react badly if used simultaneously with an MAOI.

Cancer. The nut is rich in tannins, chemicals that inhibit utilization of dietary protein and that promote cancer. An experiment injecting an areca nut extract into rats for almost a year and a half gave tumors to every rat. Various other animal experiments also indicate a danger of cancer from using areca nut, but

Areca Nut 51

scientists are uncertain that the substance causes cancer in humans unless used in combination with tobacco.

In a mice experiment a small percentage of animals receiving pan masala developed assorted cancers, but animals receiving no pan masala developed no cancers. Humans who habitually chew the nut can get noncancerous and precancerous abnormalities in the mouth. Fatal oral tumors may develop, but reports are not always clear about persons’ use of other substances that may promote cancer. Oral submucous fibrosis (OSF) is a serious mouth disease directly attributed to chewing plain areca nut or pan masala. Some victims also chew or smoke tobacco. In evaluating precancerous and cancerous growths in the mouth, however, some researchers analyzing medical cases have found areca nut to be a far more likely cause of such afflictions than tobacco. (That type of research examines outcomes of drug usage, not mech- anisms by which usage promotes cancer.) Animal experiments suggest that consuming alcohol may heighten the risk of mouth cancer from pan masala, a suggestion supported by clinical experience. Tests on pan masala users find them to suffer from increased DNA damage in tissues exposed to pan masala, a tendency duplicated in laboratory tests of pan masala and areca nut. Such chromosome damage is suspected of causing mouth, throat, and esophageal cancers ascribed to areca nut. A study examining the combined effects of pan masala, tobacco smoking, and alcohol drinking found that persons who do all three are 123 times more likely to get mouth cancer than persons who do none. Experiments suggest that vitamins A and E might help reduce the health risks of pan masala.

Pregnancy. In male mice pan masala damages chromosomes and sperm, and ingestion of pan masala by male rats has caused their gonads to shrink in weight. Examination of human uterine cells indicates mutation from chew- ing areca nut preparations. Examination of human white blood cells shows increased chromosome damage in pregnant women who chew areca nut prep- arations and still more damage if nonpregnant chewers use birth control pills. Chicken experiments produce birth defects when an alcohol extract of areca nut is injected into embryos, but results from chicken embryo testing are not accepted as evidence of human risk. One human study found that pregnant chewers were almost three times more likely to have adverse pregnancy out- comes than nonchewers. Another study found that infants of pregnant chew- ers had lower birth weight but were also less likely to have jaundice.

Additional information. Betel pepper leaves are chewed, but this plant (Piper betle, also called Piper betel) is not Areca catechu. Betel pepper leaves, areca nut, and mineral lime (not the fruit) are combined into a product called betel. Studies indicate that leaves of betel pepper reduce areca nut’s ability to cause chromosome damage. Chewing betel is thought to convert arecoline into arecaidine, which some researchers consider more benign in its effects than arecoline.

Additional scientific information may be found in:

Burton-Bradley, B.G. “Arecaidinism: Betel Chewing in Transcultural Perspective.” Ca- nadian Journal of Psychiatry 24 (1979): 481–88.

52 Areca Nut

Burton-Bradley, B.G. “Papua and New Guinea Transcultural Psychiatry: Some Impli- cations of Betel Chewing.” Medical Journal of Australia 16 (1966): 744–46. Chittivelu, S., and K.S. Chittivelu. “Betel Nut Chewing and Cardiac Arrhythmia.” Vet-

erinary and Human Toxicology 40 (1998): 368.
Nelson, B.S., and B. Heischober. “Betel Nut: A Common Drug Used by Naturalized

Citizens from India, Far East Asia, and the South Pacific Islands.” Annals of

Emergency Medicine 34 (1999): 238–43.
Norton, S.A. “Betel: Consumption and Consequences.” Journal of the American Academy

of Dermatology 38 (1998): 81–88.
Pickwell, S.M., S. Schimelpfening, and L.A. Palinkas. “ ‘Betelmania.’ Betel Quid Chew-

ing by Cambodian Women in the United States and Its Potential Health Effects.”

Western Journal of Medicine 160 (1994): 326–30.
Reichart, P.A., and H.P. Phillipsen. “Betel Chewer’s Mucosa—A Review.” Journal of

Oral Pathology and Medicine 27 (1998): 239–42.
Wyatt, T.A. “Betel Nut Chewing and Selected Psychophysiological Variables.” Psycho-

logical Reports 79 (1996): 451–63.


Pronunciation: bell-uh-DON-uh
Chemical Abstracts Service Registry Number: 8007-93-0 Formal Names: Atropa belladonna

Informal Names: Black Cherry, Deadly Nightshade, Death’s Herb, Devil’s Cher- ries, Devil’s Herb, Divale, Dwale, Dwayberry, Great Morel, Love Apple, Mur- derer’s Berry, Naughty Man’s Cherries, Poison Black Cherry, Sleeping Nightshade, Sorcerers Berries, Sorcerer’s Cherry, Witch’s Berry

Type: Hallucinogen. See page 25

Federal Schedule Listing: Unlisted as natural product

USA Availability: Nonprescription natural product; some pharmaceutical prepa- rations are prescription

Pregnancy Category: None

Uses. Belladonna bushes thrive in the United States, Europe, North Africa, and Southeast Asia. Some persons seeking a hallucinogenic effect eat the ber- ries. Leaves and roots are used medically. The wood has an even higher drug content but does not seem to be exploited medically. The plant grows wild and has also been cultivated on a commercial scale for the pharmaceutical industry. Drugs found in the plant include atropine, hyoscyamine, and sco- polamine, all of which are also found in jimson weed and European man- drake.

Belladonna substances can ease premenstrual syndrome. They can reduce spasms in smooth muscles of the digestive tract, but they cause tremors or stiffness in other muscles. Heart rate is accelerated. Migraine headaches can lessen. An experiment showed that belladonna can reduce breathing abnor- malities in infants. Some medical traditions have used belladonna for reducing sweat and other secretions and against tonsilitis, meningitis, scarlet fever, whooping cough, and epilepsy. At one time medical practitioners gave bel- ladonna to fight Parkinson’s disease and drug addiction, but those treatments have been superseded by others. Belladonna preparations have modern usage against vesico-ureteral reflux, a condition in which urine flows back toward the kidney from the bladder. Caregivers have administered belladonna to treat various pains, ranging from kidney stones to sore throat. Belladonna powders and cigarettes have been used against asthma. The natural product is consid- ered effective against afflictions of the gallbladder and liver. Belladonna is

54 Belladonna

used with uncertain results for depression, middle ear inflammation, and some heart complaints and for attempts to promote weight loss. Depending on dosage, the substance can act as a depressant or as a stimulant.

At one time the plant had cosmetic uses from which it supposedly gained its Italian name meaning “beautiful lady.” The precise cosmetic usage is un- certain: One authority mentions a rouge; another authority says the substance whitened the skin; still another says that belladonna was simply a medicinal application to remove pimples and other skin blemishes. Many accounts today say that the cosmetic function was to make women more alluring by dilating the eyes’ pupils, but those stories do not explain how flirting women would have handled the pain and near-blindness caused by artificial dilation. Mod- ern medicine uses the belladonna component atropine to dilate pupils.

Erotic dreams may occur from ingestion, and reputedly belladonna is con- sidered an aphrodisiac in Morocco. Users have reported hallucinating inter- actions with landscapes and other persons, experiences so compelling that their hallucinatory nature was unapparent until the belladonna dose wore off.

Drawbacks. Dosage with the natural product belladonna is so risky that persons are routinely advised to use it only under guidance of a trained expert. For example, depending on circumstances a fatal dose can vary by a factor of 10, meaning that a given ingestion might be survivable, but on an- other occasion one tenth that amount could just as easily be fatal. Three berries have been enough to kill youngsters. People have been poisoned by meat from animals that ate belladonna. Just handling the plant can pass its drugs into cuts and scrapes and even through unbroken skin. During World War II troops stationed in East Africa suffered “wholesale poisoning” from bella- donna, presumably due to recreational usage. Yet despite powerful effects on humans, some nonhuman species (including birds, rabbits, pigs, and sheep) can consume the plant without injury—an example of why caution is needed in reaching conclusions from drug experiments on animals.

Experiments show that the scopolamine component of belladonna reduces attention and vigilance while interfering somewhat with memory. Some vol- unteers testing the drug report dizziness and blurred vision. Nonetheless, aer- ospace researchers have concluded that scopolamine is a satisfactory motion sickness medicine for active-duty crews.

Belladonna can interfere with urination and bowel movements—drug ac- tions that are sometimes desirable, as in persons who have lost the ability to restrain such body functions. Unwanted belladonna effects include delayed passage of food from the stomach, overheating (aggravated by diminished perspiration), dry mouth, skin rash, glaucoma, hyperactivity, jabbering (or sometimes an opposite inability to speak), mania, anxiety, delirium, and con- vulsions. Psychedelic drug advocate Timothy Leary is reputed to have claimed he was unaware of anyone ever having a good experience with using bella- donna as a hallucinogen, and firsthand accounts do seem mostly negative. Stories say that in olden times belladonna was a component of witch’s brews; if so, such persons certainly partook of it for purposes rather different from those of modern recreational drug users. A medical journal author who ob- served several recreational belladonna sessions judged the substance to be powerful, but none of the users needed medical aid. Modern negative ac-

Belladonna 55

counts often derive from hospitalized individuals, and they are not necessarily a representative sample of typical users. For example, compilers of one series of case reports noted that six of the seven patients were psychologically ab- normal before using belladonna. Another pair of case reports noted that both patients had histories of depression and drug abuse.

Abuse factors. Not enough scientific information to report about likelihood of addiction, tolerance, dependence, or withdrawal.

Drug interactions. Not enough scientific information to report about the natural product.

Cancer. Not enough scientific information to report.

Pregnancy. Belladonna is suspected of causing birth defects if used during pregnancy. Belladonna drugs have been given to pregnant women, however, to control excessive salivation and vomiting, without apparent injury to off- spring.

Additional information. “Belladonna” is a nickname for PCP, but the sub- stances have no other connection.

Additional scientific information may be found in:

Forbes, T.R. “Why Is it Called ‘Beautiful Lady’? A Note on Belladonna.” Bulletin of the New York Academy of Medicine 53 (1977): 403–6.

Gowdy, J.M. “Stramonium Intoxication: Review of Symptomatology in 212 Cases.” Journal of the American Medical Association 221 (1972): 585–87.

Nuotto, E. “Psychomotor, Physiological and Cognitive Effects of Scopolamine and Ephedrine in Healthy Man.” European Journal of Clinical Pharmacology 24 (1983): 603–9.

Schneider, F., et al. “Plasma and Urine Concentrations of Atropine after the Ingestion of Cooked Deadly Nightshade Berries.” Journal of Toxicology: Clinical Toxicology 34 (1996): 113–17.

Southgate, H.J., M. Egerton, and E.A. Dauncey. “Lessons to Be Learned: A Case Study Approach. Unseasonal Severe Poisoning of Two Adults by Deadly Nightshade (Atropa belladonna).” Journal of the Royal Society of Health 120 (2000): 127–30.


Pronunciation: benz-FET-ah-meen
Chemical Abstracts Service Registry Number: 156-08-1 Formal Names: Didrex, Inapetyl
Type: Stimulant (anorectic class). See page 15
Federal Schedule Listing: III (DEA no. 1228)
USA Availability: Prescription
Pregnancy Category: X

Uses. This amphetamine was created in a laboratory in 1953 and is used as an appetite suppressant. Its qualities are similar to dextroamphetamine, al- though users perceive benzphetamine as the weaker of the two in various aspects and—with one notable exception—do not particularly find benzphet- amine to be a substitute for dextroamphetamine. The exception is that some persons wanting to boost alertness use benzphetamine in order to avoid the jumpiness caused by dextroamphetamine.

Experiments with rhesus monkeys show dextroamphetamine to be about 14 times stronger than benzphetamine when used as an appetite depressant; in dogs the difference is 5 times. Difference in potency also varies depending on the effect being measured (locomotion, blood pressure). In terms of end result, studies have been inconclusive when comparing benzphetamine, phenmetra- zine, and dextroamphetamine. One experiment found benzphetamine supe- rior to dextroamphetamine in weight reduction. In that same study benzphetamine maintained appetite reduction longer than other drugs did, but benzphetamine users in another comparison test detected no change in their feelings of hunger. The drug has little effect on levels of blood pressure or blood sugar, which some scientists see as positive factors for hypertensive or diabetic patients.

Benzphetamine is known to cause euphoria, yet that response apparently is uncommon. Volunteers taking the substance in an experiment acted more friendly but not euphoric, although they did feel more energetic. In another study the psychological state of users remained the same as with persons taking a placebo. In contrast to results from animal experiments, electroen- cephalograms (brain wave readings) taken from humans fail to show brain stimulation by benzphetamine.

Drawbacks. Users occasionally report wooziness, eyesight difficulty, and

Benzphetamine 57

mild insomnia. The compound’s ability to mask fatigue can also cause persons to overextend themselves—a hazard when operating dangerous machinery such as motor vehicles. In an experiment, complaint of dry mouth was routine, and insomnia less so, but the drug did not make people particularly active or ill-tempered. Once ingested, benzphetamine will convert into amphetamine and methamphetamine and may cause a person to fail a drug test for those substances, although skilled interpretation of test results can sometimes sug- gest benzphetamine as the source.

People with diabetes, thyroid trouble, epilepsy, or anxiety should use benzphetamine with caution. Persons with glaucoma, cardiac ailment, high blood pressure, or narrowed arteries are supposed to avoid benzphetamine altogether.

Abuse factors. Experiments with rhesus monkeys have been interpreted as meaning benzphetamine may be more effective in producing desire for the drug than in producing appetite loss. Human tests find the drug about as appealing as phenmetrazine. In an experiment with 75 human subjects, 5 re- ported experiences likened to those induced by mescaline. Drug abusers may find benzphetamine attractive, but it lacks a reputation for illicit use. Depen- dence can develop.

Drug interactions. People using a monoamine oxidase inhibitor (MAOI, found in some antidepressants and other medicines) are supposed to stop taking any such drug two weeks before using benzphetamine. Tricyclic anti- depressants may reduce benzphetamine’s effectiveness. The drug may inter- fere with the blood pressure medicine guanethidine, causing pressure to rise.

Cancer. The digestive system can convert benzphetamine into methylben- zylnitrosamine, a substance identified as causing cancer.

Pregnancy. Benzphetamine is considered to have high potential for causing birth defects if used by a pregnant woman. The drug may pass into breast milk.

Additional scientific information may be found in:

Chait, L.D., and C.E. Johanson. “Discriminative Stimulus Effects of Caffeine and Benzphetamine in Amphetamine-Trained Volunteers.” Psychopharmacology (Ber- lin) 96 (1988): 302–8.

Chait, L.D., E.H. Uhlenhuth, and C.E. Johanson. “Reinforcing and Subjective Effects of Several Anorectics in Normal Human Volunteers.” Journal of Pharmacology and Experimental Therapeutics 242 (1987): 777–83.

Patel, N., D.C. Mock, Jr., and J.A. Hagans. “Comparison of Benzphetamine, Phenmet- razine, D-Amphetamine, and Placebo.” Current Pharmacology and Therapeutics 4 (1963): 330–33.

Poindexter, A. “Appetite Suppressant Drugs: A Controlled Clinical Comparison of Benzphetamine, Phenmetrazine, D-Amphetamine and Placebo.” Current Thera- peutic Research: Clinical and Experimental 2 (1960): 354–63.

Veldkamp, W., et al. “Some Pharmacologic Properties of Benzphetamine Hydrochlo- ride.” Toxicology and Applied Pharmacology 6 (1964): 15–22.


Pronunciation: BOHL-duh-nohn
Chemical Abstracts Service Registry Number: 846-48-0. (Undecylenate form

Formal Names: Dehydrotestosterone, Equipoise, Parenabol, Vebonol Type: Anabolic steroid. See page 24
Federal Schedule Listing: III (DEA no. 4000)
USA Availability: Prescription

Uses. Boldenone has had experimental use to explore whether it is beneficial in the treatment of persons suffering from osteoporosis. This disease not only makes bones fragile, but it also causes pain and loss of appetite. Patients in the study reported feeling better, but scientific measurements failed to confirm improvement.

The drug has been given to pigeons, greyhounds, and horses in order to enhance their racing abilities. Boldenone can promote weight gain in horses.

Drawbacks. A research study administering the drug to stallions found their testes to be smaller than those of stallions receiving a placebo, and the bol- denone animals had less sperm production. Mares receiving the drug in an experiment had a shortened breeding season and abnormal sexual behavior (mounting and male-like conduct), though they seemed to recover several weeks after drug cessation. The drug has been used illegally to increase cattle growth, usage that might harm consumers of the meat.

Horses can become aggressive after receiving the drug, a trait that may continue for weeks after administration stops. A human case is reported in which a pleasant and easygoing person became rageful after using the drug at a dosage 20 times higher than an amount sufficient to make horses aggres- sive.

Abuse factors. A case report notes that someone taking boldenone and other anabolic steroids for bodybuilding suffered serious temporary depression after the supply was cut off. Until then the person had been psychologically normal.

Drug interactions. Not enough scientific information to report.
Cancer. Not enough scientific information to report.
Pregnancy. Female rats on boldenone showed lower fertility, and their off-

spring had a higher than normal death rate.

Boldenone 59

Additional information. The substance is banned from sporting competi- tions.

Additional scientific information may be found in:

Cowan, C.B. “Depression in Anabolic Steroid Withdrawal.” Irish Journal of Psychological Medicine 11 (1994): 27–28.

Dalby, J.T. “Brief Anabolic Steroid Use and Sustained Behavioral Reaction.” American Journal of Psychiatry 149 (1992): 271–72.

Melick, R.A., and C.W. Baird. “Effect of Parenabol on Patients with Osteoporosis.” Medical Journal of Australia 2 (1970): 960–62.

Melloni, R.H., et al. “Anabolic-Androgenic Steroid Exposure during Adolescence and Aggressive Behavior in Golden Hamsters.” Physiology and Behavior 61 (1997): 359–64.

Moss, H.B., and G.L. Panzak. “Steroid Use and Aggression.” American Journal of Psy- chiatry 149 (1992): 1616.


Pronunciation: boo-foh-TEN-een
Chemical Abstracts Service Registry Number: 487-93-4 Formal Names: Chan Su, Mappine, N,N-dimethylserotonin Informal Names: Cohoba
Type: Hallucinogen. See p. 25
Federal Schedule Listing: Schedule I (DEA no. 7433)
USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This drug occurs naturally in a number of plants and animals, ap- parently including trace amounts in humans. Rainforests in the Amazon and deserts in the U.S. Southwest have been key regions for natural sources of the drug, although plants and animals with the substance are found elsewhere as well. Accounts about natural products containing bufotenine reach back to ancient times. Amanita mushrooms containing the substance are believed to have been available to ancient Vikings, and some students of the topic wonder if the drug powered the Vikings’ famed Berserker rage, in which they would descend upon opponents and attack them (just as modern soldiers sometimes take drugs to improve performance in battle). Native American religious use of a bufotenine snuff called cohoba was reported in 1496. Although bufotenine gained notoriety from research conducted by the U.S. military and Central Intelligence Agency in hopes that the substance would be effective in brain- washing efforts, the drug is perhaps best known for its presence in skins of certain toads. This source is speculated as the origin of fairy tales about won- drous experiences that happen when a woman kisses a frog. Such toads were a traditional component of witches’ brews.

A tropical aphrodisiac compounded from the dried venom of toads has been found to contain bufotenine. A traditional Chinese medicine called Chan Su is rubbed on a spot of the body to numb the area and is also used for heart ailments and to fight nosebleeds; Chan Su is prepared from toads and contains bufotenine. Other toad venom preparations have been used to relieve tooth- ache, to help bleeding gums, to promote urination, and to help people cough up phlegm.

Drawbacks. When scientists administered bufotenine to some individuals they showed alarming physical symptoms ranging from faces turning purple

Bufotenine 61

to production of so much saliva that medical observers intervened to prevent the person from breathing it into her lungs and drowning. Other physical effects can include high blood pressure and a feeling that one’s air supply is inadequate. Researchers who gave the substance to dogs reported that they howled in an unnerving manner for hours.

Although bufotenine lowers pulse rate, it has been described as a heart stimulant. Overdose from products with the substance can cause death from heart failure, although the fatal poisoning may be from chemicals other than bufotenine in the products.

Abuse factors. Stories claim that licking bufotenine toads can produce hal- lucinations. Some persons familiar with the animals scoff at those tales, but there is a known case of a child being poisoned from licking one. Controversy arose when an Australian horse won a race and tested positive for bufotenine, a substance banned from the sport. Lacking any other explanation, bewildered observers at first jokingly speculated that the horse had eaten a toad, but investigators later focused on a variety of pasture grass containing bufotenine.

Typically toad venom is harvested, dried, and smoked. One authority says that swallowing enough venom to cause hallucinations would be fatal. Smok- ers, however, are apparently not automatically poisoned by the product, al- though reportedly some persons have instantly passed out upon inhaling the smoke. Smokers have reported altered consciousness and hallucinations in- volving sight, sound, smell, and touch. In research studies volunteers who took bufotenine have experienced psychedelic effects, such as mild visual hal- lucinations (seeing geometric shapes), distortions of time and space, and in- tense emotional experiences.

One authority notes that analysis of seeds used by Argentine shamans re- veals bufotenine as their sole alkaloid, a finding suggesting that bufotenine is indeed psychedelic. Nonetheless, scientific research has not confirmed that the pure drug, as opposed to natural products containing this drug along with many other chemicals, is a psychedelic. For example, some toad venom having bufotenine is also a source of a hallucinogen called 5-MeO-DMT, and a person who uses this venom may be experiencing effects from 5-MeO-DMT rather than bufotenine. (Not everyone finds 5-MeO-DMT pleasant. Scientist A. McDonald, who engaged in self-experimentation, reported “an intense feeling of unease quite unlike the effects of DMT. My scientific curiosity has not yet proved sufficient to try it a second time.”)

Although news media stories have described bufotenine as more powerful than LSD, researchers find that the substance does not readily cross from the bloodstream into brain tissue. Evidence also exists that a person’s physical condition might affect bufotenine’s hallucinogenic impact. Some authorities say the drug’s apparent hallucinogenic qualities are caused instead by its abil- ity to lower heart rate enough to produce oxygen starvation in the optic nerves, causing a person to “see stars.” Some natural products containing bufotenine (such as some kinds of seeds and toads) are unquestionably psy- chedelic, but no scientific consensus exists about the psychedelic qualities of pure bufotenine.

Drug interactions. Not enough scientific information to report. Cancer. Not enough scientific information to report.

62 Bufotenine

Pregnancy. Not enough scientific information to report.

Additional information. Studies have found that levels of the substance are often elevated in the urine of schizophrenics, in some types of autistic indi- viduals, and in depressed persons but rarely in psychologically normal people. Although cause and effect is by no means established, a study found higher bufotenine levels in urine of paranoid persons convicted of violent crimes than in urine from nonparanoid violent offenders.

Additional scientific information may be found in:

“Deaths Associated with a Purported Aphrodisiac—New York City, February 1993– May 1995.” Morbidity and Mortality Weekly Report 44 (1995): 853–55, 861. Fabing, H.D., and J.R. Hawkins. “Intravenous Bufotenine Injection in the Human Be-

ing.” Science 123 (1956): 886–87.
Horgan, J. “Bufo Abuse: A Toxic Toad Gets Licked, Boiled, Teed up and Tanned.”

Scientific American 263 (August 1990): 26–27.
Lyttle, T. “Misuse and Legend in the ‘Toad Licking’ Phenomenon.” The International

Journal of the Addictions 28 (1993): 521–38.
Lyttle, T., D. Goldstein, and J. Gartz. “Bufo Toads and Bufotenine: Fact and Fiction

Surrounding an Alleged Psychedelic.” Journal of Psychoactive Drugs 28 (1996):

McBride, M.C. “Bufotenine: Toward an Understanding of Possible Psychoactive Mech-

anisms.” Journal of Psychoactive Drugs 32 (2000): 321–31.
McDonald, A. “Mushrooms and Madness. Hallucinogenic Mushrooms and Some

Psychopharmacological Implications.” Canadian Journal of Psychiatry 25 (1980):

Sandroni, P. “Aphrodisiacs Past and Present: A Historical Review.” Clinical Autonomic

Research 11 (2001): 303–7.
Siegel, D.M., and S.H. McDaniel. “The Frog Prince: Tale and Toxicology.” American

Journal of Orthopsychiatry 61 (1991): 558–62.


Pronunciation: boo-preh-NOHR-feen
Chemical Abstracts Service Registry Number: 52485-79-7. (Hydrochloride form


Formal Names: Buprenex, Subutex, Temgesic, Tidigesic

Type: Depressant (opiate class). See page 22

Federal Schedule Listing: Schedule V (DEA no. 9064). In 2002 a rescheduling to III was underway.

USA Availability: Prescription Pregnancy Category: C

Uses. This pain reliever is produced from thebaine and is both longer last- ing than morphine and 25 to 50 times stronger. Buprenorphine is given to persons suffering from conditions causing great discomfort, such as cancer, pancreatitis, and surgery. Experimental use of the drug to treat depression and schizophrenia has had promising results.

Drawbacks. Typical unwanted effects are sedation, nausea, constipation, dizziness, sweating, and low blood pressure. Impairment of breathing can occur. The drug can interfere with skills needed to operate a car or other dangerous machinery; volunteers in one experiment still had trouble eight hours after a dose. Visual or auditory hallucinations are possible. A medical case report tells of a heart attack after someone inhaled powder from a pul- verized oral buprenorphine tablet. Heart trouble has also been noted when the drug is used medically, but in a therapeutic context, such difficulty is very unusual. Long-term administration of the drug in mice can change their blood composition, including a drastic decline in the number of white blood cells, but these changes clear up after administration of buprenorphine stops.

Abuse factors. Although the drug produces sensations likened to those of morphine, when this book was written, buprenorphine was a Schedule V con- trolled substance, a classification reserved for drugs with the lowest addictive potential. Research conducted on behalf of the National Institute on Drug Abuse and published in 2001 found no illicit buprenorphine use in the United States but described the drug as having appeal to street markets. Such a mar- ket may develop; in an experiment testing opiate users’ ability to detect dif- ferences among drugs, the volunteers misidentified buprenorphine as heroin.

64 Buprenorphine

Buprenorphine abuse is well documented in other countries, ranging from Scotland and France to India and New Zealand.

People can become addicted to buprenorphine; one study found no differ- ence other than age between buprenorphine addicts and heroin addicts, sug- gesting the two drugs appeal to the same kinds of people. Given that finding, it is unsurprising that buprenorphine’s experimental use as an alternative to methadone has been successful in switching heroin addicts to buprenorphine. Various studies note that buprenorphine may create euphoria, an effect that is normally considered a drawback if a drug is used for treating addiction. Some researchers feel that buprenorphine has large potential for abuse. Treat- ing cocaine addiction with buprenorphine has had mixed success. Indeed, an experiment indicated that buprenorphine increases pleasurable effects from cocaine.

After a certain point, buprenorphine’s effects no longer increase as much when dosage size increases; this characteristic may deter addicts from taking too much buprenorphine and thereby make it a relatively safe substitute for heroin. An experiment demonstrated that persons lacking dependence with opiates could receive 70 times the normal medical dose of buprenorphine without harm, a safety factor of significance in addiction treatment programs, particularly since dependent persons (such as those in addiction treatment) normally can withstand even higher opiate doses than nondependent persons can. A statistical analysis of drug abuser fatalities in France concluded that the death rate from buprenorphine is far less than the rate from methadone. Another advantage to buprenorphine is that maintenance doses can be given less often than with methadone. Still another advantage is that, unlike most opiates, buprenorphine can provoke withdrawal symptoms when taken with another opiate. Thus addicts may be deterred from continuing to take heroin or other opiates while using buprenorphine. Some addicts, however, are able to take both heroin and buprenorphine simultaneously.

Tolerance does not necessarily develop with long-term use, although evi- dence of tolerance exists among buprenorphine addicts. Animals that are dosed on buprenorphine develop little or no dependence, a finding duplicated in a study of heroin addicts receiving maintenance doses of buprenorphine. Experiments show, however, that when buprenorphine addicts receive a drug that counteracts opiate actions, subjects experience classic symptoms of with- drawal from opiate dependence: yawning, muscle ache, and general uneasi- ness.

Drug interactions. An experiment showed that buprenorphine further ac- celerates pulse rates that are already raised by cocaine. Another human study and a monkey experiment found no significant interaction between cocaine and buprenorphine, but still another primate study showed buprenorphine as boosting cocaine effects. Researchers operating a rat study concluded that bu- prenorphine boosts cocaine actions, but mice studies found that buprenor- phine diminished some cocaine effects; such varying results from different animal species indicate the difficulty of applying those results to humans. A human experiment showed that blood flow damage in the brain caused by cocaine can improve after taking buprenorphine.

People using buprenorphine have suffered collapse of breathing and blood

Buprenorphine 65

circulation when also taking diazepam. Taking a monoamine oxidase inhibitor (MAOI—a component in some antidepressants and other medication) may be risky when using buprenorphine. Evidence exists that the drug may promote bleeding under the skin when taken with the anti–blood clot medicine phen- procoumon. Adverse interaction is also reported between buprenorphine and flunitrazepam. Antihistamines can add to buprenorphine’s general depressant effects. Another possible drug interaction involves nicotine; people using bu- prenorphine tend to increase their tobacco cigarette consumption. Buprenor- phine should be used with particular carefulness if a person suffers from enlarged prostrate, urination difficulty, alcoholism, thyroid gland deficiency, or adrenal gland deficiency.

Cancer. Animal experiments have not indicated that the compound pro- duces cancer.

Pregnancy. Pregnant rats receiving 1,000 times the normal human dose have had difficulty when giving birth. Early pregnancy failure and fetal deaths occurred when rats received 10 to 100 times the normal human dose, but not if they had 1,000 times the standard dose. No birth defects were seen at any of those dose levels. More experimentation shows that buprenorphine alters brain development in fetal rats, but the practical effects of those changes are unclear. Results from other research demonstrate long-term effects on behav- ior of offspring if pregnant rats receive high doses of buprenorphine; those measurements do not indicate what the human outcome would be but none- theless serve as a warning. Malformations occurred when pregnant rabbits received 1,000 times the recommended human dose. A case report says no malformations occurred when a pregnant heroin addict was switched to daily doses of buprenorphine for several months; the infant showed mild depen- dence but quickly got through the withdrawal symptoms. One group of re- searchers who gave daily doses of the drug to pregnant women observed no withdrawal symptoms in the infants, and offspring also had normal weight. Another group of researchers found no adverse effect on fetal development and no harm in infants born to pregnant women who were also using nicotine and marijuana in addition to buprenorphine. Buprenorphine has been given to premature newborns with no apparent ill effect.

Milk production declined after nursing rats received buprenorphine, and the same effect has been observed in women who received the drug during Caesarean section. The drug passes into human milk, but a case report indi- cates the amount is not enough to cause dependence in the infant.

Additional scientific information may be found in:

Agar, M., et al. “Buprenorphine: ‘Field Trials’ of a New Drug.” Qualitative Health Re- search 11 (2001): 69–84.

Bedi, N.S., et al. “Abuse Liability of Buprenorphine—A Study among Experienced Drug Users.” Indian Journal of Physiology and Pharmacology 42 (1998): 95–100.

Hammersley, R., T. Lavelle, and A. Forsyth. “Predicting Initiation to and Cessation of Buprenorphine and Temazepam Use amongst Adolescents.” British Journal of Addiction 87 (1992): 1303–11.

Heel, R.C. “Buprenorphine: A Review of Its Pharmacological Properties and Thera- peutic Efficacy.” Drugs 17 (1979): 81–110.

66 Buprenorphine

Lewis, J.W. “Buprenorphine.” Drug and Alcohol Dependence 14 (1985): 363–72. Pickworth, W.B. “Subjective and Physiologic Effects of Intravenous Buprenorphine in

Humans.” Clinical Pharmacology and Therapeutics 53 (1993): 570–76.
Zacny, J.P., K. Conley, and J. Galinkin. “Comparing the Subjective, Psychomotor and Physiological Effects of Intravenous Buprenorphine and Morphine in Healthy Volunteers.” Journal of Pharmacology and Experimental Therapeutics 282 (1997):



Pronunciation: byoo-TAL-bi-tall
Chemical Abstracts Service Registry Number: 77-26-9 Formal Names: Esgic, Fioricet, Fiorinal, Phrenilin, Sedapap Type: Depressant (barbiturate class). See page 20
Federal Schedule Listing: Schedule III (DEA no. 2100) USA Availability: Prescription
Pregnancy Category: C

Uses. The drug is a potent sedative. Butalbital’s primary medical use is for headache relief, and a product containing butalbital has also been found ef- fective in treating pain of oral surgery.

Drawbacks. In excessive amounts butalbital can interfere with breathing and induce coma. The drug can increase body temperature, cause reddening of the skin, slow manual dexterity, and bring on confusion and glumness, all rather reminiscent of what alcohol can do. Compared to other barbiturates butalbital is rather short acting, which can have the advantage of lessening the time that users experience unwanted effects.

Abuse factors. Excessive use can cause problems both when actively taking the drug and when the drug is stopped. A case is reported when butalbital was suspected of promoting periods of wandering with the person having no recollection of what happened during those times. A single dose of one thou- sand milligrams (mg) is considered a poisonous dose, and a woman who took 900 mg daily for more than two years developed hallucinations, seizures, and delirium when she stopped the drug; hospitalization was needed to cure those symptoms. Two individuals taking 1,500 mg daily for months became con- fused, experienced hallucinations, and needed medical help to wean them- selves from the drug. Persons taking butalbital for migraine have had grand mal brain seizures upon stopping the drug. Some medical practitioners feel that drug abuse is a cause of chronic headache, a belief that may make pre- scribing a controlled substance such as butalbital a touchy issue if a patient complains of daily headache.

Drug interactions. Monoamine oxidase inhibitors (MAOIs) can boost the effects of butalbital. Like other barbiturates, butalbital can increase the effects of alcohol and tranquilizers. Butalbital is suspected of decreasing the blood

68 Butalbital

levels of imipramine, so persons taking tricyclic antidepressants such as imip- ramine may need to have blood levels monitored.

Cancer. Not enough scientific information to report.

Pregnancy. Animal experiments apparently do not indicate butalbital’s po- tential for causing birth defects, but a large study of human pregnancy out- comes found no link between the drug and birth defects. In one case when a pregnant woman using butalbital gave birth, the child experienced seizures identified as butalbital withdrawal symptoms. Those symptoms disappeared when the infant received another barbiturate on a gradually decreasing dose that weaned the child off the drug.

Combination products. Fiorinal is a headache remedy that has had several formulations but is typically butalbital, aspirin, and caffeine. The product has been found useful for pain relief among women who have recently given birth, apparently more effective than propoxyphene. Also oral surgery patients have received good pain relief from Fiorinal and codeine. Fiorinal is known to produce a false positive for phenobarbital in body fluid testing. Abuse of the butalbital, aspirin, and caffeine (BAC) combination headache remedy can in itself cause rebound headaches. Although most persons feel no particular at- traction to that combination when they take it, a minority of users experience elevation of physical energy and psychic mood, which makes the tablets at- tractive. Persons have been known to take from 150 to 420 BAC tablets a month for years, habits requiring hospitalization and psychological help to overcome. Substituting acetaminophen for aspirin in this combination has been found to be just as good for treating headache and less likely to cause unwanted effects. This latter combination, under the brand name Fioricet, has been found to have the additional effect of relieving tension.

Sedapap and Phrenilin (both with butalbital and acetaminophen) are rem- edies for headaches produced by tension or muscle contraction. The combi- nation is not recommended for preadolescents or for persons suffering from porphyria, a condition involving disturbances in body chemistry and abnor- mal sensitivity to light. Potential for causing cancer or birth defects is un- known, and the combination is assigned to Pregnancy Category C. The combination passes into the milk supply of nursing mothers with unknown effect.

Additional scientific information may be found in:

Forbes, J.A. “Analgesic Effect of an Aspirin-Codeine-Butalbital-Caffeine Combination and an Acetaminophen-Codeine Combination in Postoperative Oral Surgery Pain.” Pharmacotherapy 6 (1986): 240–47.

Friedman, A.P., and F.J. DiSerio. “Symptomatic Treatment of Chronically Recurring Tension Headache: Placebo-Controlled, Multicenter Investigation of Fioricet and Acetaminophen with Codeine.” Clinical Therapeutics 10 (1987): 69–81.

Good, M.I. “Organic Dissociative Syndrome Associated with Antimigraine Pharma- cotherapy.” Canadian Journal of Psychiatry 36 (1991): 597–99.

Preskorn, S.H., R.L. Schwin, and W.V. McKnelly. “Analgesic Abuse and the Barbiturate Abstinence Syndrome.” Journal of the American Medical Association 244 (1980): 369–70.

Raja, M. “Severe Barbiturate Withdrawal Syndrome in Migrainous Patients.” Headache 36 (1996): 119–21.


Pronunciation: BYOO-tain

Chemical Abstracts Service Registry Number: 106-97-8

Formal Names: Butyl Hydride, Liquefied Petroleum Gas, Methylethylmethane, Pyrofax

Type: Inhalant. See page 26
Federal Schedule Listing: Unlisted
USA Availability: Nonprescription chemical Pregnancy Category: None

Uses. Some recreational use is for psychic effects: During butane intoxica- tion, time may appear to pass more slowly, and thoughts may seem to come faster. Other recreational usage has nothing to do with altered consciousness: Some persons ingest butane to perform the stunt of fire breathing, appearing to exhale flames by filling the mouth with butane and then exhaling over a flame source.

Drawbacks. Inhaling butane to achieve euphoria, hallucinations, and sen- sory distortion is one of the riskier forms of substance abuse. The amount required for hallucinatory action can be close to a lethal dose, making a slight miscalculation fatal.

Users have complained of headache and coughing. Lung injury is reported, ranging from fluid build-up and congestion to impaired breathing function and lung collapse. Unwanted effects can also include cardiac arrest, from which persons can seldom be resuscitated. A case report tells of a 14-year-old male who suffered a heart attack due to inhaling butane. Another case report describes a teenager who became paralyzed on one side of the body due to butane inhalation. Explosion is a common misadventure; one hospital in South Korea found that 1.6% of all flame burn patients had been abusing butane. Most were teenagers. Accidents often happened in a group setting in bed- rooms or motel rooms. Burns typically covered more than 25% of the body: face, hands, arms, midsection. About half the victims required skin grafts, and the overall death rate was just over 10%. An American case study noted how treacherous treatment can be for such injuries. A female was hospitalized after striking a match in a closed vehicle while inhaling butane. She was released after a couple of days but died a week later. In addition to external burns, the explosion had burned interior airways into the lungs, an injury that gradually

70 Butane

destroyed her ability to breathe. Medical caregivers emphasize the importance of victims honestly describing circumstances of a butane injury so that their lung condition will be properly examined in detail. Caregivers also emphasize that a person who experiences seemingly minor burns in a butane explosion should always seek immediate medical examination of the lungs, because breathing distress may not occur until several days later, when successful treatment is less likely.

Butane is suspected of causing liver damage and is suspected of making users ill-tempered.

Some recreational butane sniffers use sources also containing other ingre- dients. Those other substances can be harmful as well. For example, a case report notes problems encountered by someone who inhaled spray from oven cleaner that contained butane. Butane spray from aerosol cans and other pres- surized containers can be cold enough to cause frostbite. Cases have been seen of skin burns from the severe cold, also frostbite damage to the throat, lungs, and esophagus. Associated inflammation of stomach lining is also known. The instant severe cold can affect the vagus nerve, which influences voice qual- ity and affects heartbeat; such impact on the vagus nerve can produce heart failure.

A case report notes a habitual practitioner of the fire breathing stunt who developed stomach inflammation and a bleeding esophagus from irritation caused by repeated exposure to butane. Another case report tells of severe lung damage caused by exposure to unignited fumes. Judging from the ex- pected progress of such disease and from autopsy findings, such lung damage can be fatal. Because butane is heavier than air, it can flow into the lungs even if a person is trying to hold butane in the mouth without inhaling. One fire breather routinely swallowed some of the butane, numbing the rear of the mouth.

Abuse factors. Authorities have described butane’s effects as weaker and having less addictive appeal than those of toluene. Tolerance and dependence are reported. Withdrawal may involve several days of nausea, perspiration, crankiness, troubled sleep, abdominal cramps, and general shakiness.

Drug interactions. Not enough scientific information to report. Cancer. Potential for causing cancer is unknown.
Pregnancy. Potential for causing birth defects is unknown. Additional scientific information may be found in:

Evans, A.C., and D. Raistrick. “Patterns of Use and Related Harm with Toluene-Based Adhesives and Butane Gas.” British Journal of Psychiatry 150 (1987): 773–76.

Evans, A.C., and D. Raistrick. “Phenomenology of Intoxication with Toluene-Based Adhesives and Butane Gas.” British Journal of Psychiatry 150 (1987): 769–73.

Gomibuchi, K., T. Gomibuchi, and H. Kurita. “Treatment and 9-Year Outcome of Butane-Induced Psychotic Disorder in a Butane-Dependent Japanese Male Ad- olescent.” Psychiatry and Clinical Neurosciences 55 (2001): 163.

Gray, M.Y., and J.H. Lazarus. “Butane Inhalation and Hemiparesis.” Journal of Toxicol- ogy: Clinical Toxicology 31 (1993): 483–85. Hemiparesis is paralysis on one side of a person’s body.

Butane 71

Marsh, W.W. “Butane Firebreathing in Adolescents: A Potentially Dangerous Practice.” Journal of Adolescent Health Care 5 (1984): 59–60.

Oh, S.J., et al. “Explosive Burns during Abusive Inhalation of Butane Gas.” Burns 25 (1999): 341–44.

Rieder-Scharinger, J., et al. “Multiorganversagen nach Butangasinhalation: Ein Fallbe- richt [Multiple Organ Failure Following Inhalation of Butane Gas: A Case Re- port].” Wiener Klinische Wochenschrift 112 (2000): 1049–52. Abstract in English.

Rohrig, T.P. “Sudden Death Due to Butane Inhalation.” American Journal of Forensic Medicine and Pathology 18 (1997): 299–302.


Pronunciation: byoo-TOR-fa-nohl
Chemical Abstracts Service Registry Number: 42408-82-2. (Tartrate form 58786-

Formal Names: Dorphanol, Stadol, Stadol NS, Torbugesic Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule IV (DEA no. 9720) USA Availability: Prescription
Pregnancy Category: C

Uses. This pain reliever is a narcotic agonist/antagonist, meaning that it acts like an opioid when used by itself but counteracts other opioids if given simultaneously with them; the counteraction can be significant enough to pro- voke a withdrawal syndrome if a person is dependent on the other opioids.

Butorphanol is used to control pain in conditions ranging from cancer and surgery to migraine headache and dental work. Women seem to achieve better pain control from butorphanol than men. The drug also suppresses coughs, and researchers have found that it improves appetite. The substance has been used illicitly by the type of bodybuilders who take nalbuphine and for the same reasons (to reduce pain from workouts and in hopes of promoting mus- cle mass).

Experiments show butorphanol to be about 4 to 7 times stronger than mor- phine, 20 to 30 times stronger than pentazocine, and 30 to 50 times stronger than meperidine. Butorphanol is powerful enough that it has been used to help sedate rhinoceroses. The substance has other veterinary uses as well, including illicit doping of racehorses to improve performance (at certain dos- ages opioids can both excite the animals and mask pain).

Drawbacks. Unwanted effects include uneasy feelings, ill temper, sleepi- ness, dizziness, nausea, vomiting, blood pressure changes (up or down), and impaired breathing. Reports of hallucinations and psychoses exist. People us- ing the drug can feel faint if they suddenly stand up. The drug can make people woozy and cloud their thinking, impeding their ability to operate dan- gerous machinery. Illicit users who inject butorphanol into muscles can cause damage that is long-lasting, if not permanent.

Abuse factors. Tolerance and dependence can develop. Withdrawal symp- toms are characterized as minor. Addiction is possible but is not commonly

Butorphanol 73

reported in scientific literature. Two investigators say, however, that depen- dency and addiction were the most frequent adverse reaction reports about the drug received by the U.S. Food and Drug Administration in the early 1990s. Heroin users who received butorphanol in an experiment described butorphanol as unpleasant. Former opioid addicts have said it reminded them of pentazocine. At one time in the United States butorphanol was not a con- trolled substance, but instances of addiction prompted government authorities to change the drug’s status to Schedule IV in 1997.

Drug interactions. Some recreational users combine butorphanol with the common cold and allergy remedy diphenhydramine to produce a typical opiate-type stupor. Users of that combination sometimes report loss of interest in other drugs. Unwanted results can include emotional flip-flops, dizziness, nausea, vomiting, breathing difficulty, and general reduction of mental and physical abilities. Withdrawal symptoms from the combination may involve impaired concentration, mental restlessness and unease, and emotional insta- bility and peevishness.

In a mice experiment butorphanol and acetaminophen (Tylenol and similar products) boosted each other’s pain relieving effects.

Cancer. Laboratory tests and two-year animal experiments have not indi- cated that butorphanol causes cancer.

Pregnancy. Research using rats, mice, and rabbits has not yielded evidence of birth defects caused by butorphanol, but some of the experiments produced fetal death. The drug passes from a pregnant woman into the fetus and can cause abnormal fetal heartbeat. When used in childbirth, impact on newborns is similar to that of meperidine; respiratory distress can occur in the infant. One study found the average drug level in newborns to match the maternal level at time of birth. The amount of drug that passes into milk is believed unharmful to nursing infants.

Additional scientific information may be found in:

Fisher, M.A., and S. Glass. “Butorphanol (Stadol): A Study in Problems of Current Drug Information and Control.” Neurology 48 (1997): 1156–60.

Gillis, J.C., P. Benfield, and K.L. Goa. “Transnasal Butorphanol: Review of Its Phar- macodynamic and Pharmacokinetic Properties, and Therapeutic Potential in Acute Pain Management.” Drugs 50 (1995): 157–75.

Rosow, C.E. “Butorphanol in Perspective.” Acute Care 12 (1988, Suppl. 1): 2–7.
Smith, S.G., and W.M. Davis. “Nonmedical Use of Butorphanol and Diphenhydra-

mine.” Journal of the American Medical Association 252 (1984): 1010.
Vogelsang, J., and S.R. Hayes. “Butorphanol Tartrate (Stadol): A Review.” Journal of

Post Anesthesia Nursing 6 (1991): 129–35.
Zacny, J.P., et al. “Comparing the Subjective, Psychomotor and Physiological Effects of

Intravenous Butorphanol and Morphine in Healthy Volunteers.” Journal of Phar-

macology and Experimental Therapeutics 270 (1994): 579–88.
Zacny, J.P., et al. “The Effects of Transnasal Butorphanol on Mood and Psychomotor

Functioning in Healthy Volunteers.” Anesthesia and Analgesia 82 (1996): 931–35.


Pronunciation: KAFF-een
Chemical Abstracts Service Registry Number: 58-08-2
Type: Stimulant. See page 11
Federal Schedule Listing: Unlisted
USA Availability: Prescription and nonprescription drug; also in food Pregnancy Category: C

Uses. This drug is responsible for the stimulating jolt that coffee drinkers get. Many drinkers would probably be surprised to see caffeine listed as an ingredient in medicines they take. Caffeine is so widely used (typically in coffee, tea, soda, and chocolate) that it is scarcely considered a drug. Yet an overdose can be fatal.

Caffeine makes people more alert, and experimentation finds that it can help persons function more effectively during sleep deprivation. Caffeine is com- monly used in the workplace to increase employees’ energy and output. Lab- oratory measurements indicate that a single dose of 250 mg to 400 mg at the beginning of a night work shift is more effective than several smaller doses spread out during the work period. Some studies find that caffeine helps ex- troverts perform simple physical assignments but overstimulates introverts and thereby worsens their performance. Scientific measurements prove that caffeine, by itself or in combination with ephedrine, improves athletic perfor- mance.

Like some amphetamine class stimulants, caffeine has reduced hyperactivity in children when they received 600 mg daily, but it has been found ineffective for attention deficit hyperactivity disorder (ADHD).

Studies demonstrate caffeine can mildly help asthma sufferers. Theophyl- line, a drug commonly used to widen airways and help asthmatics breathe, is related to caffeine. Caffeine is a standard drug to help premature infants that have interruptions in breathing.

Rat experiments indicate that caffeine can promote weight loss. In humans a combination of caffeine and ephedrine has been used for that purpose. A study found that caffeine increased women’s energy outlay and body tem- perature but that the temperature change correlated with smaller weight and waistlines only in younger women.

Caffeine has been suspected of promoting osteoporosis, a disease causing

Caffeine 75

loss of bone density in older women; studies controlling other factors (such as cigarettes and drugs promoting calcium loss) found that caffeine had no tendency to reduce bone density, but one study published in 2000 and tracking almost 35,000 postmenopausal women found a slight correlation of caffeine usage to broken bones—a correlation implying loss of density. Coffee drinking is associated with loss of density. In contrast, examination of over 1,200 older women in England showed that tea drinkers were less likely to have osteo- porosis, leading investigators to wonder if something in tea, other than caf- feine, affects bone density.

Investigators examining caffeine consumption in a group of 8,000 men who were tracked for three decades discovered that the more caffeine someone ingested over the years, the less likely the person was to come down with Parkinson’s disease. In a group of 46,000 men tracked for a decade, increased consumption of caffeinated coffee was linked to decreased likelihood of having gallstones; consumption of decaffeinated coffee did not have such a link. As one analyst pointed out, such associations are interesting but do not prove cause and effect; for example, perhaps some physical aspect leading to Parkinson’s disease also makes caffeine beverages unappealing—thus persons without the disease would consume more caffeine beverages than sufferers do, but that consumption would not mean that caffeine prevents the affliction.

Mice experiments demonstrate that if caffeine is administered in the right amount and at the right time before exposure to radiation, the drug will allow mice to survive otherwise lethal amounts of radiation.

Drawbacks. In the 1990s, 20% of the U.S. population was believed to be using over 700 mg of caffeine each day. That is enough to produce behavior mimicking an anxiety neurosis. If a person only ingests caffeine through phar- maceutical preparations or food products with labels listing caffeine amounts, intake can easily be measured. The amount in a restaurant cup of coffee is more difficult to measure; one rule of thumb says 100 mg to 150 mg.

The substance can accelerate pulse rate; it can also make people more pee- vish and jumpy (even promote panic attacks) and interfere with getting good sleep. Caffeine can cause heartburn and increase urine output. Experimenta- tion has confirmed that the drug’s tendency to promote loss of body fluid will dry the vocal cords and affect voice quality.

Analysis of over 30 years of reports about caffeine and blood pressure found that the drug reliably increased blood pressure when persons began using it but that the effect did not persist in all users. Investigators measuring blood pressure among medical students found caffeine raising the readings far enough that anyone at risk for high blood pressure should avoid the drug during times of stress. Persons with coronary artery disease may be at signif- icant risk for sudden cardiac arrest if they drink more than 10 cups of coffee a day.

Excessive doses can dangerously reduce blood potassium levels, damage muscles, produce extremely rapid heartbeat, and cause delirium and seizures. As the twenty-first century began a case report associated caffeine with retina damage in several persons.

Abuse factors. Coffee was formerly treated as an illicit drug. Centuries ago possession was a death penalty offense in Spain and the Near East. In the

76 Caffeine

early twentieth century one standard medical textbook warned of coffee ad- diction peril, and another medical volume described coffee as a gateway to opiate addiction. In a modern study volunteers showed no particular desire for caffeine but did find that 300 mg mimicked some effects of dextroam- phetamine. Although caffeine is not a scheduled substance, users can develop a physical dependence on the drug that results in withdrawal symptoms in- cluding weariness and headache. Such symptoms are not inevitable nor are they necessarily troubling to persons experiencing them. In 2000 an interna- tional panel of experts convened by European drug regulation agencies de- scribed caffeine’s potential for dependence as low. Tolerance can develop to some of caffeine’s effects.

Drug interactions. Caffeine itself can reduce headache, and an experiment involving hundreds of participants showed caffeine to substantially improve ibuprofen’s ability to relieve headache. Phenylpropanolamine is a drug com- monly found in remedies for colds. It seems to increase caffeine levels in a person using both drugs, and together the two can produce mood elevation, hyperactivity and manic behavior, confusion, high blood pressure, and stroke. In rat experiments, caffeine boosts the effects of cocaine and amphetamine, enough to transform normally tolerable doses into fatal ones. Human obser- vations show that cocaine users tend to take lower doses of that drug if they also use caffeine. Perhaps the most common drug taken with caffeine is nic- otine. Animal experiments find that interactions of that combination may make cigarette smoking more pleasurable. Cigarette smoking increases the body’s rate of metabolizing caffeine, which decreases the influence from a given amount of caffeine; British researchers found that smokers tend to use more caffeine than nonsmokers. Birth control pills can double the time that a given amount of caffeine lasts in the body. The drug can reduce drowsiness produced by pentobarbital, and it can reduce diazepam’s interference with cognitive function. Caffeine is a traditional remedy for alcohol intoxication, but in fact it does not speed alcohol’s elimination from the body, although caffeine’s stimulant properties may help a drunken person function better. Estrogen replacement therapy appears to interfere with women’s ability to metabolize caffeine.

Cancer. Caffeine does not seem to produce cancer in animal experiments. Indeed, green and black tea reduce development of cancer in mice, an effect in which caffeine is believed to play a part. In humans, however, caffeine is suspected of promoting premenopausal ovarian cancer and also cancer of the pancreas and bladder.

Pregnancy. Experiments examining caffeine’s influence on pregnancy yield conflicting results, which may indicate the question is particularly complex or may simply mean that caffeine is an “invalid variable” having no effect. Here are examples. A 1994 survey of 259 women in the Netherlands found that caffeine raised the likelihood of becoming pregnant, but when the same subject was examined in the 1980s among almost 2,000 women in Connecticut, caf- feine was found to suppress fertility. During the 1990s a study of farm couples in Canada found that caffeine had no effect on fertility but that coffee-drinking women and tea-drinking men had lower birthrates, suggesting involvement of something besides caffeine in the natural products’ effect. Rat experimen-

Caffeine 77

tation shows that caffeine reduces female fertility, produces smaller than usual offspring, and may affect brain development.

Research in Yugoslavia indicates that pregnant women who do not smoke cigarettes but do take more than 71 mg of caffeine daily have smaller infants. A British study found the opposite; slightly smaller infants came from cigarette-smoking women who used 1,000 mg or more of caffeine a week, but the effect was not seen in nonsmokers. Still other studies find no connection between caffeine and either birthweight or prematurity.

Caffeine affects vital signs in a human fetus even when the dose is so low as to have no influence on the pregnant woman.

Question has arisen about whether caffeine promotes spontaneous abortion; a study published in 1994 found 140 mg to 280 mg a day to pose a significant risk; a rigorous study published in 1999 was unable to find such a hazard among moderate caffeine users; and a study published in 1993 saw caffeine as reducing the incidence of spontaneous abortion. Still another study found that women who drank decaffeinated coffee were even more likely to expe- rience a spontaneous abortion than women who drank caffeinated coffee. Re- search in New Zealand indicated that sudden infant death syndrome (SIDS) was more likely if a woman had ingested more than 400 mg of caffeine daily during pregnancy, but an examination of SIDS in Scandinavia found no cor- relation with caffeine use during or after pregnancy.

Instant coffee can damage DNA, but implications for general health or birth defects are unclear. Testing caffeine on mice produced birth defects in limbs, and tests on chicken embryos produced heart deformities. Chicken embryos, however, are so sensitive to various chemicals that such results are not con- sidered a warning of human danger. Indeed, a substantial body of research indicates that caffeine causes no human birth defects.

Evidence does exist that caffeine can increase the likelihood of birth defects caused by alcohol and tobacco. An Egyptian study found that caffeine in- creases alcohol birth defects in rats.

A statistical study showed that women who use more than 300 mg of caf- feine daily around the time of conception and who do not smoke are less likely to have infants with Down syndrome.

Given all the uncertainties, pregnant women are advised to use caffeine “moderately”—no more than 200 mg to 300 mg daily (150 mg or less is con- sidered “minimal”).

Caffeine increases milk production in nursing mothers and passes into the milk but appears unharmful to infants if the women are moderate users. On occasions when mothers use a lot of caffeine, however, their nursing infants may be fussier and have more trouble sleeping. A dose lasts longer in infants than in older persons.

Additional scientific information may be found in:

Anderson, M.E., et al. “Improved 2000-Meter Rowing Performance in Competitive Oarswomen after Caffeine Ingestion.” International Journal of Sport Nutrition and Exercise Metabolism 10 (2000): 464–75.

Eskenazi, B. “Caffeine—Filtering the Facts.” New England Journal of Medicine 341 (1999): 1688–89.

78 Caffeine

Golding, J. “Reproduction and Caffeine Consumption—A Literature Review.” Early Human Development 43 (1995): 1–14.

Marsden, G., and J. Leach. “Effects of Alcohol and Caffeine on Maritime Navigational Skills.” Ergonomics 43 (2000): 17–26.

Nurminen, M.-L., et al. “Coffee, Caffeine and Blood Pressure: A Critical Review.” Eu- ropean Journal of Clinical Nutrition 53 (1999): 831–39.

Reyner, L.A., and J.A. Horne. “Early Morning Driver Sleepiness: Effectiveness of 200 Mg Caffeine.” Psychophysiology 37 (2000): 251–56.

Smit, H.J., and P.J. Rogers. “Effects of Low Doses of Caffeine on Cognitive Performance, Mood and Thirst in Low and Higher Caffeine Consumers.” Psychopharmacology (Berlin) 152 (2000): 167–73.

Tanda, G., and S.R. Goldberg. “Alteration of the Behavioral Effects of Nicotine by Chronic Caffeine Exposure.” Pharmacology, Biochemistry, and Behavior 66 (2000): 47–64.

Chloral Hydrate

Pronunciation: KLOHR-ul HIGH-drait
Chemical Abstracts Service Registry Number: 302-17-0
Formal Names: Aquachloral, Chloradorm, Chloralex, Felsules, Noctec, Somnos Informal Names: Jelly Beans, Knockout Drops, Mickey Finn, Mickeys
Type: Depressant. See page 19.
Federal Schedule Listing: Schedule IV (DEA no. 2465)
USA Availability: Prescription
Pregnancy Category: C

Uses. This substance is the first synthetic central nervous system depressant, created in the 1830s. After that creation, however, several decades passed be- fore chloral hydrate’s medical usage as a sleep inducer began. The anesthetic chloroform is produced from it. Chloral hydrate has also been used against pain of rheumatism. In the nineteenth century the drug was popular among middle-class women and middle-aged men for reducing anxiety.

In former times chloral hydrate was routinely administered to produce an- esthesia, but such use is tricky; the difference between an effective dose and a poisonous one is so close that the drug has been replaced by other substances for human anesthesia, although chloral hydrate is still used for that purpose in animals. The substance has been largely superseded by barbiturates but still has medical applications as a sedative and to induce sleep. Chloral hydrate is also used to treat seizures caused by fever and is a secondary choice for con- trolling the seizures of status epilepticus (an emergency in which persons keep having epileptic seizures, one after another, with little or no letup). Medical caregivers sometimes administer chloral hydrate to help withdrawal from her- oin and GHB dependence and to help alcohol addicts withstand delirium tremens during withdrawal. The famed “Mickey Finn” drug used by criminals to knock out victims was a combination of chloral hydrate and alcohol, but animal and human experiments have failed to demonstrate that the combi- nation worked as advertised.

Drawbacks. Chloral hydrate users may act drunken and confused. An ex- periment found reduction in abilities needed to drive an automobile. The same research, however, also showed that if the product was taken to induce sleep the night before, persons performed better the next day after the drug had worn off, presumably because they were better rested than usual. At normal

80 Chloral Hydrate

doses gastrointestinal distress may occur, and persons suffering from stomach irritation are supposed to avoid the compound. A case report notes a delib- erate overdose that destroyed part of a patient’s stomach. Heart attack has occurred from chloral hydrate overdose, but that is unusual. In high quantities the compound interferes with heart rhythm and reduces blood pressure and breathing; seizures are possible. Experiments using chloral hydrate on rats and mice have injured the liver, and inhaling the drug’s vapor has caused lung damage in mice. Human physical contact with the compound can irritate the skin, lungs, and eyes. The substance is suspected of causing kidney damage and colon cysts and of aggravating a disease called porphyria. Reduction may occur in the number of white blood cells. Although the substance is a de- pressant, some persons are stimulated by the drug.

Abuse factors. In the 1800s a number of prominent persons became addicted to chloral hydrate: English poet and painter Dante Gabriel Rossetti, German literary figure Karl Ferdinand Gutzkow, and renowned German philosopher Friedrich Wilhelm Nietzsche. Such addiction grew uncommon in the twentieth century as the drug itself grew less common. As is so often the case with drug abuse, chloral hydrate addicts were typically polydrug abusers, often using alcohol, opium, or morphine as well. Today chloral hydrate does not seem to be a popular recreational intoxicant, quite possibly because the kind of person who would enjoy chloral hydrate may instead be attracted to barbiturates, a type of drug that was unavailable in the nineteenth century.

No dependence developed after experimenters gave chloral hydrate to mon- keys twice a day for six weeks, but tolerance and dependence can develop in humans. The most common origin of dependence is medical usage. Chloral hydrate withdrawal symptoms include tremors, worry, sleeping difficulty, confusion, delirium, hallucinations, and convulsions. Some authorities de- scribe the syndrome as delirium tremens. Withdrawal may have a fatal out- come.

Drug interactions. Actions of anti–blood clotting medicines may be tem- porarily boosted by chloral hydrate, but the amount of change and its medical significance are disputed. The drug may reduce blood levels of the epilepsy medicine phenytoin, thereby impeding phenytoin’s therapeutic actions. In mice experimentation chloral hydrate had inconsistent impact on alcohol blood level (sometimes raising it, sometimes reducing it) but extended the time that intoxication lasted. In humans the combination produces changes in heart rate and blood pressure that might harm cardiac patients (the face and neck of one volunteer turned reddish purple from the combination). Alcohol and chloral hydrate are both depressants, and taking them together is like taking an extra dose of one or the other. Injecting marijuana’s main active ingredient THC (tetrahydrocannabinol) into animals increases chloral hy- drate’s potency.

Cancer. Lab tests of chloral hydrate’s potential for causing cancer have pro- duced mixed results. The compound has increased the liver cancer rate in mice, but skepticism exists about human relevance of those mice results be- cause dosage was long term and so high as to be poisonous—circumstances not at all similar to an occasional normal therapeutic dose. Experimenters administered the substance to hundreds of rats every day for over two years

Chloral Hydrate 81

without evidence developing that the drug causes cancer. The cancer-causing potential in humans is uncertain.

Pregnancy. Chloral hydrate passes from a pregnant woman into the fetus but is not considered a cause of birth defects. Infants born to such women are, however, more likely to have a condition called hyperbilirubinemia, which can lead to jaundice. Some investigators also believe that administering the drug to infants after birth causes hyperbilirubinemia. The compound passes into the milk of a nursing mother, enough to slightly sedate the infant.

Additional scientific information may be found in:

Butler, T.C. “The Introduction of Chloral Hydrate into Medical Practice.” Bulletin of the History of Medicine 44 (1970): 168–72.

Miller, R.R., and D.J. Greenblatt. “Clinical Effects of Chloral Hydrate in Hospitalized Medical Patients.” Journal of Clinical Pharmacology 19 (1979): 669–74.

Robinson, J.T. “A Case of Chloral Hydrate Addiction.” International Journal of Social Psychiatry 12 (1966): 66–71.

Sellers, E.M., et al. “Interaction of Chloral Hydrate and Ethanol in Man. II. Hemodyn- amics and Performance.” Clinical Pharmacology and Therapeutics 13 (1972): 50–58. Sourkes, T.L. “Early Clinical Neurochemistry of CNS-Active Drugs. Chloral Hydrate.”

Molecular and Chemical Neuropathology 17 (1992): 21–30.
Steinberg, A.D. “Should Chloral Hydrate Be Banned?” Pediatrics 92 (1993): 442–46.


Pronunciation: klor-dye-az-uh-POX-ide
Chemical Abstracts Service Registry Number: 58-25-3. (Hydrochloride form 438-

Formal Names: Libritabs, Librium, Limbitrol
Informal Names: Libs
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2744) USA Availability: Prescription
Pregnancy Category: D

Uses. Chlordiazepoxide was the first benzodiazepine tranquilizer and has been commonly used since 1960. It is considered one of the safer psychiatric drugs and has actions comparable to those of barbiturates and alcohol.

This classic benzodiazepine is used mainly for calming anxiety and for treat- ing symptoms of alcohol withdrawal, including delirium tremens. Studies have found, however, that alcoholics receiving this drug to help them through withdrawal are about three times more likely to resume drinking than alco- holics who receive a placebo. The substance is also used to overcome convul- sions and to treat insomnia, migraine headache, gastric ulcers, and irritable bowel syndrome (persistent cramps and diarrhea). Actions from a dose of this drug take longer to appear than actions from a dose of lorazepam or diaze- pam, so those latter substances are sometimes preferred when faster results are needed.

Researchers have used rats and mice to demonstrate partial cross-tolerance between pentobarbital, alcohol, and chlordiazepoxide, and that relationship may contribute to the latter’s therapeutic role in treating alcohol withdrawal. An argument has been made that when clinical signs of alcohol withdrawal can be treated as well with chlordiazepoxide as with lorazepam, the former is preferable because of cheaper cost. Chlordiazepoxide can be substituted for alprazolam to wean someone from that drug, although one study found chlor- diazepoxide to be about 86 times weaker than alprazolam (consistent with animal experiments, where large doses of chlordiazepoxide are needed to pro- duce dependence). Chlordiazepoxide can be used in place of most benzodi- azepines if someone who stops taking one of those drugs is troubled by

Chlordiazepoxide 83

withdrawal. An experiment found chlordiazepoxide to be as effective as meth- adone in easing opiate withdrawal symptoms experienced by heroin addicts. Drawbacks. Chlordiazepoxide is one of the longer-lasting benzodiazepines, which can have advantages—but it can also have disadvantages; for example, the drug is associated with higher chance of hip fractures in older persons,

perhaps because it makes them unsteady longer and more likely to fall. Blood disorders can be an unusual unwanted effect, and a case is reported in which long-term use produced purpura, tiny purple spots in the skin caused by bleeding under the skin surface. Although the drug is used to re- lieve anxiety, studies conflict on whether it increases users’ hostility. The drug reduces aggression in animal experiments, and human aggression is certainly not a typical result of a dose; perhaps lowered anxiety among resentful per- sons also lowers inhibitions, allowing those angry individuals to engage in aggression they had been afraid to attempt. That outcome is more likely when a person using chlordiazepoxide has also been drinking alcohol, and alcohol definitely can lower inhibitions. Chlordiazepoxide can make people weary, degrade verbal communication ability, and raise or lower interest in sex. Among alcoholics, measurements find that chlordiazepoxide reduces rapid eye movement (REM) sleep and delta (deep) sleep; those types are considered important for maintaining normal mental functioning. A case report indicates that the substance may worsen symptoms of Parkinson’s disease, possibly due to untoward reaction with the Parkinson’s drug levodopa. Another case report notes a diabetic whose blood sugar levels rose substantially while taking chlor- diazepoxide. An instance is known of continual hiccups starting soon after a person started taking the drug and stopping soon after the drug dosage

stopped. Still another case report associated the drug with gout.
Persons who receive chlordiazepoxide by injection should avoid hazardous activity (such as driving a car) for several hours; a test of the oral format showed that it lowered driving ability as well. Drivers can be unaware that chlordiazepoxide is affecting them. A study of bronchitis patients found that the drug worsened their breathing, and in general the compound impairs respiration. Chlordiazepoxide is also suspected of worsening porphyria, a dis- ease involving body chemistry and that makes a person extremely sensitive to light. Porphyria caused the madness of George III, king of Great Britain

during the American Revolution.
Abuse factors. Sudden stoppage of chlordiazepoxide dosage can produce

symptoms similar to those of alcohol or barbiturate withdrawal: tremors and cramps, vomiting, perspiring, and even convulsions.

Drug interactions. When delta-9-tetrahydrocannabinol (also called THC, the main psychoactive chemical in marijuana) was given to pregnant mice in an experiment, administering chlordiazepoxide along with THC raised the blood level of THC. Another mice experiment showed an increase in THC’s catalep- tic effect when chlordiazepoxide was administered. In mice chlordiazepoxide can increase potency of the anticancer drug ifosfamide, and in both mice and humans alcohol can boost chlordiazepoxide’s potency (though a rat experi- ment did not find that effect). In humans monoamine oxidase inhibitors (MAOIs) boost chlordiazepoxide actions, and the antacid-heartburn medicine cimetidine lengthens the effect of a chlordiazepoxide dose. Cigarette smoking

84 Chlordiazepoxide

reduces chlordiazepoxide actions, and morphine and meperidine each make oral dosage of chlordiazepoxide less effective. The drug is suspected of af- fecting blood clotting and is known to constrain the healing abilities of the anticoagulant medicine warfarin.

Cancer. Chlordiazepoxide has produced DNA damage in experiments de- signed to reveal potential for such defects. Under certain laboratory conditions the drug can promote DNA damage in rats, which theoretically might en- courage development of cancer, but that outcome has not been observed in practice.

Pregnancy. “Nitrosatable” drugs, of which chlordiazepoxide is one, cause birth defects in animal experiments. Some studies suggest that using chlor- diazepoxide during pregnancy may cause human birth defects, but confir- mation is elusive. For example, a study of 50,000 pregnancies published in 1975, including many women who used chlordiazepoxide, found no difference in outcome regardless of whether women used the drug. In contrast, a study of almost 20,000 pregnancies (published in 1974) compared women who took chlordiazepoxide to those who took assorted other antianxiety drugs or none at all in early pregnancy. In the chlordiazepoxide group birth defects were more than two times as frequent compared to the “other drugs” group and over four times as frequent compared to the “no drug” group. Some research- ers believe chlordiazepoxide may cause infant skull deformities if a pregnant woman uses the drug.

Combination products. Limbitrol is a combination product using chlordi- azepoxide to reduce anxiety and amitriptyline as a tricyclic antidepressant. Taking a tricyclic antidepressant along with an MAOI can be fatal. Tricyclics are not recommended for persons with glaucoma or urinary difficulties. An experiment with hamsters showed that the drug combination is more likely to produce birth defects than either drug alone. Amitriptyline is Pregnancy Category C and passes into a nursing mother’s milk supply.

Additional scientific information may be found in:

Giri, A.K. and S. Banerjee. “Genetic Toxicology of Four Commonly Used Benzodiaze- pines: A Review.” Mutation Research 340 (1996): 93–108.

Harmatz, J.S., et al. “Differential Effects of Chlordiazepoxide and Oxazepam on Hos- tility in a Small Group Setting.” American Journal of Psychiatry 132 (1975): 861–63.

Palva, E.S., and M. Linnoila. “Effect of Active Metabolites of Chlordiazepoxide and Diazepam, Alone or in Combination with Alcohol, on Psychomotor Skills Re- lated to Driving.” European Journal of Clinical Pharmacology 13 (1978): 345–50.

Salzman, C., et al. “Chlordiazepoxide-Induced Hostility in a Small Group Setting.” Archives of General Psychiatry 31 (1974): 401–5.

Sternbach, L.H. “The Discovery of Librium.” Agents and Actions 43, nos. 3–4 (1994): 82– 85.


Pronunciation: kloh-NA-zuh-pam
Chemical Abstracts Service Registry Number: 1622-61-3 Formal Names: Iktorivil, Klonopin, Lansden, Rivotril Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2737) USA Availability: Prescription
Pregnancy Category: D

Uses. Clonazepam is considered one of the more powerful benzodiazepine class drugs. Primary medical uses are against some kinds of convulsions, par- ticularly in certain kinds of epilepsy, and against panic attacks. For persons suffering from panic attacks, measurements indicate the drug improves both quality of life and work productivity. The drug is also used as an antidepres- sant and to treat anxiety, catatonia, obsessive-compulsive disorder, the manic phase of manic-depressive behavior, and social phobia in general. A two-year follow-up study of persons receiving brief clonazepam treatment for social phobia found their improvement to be sustained after dosage stopped, and at the two-year mark they were doing better than a control group that had re- ceived a placebo. Clonazepam is sometimes preferred over alprazolam in treating anxiety because that condition seems less likely to reappear between doses of clonazepam than between doses of alprazolam. Clonazepam can be substituted for alprazolam in order to withdraw persons who have depen- dence with the latter drug. Clonazepam has been used to fight tics and also to treat muscle control diseases such as akathisia and tardive dyskinesia. Among children with attention deficit hyperactivity disorder (ADHD) who also have tics, a study found clonazepam could help suppress tics without harming the psychiatric effect of ADHD medicine. Although clonazepam is not a multiple sclerosis medicine, it is administered to relieve the affliction’s symptoms. Clonazepam has helped reduce fainting spells. It is prescribed to relieve insomnia and to reduce a disorder in which sleeping persons thrash about. The substance has promoted cure of sleepwalking, including a docu- mented extreme case in which a sleeping person would drive a car and engage in violence involving knives. The drug can relieve pain caused by jaw trouble and has been given to cancer patients to reduce vomiting from chemotherapy. Clonazepam and the antimania medicine lithium have been experimentally

86 Clonazepam

administered together as a successful treatment for cluster headaches. Clona- zepam has eased burning mouth syndrome, a self-descriptive sensation that can persist for years. The drug has been used experimentally with limited success to treat ringing in the ears.

Drawbacks. Clonazepam is not recommended for persons suffering from narrow-angle glaucoma. The compound may worsen respiratory disease. The substance increases saliva production. It often makes people tired, interferes with muscular coordination, and can impede decision making; such effects hinder ability to operate dangerous machinery. Dozens of less common ad- verse effects are described, ranging from skin rash to painful gums. One case report concludes that clonazepam may promote porphyria, a body chemistry disorder that can make a person violent and supersensitive to light, but such a result is virtually unheard of. A review of medical records of men being treated for posttraumatic stress disorder suggested that the drug may com- monly inhibit sexual performance in such a population. Some persons suffer from a disquieting affliction called apnea in which they temporarily stop breathing; case reports say clonazepam can cause apnea attacks. An experi- ment noted a rebound effect when people stop taking the drug for insomnia, meaning the condition is not cured but instead returns worse than ever, at least for awhile.

Contrary to normal expectations, the drug has occasionally been reported to bring on mania and even aggression. One case report noted that if panic attacks act as a warning against certain behavior, clonazepam’s ability to re- duce or eliminate panic attacks can also remove a person’s inhibitions against the behavior. A small study suggests that clonazepam may reduce inhibitions in children, and case reports exist about the same effect in children, teenagers, and adults. Researchers curious about whether clonazepam especially reduces inhibitions examined medical records of 323 persons institutionalized for psy- chiatric disturbance, a population in which such a clonazepam effect might be particularly evident; although the study was not designed to demonstrate cause and effect, the records were consistent with a low risk of reduced in- hibition from clonazepam and other benzodiazepine class drugs.

Abuse factors. Clonazepam has a withdrawal syndrome similar to alcohol’s: cramps and tremors, convulsions, hallucinations, and general mental distress. The syndrome can be avoided if a person reduces dosage gradually. Suddenly halting the drug after taking it for an extended period of time can cause ep- ileptic seizures.

Drug interactions. Clonazepam’s actions can be boosted by alcohol, barbi- turates, opiates, tricyclic antidepressants, and monoamine oxidase inhibitors (MAOIs). A case report suggests that effects may also be boosted by the heart medicine amiodarone. Another case report indicates that clonazepam reduces blood levels of the epilepsy medicine phenytoin. Taking clonazepam with the antidepressant paroxetine is suspected of causing a dangerous reaction called serotonin syndrome, a serious condition which can involve confusion, tremors, and high body temperature. Combining clonazepam with the antimania med- icine lithium is suspected of causing muscular discoordination, including muscles used for speech. A case report noted delirium brought on by simul- taneously taking clonazepam and the schizophrenia medicine clozapine.

Clonazepam 87

Cancer. Not enough scientific information to report.

Pregnancy. No increase in birth defects was noted when pregnant rats and mice received many times the recommended human dose while embryos were in the organ-forming stage. Pregnant rabbits receiving clonazepam during the same stage, however, have produced offspring with birth defects such as limb malformations and cleft palate. Because other drugs in the benzodiazepine class are assumed to have potential for causing human birth defects, clona- zepam is considered inadvisable for pregnant women unless they and their physicians have considered the issue. Among 51 infants whose mothers took clonazepam during pregnancy, almost 10% had “major malformations”; al- though that small sample did not compare outcomes in matched women who took no such drug, the study’s finding nonetheless raises a caution. A much larger study said that clonazepam taken in combination with other epilepsy drugs increased the chance of birth defects but said nothing about using clona- zepam alone. Clonazepam may disturb fetal heartbeat. Offspring with fetal exposure may be sedated, show poor muscle tone, and have low body tem- perature. Infants can be born with dependence to the drug. Clonazepam passes into human milk at levels high enough to affect infants, and breast- feeding mothers are counseled to avoid clonazepam.

Additional scientific information may be found in:

Cohen, L.S., and J.F. Rosenbaum. “Clonazepam: New Uses and Potential Problems.” Journal of Clinical Psychiatry 48 (1987, Suppl.): 50–56.

Commander, M., S.H. Green, and M. Prendergast. “Behavioural Disturbances in Chil- dren Treated with Clonazepam.” Developmental Medicine and Child Neurology 33 (1991): 362–63.

Davidson, J.R., and G. Moroz. “Pivotal Studies of Clonazepam in Panic Disorder.” Psychopharmacology Bulletin 34 (1998): 169–74.

Davidson, J.R., et al. “Treatment of Social Phobia with Clonazepam and Placebo.” Jour- nal of Clinical Psychopharmacology 13 (1993): 423–28.

Morishita, S., S. Aoki, and S. Watanabe. “Clonazepam as a Therapeutic Adjunct to Improve the Management of Psychiatric Disorders.” Psychiatry and Clinical Neu- rosciences 52 (1998): 75–78.

Rosenbaum, J.F., G. Moroz, and C.L. Bowden. “Clonazepam in the Treatment of Panic Disorder with or without Agoraphobia: A Dose-Response Study of Efficacy, Safety, and Discontinuance.” Journal of Clinical Psychopharmacology 17 (1997): 390–400.

Worthington, J.J., III, et al. “Long-term Experience with Clonazepam in Patients with a Primary Diagnosis of Panic Disorder.” Psychopharmacology Bulletin 34 (1998): 199–205.


Pronunciation: klor-AZ-uh-pait
Chemical Abstracts Service Registry Number: 23887-31-2. (Dipotassium form

Formal Names: Tranxene
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2768) USA Availability: Prescription
Pregnancy Category: D

Uses. Clorazepate dipotassium is a “prodrug” related to diazepam. A pro- drug is a substance that may have little effect itself but that the body metab- olizes into another chemical that does have a drug effect. For example, one metabolite of clorazepate dipotassium is desmethyldiazepam, which in turn transforms into oxazepam. Prodrugs are prescribed when direct administra- tion of the desired chemical does not work, such as when the chemical would degrade before it has time to build up in the part of the body where it is needed or when the normal dosage form cannot be given (perhaps a substance that can be absorbed through the skin is needed rather than giving an injec- tion). Although metabolites of clorazepate dipotassium generally create the medical actions, for simplicity this discussion usually refers only to the pro- drug clorazepate dipotassium and calls it a drug.

This long-acting drug’s primary medical uses are for anxiety, for convul- sions, and as a muscle relaxant. The substance can be taken on a long-term basis for successful control of epilepsy but is described as a “second-line” medication, meaning it is not used unless other drugs have been tried without success. Clorazepate dipotassium’s long-term effectiveness against anxiety is unclear. A common short-term use is to reduce nervousness in surgery pa- tients shortly before an operation. The drug is also given to ease withdrawal from zolpidem and alcohol (including delirium tremens). An injection can quickly calm a bellicose individual.

Weight, age, and gender can affect dosage. A study found that an active metabolite (desmethyldiazepam) from a dose of clorazepate dipotassium lasts almost three times as long in overweight persons compared to normal weight persons, apparently due to accumulation in body fat. Another study noted

Clorazepate 89

that the older a male was, the longer the same metabolite from a dose lasted, but that effect was not seen in women.

Although clorazepate dipotassium is used against anxiety, the drug is gen- erally considered unsuitable for depressed or psychotic persons. It has none- theless been given with success for treating depression (even though sometimes the drug can instead worsen that condition). The drug has helped reduce nightmares caused by other pharmaceuticals and has helped alleviate psychosomatic complaints. It has also been used against tetanus.

Drawbacks. People with severe breathing trouble or acute narrow-angle glaucoma should avoid clorazepate dipotassium. Loosening of the nails has been attributed to the drug in a case report, but that is unusual. Somewhat less surprising is a case report of jaundice, less surprising because many drugs add a burden to the liver. Oral overdose can provoke rage.

The drug routinely makes people sleepy, and users are cautioned against operating dangerous machinery. In experiments the drug increases reaction time and decreases attention. Nonetheless, a laboratory simulation of driving showed no effect on operating a motor vehicle. One authority contends that the substance should not impair driving performance but acknowledges that trouble arises if a driver does not use the drug as medically directed or uses alcohol simultaneously. Other unwanted effects occur less often: peevishness, headache, stomach irritation, dry mouth, rashes, double vision, and unclear speech. Therapeutic advantage sometimes comes from the drowsiness factor, with patients instructed to take the drug at bedtime to help reduce insomnia, a technique that then also allows them to obtain the long-lasting antianxiety effect during daytime hours the next day. In one study people reported more restful sleep, and measurements after they awoke showed little drug impact on performance tests (illustrating the difference a few hours can make on how well someone performs after taking a substance).

Abuse factors. If usage continues for a long time and suddenly stops, a withdrawal syndrome can occur. Withdrawal symptoms can include trouble with sleeping and memory, jitteriness and crankiness, sore muscles, and loose bowels. Those discomforts are similar to what happens in alcohol or barbi- turate withdrawal. Researchers suspect the problem may be worsened if a person has taken some other benzodiazepine class drug off and on. The with- drawal problem may be avoided by gradual discontinuation of clorazepate dipotassium. Experiments with dogs and rabbits also show withdrawal symp- toms. A canine test demonstrated that abrupt clorazepate dipotassium with- drawal can cause fatal seizures. The kinds of well-documented dependence mentioned above involve relatively brief withdrawal. Reportedly human with- drawal symptoms may continue for months, which is an unusual persistence of dependence. Long-term signs of withdrawal, however, are described as reappearance of anxiety, sometimes accompanied by psychosis and convul- sions. Such long-term “withdrawal symptoms” sound much like conditions for which the drug is prescribed, raising a question of whether the victim is experiencing long-term dependence or simply reemergence of conditions for- merly controlled by the now-absent drug.

A group of recreational drug abusers was tested to determine their likings,

90 Clorazepate

and the group declared clorazepate dipotassium to be less attractive than di- azepam or lorazepam.

Drug interactions. Members in a group of recreational drug abusers re- ported that alcohol boosted clorazepate dipotassium’s effect and that the com- bination made their mood bleaker, but when subjects in another study took that combination they felt happier than alcohol normally made them. Another experiment found that the combination impaired memory, although still an- other study found that clorazepate alone did not affect memory. In testing how long the desmethyldiazepam metabolite lasts from a clorazepate dipo- tassium dose, conflicting results have come from experiments comparing cig- arette smokers to nonsmokers. Opiates, barbiturates, and monoamine oxidase inhibitors (MAOIs) found in some antidepressants may boost actions of clora- zepate dipotassium. Clorazepate dipotassium may boost alcohol’s effects.

Cancer. Animal studies have failed to find evidence of any cancer-causing potential in clorazepate dipotassium.

Pregnancy. Experiments with pregnant rats and rabbits revealed no im- pairment of fertility and failed to produce any birth defects attributable to clorazepate dipotassium. One rat study also found no behavioral conse- quences from prenatal exposure to the drug, but another rat study discovered that offspring walked more slowly than normal and also had some learning difficulty. The drug’s potential for creating human birth defects is unknown. A case report associates it with fatal lung collapse in a newborn whose mother had used the drug during pregnancy, and another case report associates the drug with fatal birth defects. “Association” may mean caution is appropriate, but it does not demonstrate cause and effect. Breast-feeding mothers are warned to avoid the drug because its metabolite nordiazepam (which is also a metabolite of diazepam) passes into the milk and into the infant. The metab- olite desmethyldiazepam also passes into milk, as does clorazepate dipotas- sium itself.

Additional scientific information may be found in:

Fabre, L.F., and H.P. Putman III. “Depressive Symptoms and Intellectual Functioning in Anxiety Patients Treated with Clorazepate.” Journal of Clinical Psychiatry 49 (1988): 189–92.

Fujii, T., et al. “Clorazepate Therapy for Intractable Epilepsy.” Brain and Development 9 (1987): 288–91.

Henderson, J.G. “Value of a Single Night-time Dose of Potassium Clorazepate in Anx- iety: A Controlled Trial Comparison with Diazepam.” Scottish Medical Journal 27 (1982): 292–96.

Moodley, P., S. Golombok, and M. Lader. “Effects of Clorazepate Dipotassium and Placebo on Psychomotor Skills.” Perceptual and Motor Skills 61 (1985): 1121–22.

Zung, W.W. “Effect of Clorazepate on Depressed Mood in Anxious Patients.” Journal of Clinical Psychiatry 48 (1987): 13–14.


See also Cocaine

Pronunciation: KOH-kuh

Chemical Abstracts Service Registry Number: None

Formal Names: Erythroxylum coca

Informal Names: Cocaine Plant, Cocaine Tree, Cuca

Type: Stimulant (cocaine class). See page 17

Federal Schedule Listing: Schedule II (DEA no. 9040)

USA Availability: Prescription (due to Schedule II status, but not a standard med- ical drug)

Pregnancy Category: None

Uses. The coca bush is native to the Andes, where it has been harvested since ancient Inca days. Use in that era has been confirmed through analysis of hair from ancient corpses and from examination of artwork. At first only upper-class Incas and select individuals were permitted to use coca, but usage spread to Inca society as a whole after the Spanish conquest. In modern times the plant has been cultivated in India and Sri Lanka as well as Formosa, Indonesia, and Malaysia. During the 1960s Malaysia was the world’s primary source of coca. Its leaves are the natural product from which cocaine is refined, and blood measurements confirm that coca users receive cocaine from the leaves. Cocaine content is commonly 0.6% to 1.5% of the leaves by weight. Cocaine is not the only drug component of coca, but relatively little explora- tion has been made of other components. Some investigators suspect that these other drugs are more important than cocaine in producing coca’s effects.

Traditionally coca has enjoyed wide use and social acceptance in the Andes, although leaf chewing (as opposed to taking coca in tea) is associated with lower social classes. Persons from middle and higher social classes who do not engage in physical labor may use coca recreationally. Short-term mental effects of coca leaves have been likened to those of coffee. Usage is much more common among persons living at high altitudes than at sea level. Coca can be a social lubricant, much in the way that khat is traditionally utilized. As with wine, coca leaves produced in different regions under different condi- tions can have flavor characteristics making some varieties more sought after than others even if the drug content is virtually identical. Veins are stripped from the leaves, which typically are then chewed or sucked upon in a small

92 Coca

quantity for hours, much like chewing gum. Coca is a local anesthetic and numbs the mouth when a person chews coca leaves. Lime (the mineral, not the fruit) may be added to improve the body’s absorption of cocaine from the leaves. Habitual leaf chewers routinely receive a daily cocaine dose of 0.25 grams spread over several hours. Coca tea or the leaves themselves are used to aid digestion, reduce gastrointestinal colic, fight asthma, soothe vocal cords (laryngitis), relieve stress and elevate mood, alleviate cold and thirst, produce sweat, and fight motion sickness. Milk with coca has been used against colic and diarrhea in babies. Coca cigarettes have been used to treat both asthma and colds. Proposals have been made to produce coca lozenges and chewing gum to make the natural product available in formats more familiar to persons coming from a European heritage.

Habitual coca chewing interferes with the body’s insulin and thereby tends to raise blood sugar levels. That finding should interest diabetic chewers but is also relevant to persons using leaves at high altitudes (common in the An- des) because the reduced oxygen supply at upper elevations tends to lower blood sugar. Habitual coca use apparently compensates for that effect. Blood sugar tends to decline during exercise; coca can prevent that decline, and scientists suspect that coca can increase the body’s effective use of blood sugar during exercise.

Coca leaves improve a person’s access to stored energy sources in the hu- man body and thereby increase capacity for physical labor. During the nine- teenth century such qualities attracted notice in Europe, but suggestions that coca be used in industrial and military labor were apparently ignored. In the 1970s a sample of Argentine miners showed that 65% chewed coca leaves every day, and another 14% used leaves less often. The more physical power and endurance required for a particular job, the more likely that a miner used coca leaves each day. One study of coca found the typical stimulant actions of raising pulse rate and blood pressure but also found that coca had a more unusual effect of decreasing the volume of blood plasma—a condition nor- mally associated with bleeding or with not drinking enough fluids. This con- dition interferes with proper blood circulation during physical exercise, but centuries of experience suggest that coca-chewing laborers get along well enough nonetheless. The study just referred to involved habitual chewers of coca; occasional chewers may not experience the same results. For example, in another study scientists concluded that regular chewers had more access to energy stored in body fat but that occasional chewers did not and also con- cluded that occasional chewers would not show the same improved endurance during physical exercise that is demonstrated by habitual chewers. One in- vestigator has concluded that coca improves endurance but does not otherwise help physical labor (a person cannot lift more or run faster).

Like many stimulants, coca reduces feelings of hunger and can thereby re- duce food intake. The appetite suppressant effect is slight, however, simply helping a person to get by more comfortably when food is scarce. Coca chew- ers exhibit robust appetites when victuals are plentiful, and coca preparations can even be an element of meal-taking. Some research suggests that under low atmospheric pressure coca can improve the body’s metabolism of carbo- hydrates and thereby improve nutrition of users. Coca itself is a good source

Coca 93

of vitamins, iron, and phosphorus; and lime used with coca can provide al- most a gram of calcium per day—important supplements where diet is often deficient in such factors. Malnourishment exhibited by rural coca chewers seems related more to poor food supply than to use of coca. Rat experiments, however, indicate that coca slows growth rate if used in mountainous alti- tudes.

Drawbacks. Although individuals have to work hard to abuse coca enough to create problems, persons who succeed at that task can experience the kinds of hallucinations and other mental afflictions associated with stimulant abuse. That outcome is very unusual among persons who use coca in traditional ways. Contrary to what one would expect from a stimulant, scientific tests show that coca (like khat) retards reaction time and increases errors in work performance. Long-term mental effects of habitual coca usage decrease think- ing abilities in ways that are seldom noticeable in rural village life but that are clearly documented through scientific tests. Such decline would put per- sons at a disadvantage in coping with modern urban conditions, on or off the job. The decline is presumed to be evidence of organic brain damage.

Coca depresses the immune system, presumably making users more sus- ceptible to disease. Coca chewing is suspected of promoting spread of cholera, not from coca itself but from lime or other alkali substances chewed with the leaves, having the result of lowering the stomach’s acid content and thereby providing an excellent environment for growth of microscopic cholera organ- isms. Coca is suspected of causing liver damage. Archeologists examining an- cient human remains have concluded that coca chewing may cause tooth decay and loss. In contrast, modern-day chewers claim that the habit promotes dental health and makes users less susceptible to disease in general. Coca’s effects on general physical health remain uncertain. Differing backgrounds of users and abstainers hinder efforts to measure effects; factors other than coca may be affecting health.

Abuse factors. Tolerance to the drug effect (resulting in a need to keep increasing the dose) is not observed among coca chewers; lack of that classic indication of addiction is evidence of coca’s low addictive potential. Heavy coca users may exhibit mild signs of physical dependence with the drug if they stop using it, but any such transitory illness is too slight to be a factor in choosing to continue using the drug.

Drug interactions. Not enough scientific information on the natural product to report.

Cancer. Mouths of habitual chewers show tissue abnormalities but no pre- cancerous conditions. Nonetheless, coca is considered a probable cause of cancer.

Pregnancy. Coca is considered a probable cause of fetal injury.

Additional information. In the 1970s a lift of all legal controls over coca was proposed on the theory that the natural product was far less harmful than pharmaceutical stimulants and might be just as attractive to persons who were damaging themselves through stimulant abuse. The proposal was rejected.

Cocaine and ecgonine can be removed from coca leaves, and such “deco- cainized” leaves are legal to possess without a prescription. Not all leaves marketed as decocainized have undergone such treatment, and urine tests of

94 Coca

persons drinking tea steeped from such leaves may be positive for cocaine use.

Coca paste. This substance is made from coca leaves but has the same sort of relationship to them that 100 proof alcohol has to 3.2 beer. Paste is yielded midway in the process of refining cocaine from coca; by volume the paste is anywhere from about 40% to 90% cocaine, thus as potent as typical street varieties of cocaine itself. Some persons desiring cocaine sensations prefer paste, which can be smoked without the heat destroying cocaine’s drug effects. Such persons routinely add the paste to tobacco or marijuana. Because of coca paste’s high potency, a user basically receives the same impact as with using cocaine. Descriptions of coca paste smoking and crack smoking are similar: euphoria, insomnia, compulsive use. Adverse effects duplicate those of cocaine (even including “coke bugs”—a hallucination of vermin crawling under the skin). Using coca paste is very different from using coca leaves. The difference can be inferred from a 1996 report that combined surveys involving over 24,000 persons in several countries of the Andes region. In 1965 about 13% of Peru’s population apparently used coca leaves, but only 0.8% to 3% of persons in the 1996 multicountry survey reported “lifetime” coca paste or cocaine use—meaning people had tried them at least once; the percentage of regular users would be lower yet. Direct comparison of those 1965 and 1996 figures would be invalid because of difference in dates and survey designs, but the huge gap between their percentages is consistent with a general rule that the stronger a drug is, the less popular it is. Also, the kinds of persons who use coca leaves and coca paste differ. The 1965 figure included over half the la- borers in Peru’s countryside. The 1996 survey found coca paste and cocaine to be used predominantly by educated middle-class urbanites. A 1992 study of hospitalized coca paste smokers also found most to be middle class, but almost as many were from a low-income background.

Additional scientific information may be found in:

Favier, R., et al. “Effects of Coca Chewing on Hormonal and Metabolic Responses during Prolonged Submaximal Exercise.” Journal of Applied Physiology 80 (1996): 650–55.

Grinspoon, L., and J.B. Bakalar. “Coca and Cocaine as Medicines: An Historical Re- view.” Journal of Ethnopharmacology 3 (1981): 149–59.

Hamner, J.E., III, and O.L. Villegas. “The Effect of Coca Leaf Chewing on the Buccal Mucosa of Aymara and Quechua Indians in Bolivia.” Oral Surgery, Oral Medicine, and Oral Pathology 28 (1969): 287–95.

Heath, D.B. “Coca in the Andes: Traditions, Functions and Problems.” Rhode Island Medical Journal 73 (1990): 237–41.

Jeri, F.R., et al. “The Syndrome of Coca Paste.” Journal of Psychoactive Drugs 24 (1992): 173–82.

Negrete, J.C. “Coca Leaf Chewing: A Public Health Assessment.” British Journal of Ad- diction to Alcohol and Other Drugs 73 (1978): 283–90.

Weil, A.T. “Coca Leaf as a Therapeutic Agent.” American Journal of Drug and Alcohol Abuse 5 (1978): 75–86.

Zapata-Ortiz, V. “The Chewing of Coca Leaves in Peru.” International Journal of the Addictions 5 (1970): 287–94.


See also Coca

Pronunciation: koh-KAIN
Chemical Abstracts Service Registry Number: 50-36-2. (Hydrochloride form 53-


Formal Names: Methylbenzoylecgonine

Informal Names: All-American Drug, Angie, Apple Jacks, Aunt Nora, Baby T, Bad, Badrock, Ball, Barbs, Base, Baseball, Basuco, Bazooka, Bazulco, Beam, Beamer, Beans, Beat, Beautiful Boulders, Bebe, Beemer, Bernice, Bernie, Bernie’s Flakes, Bernie’s Gold Dust, Big Bloke, Big C, Big Flake, Big Rush, Bill Blass, Billie Hoke, Bings, Birdie Powder, Biscuit, B.J., Black Rock, Blanca, Blanco, Blast, Blotter, Blow, Blowcaine, Blowout, Blue, Bobo, Bolivian Marching Powder, Bollo, Bolo, Bomb, Bone, Bonecrusher, Boost, Botray, Boubou, Boulder, Boulya, Bouncing Powder, Boy, Bubble Gum, Bullia Capital, Bullyon, Bump, Bunk, Burese, Bur- nese, Bush, Butler, Butter, C, Cabello Cadillac, Caine, Cakes, California Corn- flakes, Came, Canamo, Candy, Candy C, Cap, Capsula, Carnie, Carrie, Carrie Nation, Casper, Casper the Ghost, C-Dust, Cecil, C-Game, Chalk, Charlie, Chemical, Chewies, Chippy, Chocolate Ecstasy, Choe, Cholly, Climax, Cloud, Cloud 9, Coca, Coconut, Coco Rocks, Coke, Cola, Combol, Cookies, Coolie, Corine, Corrine, Corrinne, Crack, Crank, Crib, Crimmie, Croak, Crumbs, Crunch & Munch, Crystal, Cube, Dama Blanca, Demolish, Devil, Devil Drug, Devil’s Dandruff, Devilsmoke, Dice, Dip, DOA, Double Bubble, Double Ups, Double Yoke, Dove, Dream, Duct, Dust, Eastside Player, Egg, Eightball, Esnortiar, Ev- erclear, Eye Opener, Famous Dimes, 51, Fish Scales, Flake, Florida Snow, Foo Foo, Foolish Powder, Freeze, French Fries, Fries, Friskie Powder, Garbage Rock, Geek (with marijuana), Gift of the Sun, Gift of the Sun God, Gimmie (with marijuana), Gin, Girl, Girlfriend, Glad Stuff, Glo, Gold, Gold Dust, Golf Ball, Goofball (with heroin), Gravel, Green Gold, Gremmies (with marijuana), Grit, Groceries, G-Rock, H & C (with heroin), Hail, Half Track, Hamburger Helper, Happy Dust, Happy Powder, Happy Trails, Hard Ball, Hard Line, Hard Rock, Have a Dust, Haven Dust, Heaven, Heaven Dust, Hell, Henry VIII, Her, Hit, Hooter, Hotcakes, Hubba, Hunter, Ice, Ice Cube, Icing, Inca Message, Issues, Jam, Jejo, Jelly, Jelly Beans, Johnson, Joy Powder, Junk, King, King’s Habit, Ko- kayeen, Kokomo, Kryptonite, Lady, Lady Caine, Lady Snow, Late Night, Leaf, Line, Love, Love Affair, Ma’a, Mama Coca, Marching Dust, Marching Powder, Mayo, Merck, Merk, Mixed Jive, Mojo, Monkey, Monster, Mosquitos, Movie Star Drug, Mujer, Murder 1 (with heroin), New Addition, Nieve, Nose, Nose

96 Cocaine

Candy, Nose Powder, Nose Stuff, Nuggets, Number 3, 151, Onion (quantity), Oyster Stew, Paradise, Paradise White, Parlay, Paste, Patico, Pearl, Pebbles, Pee Wee, Percia, Perico, Peruvian, Peruvian Flake, Peruvian Lady, P-Funk (crack cocaine mixed with PCP), Piece, Piedra, Piles, Pimp, Pimp’s Drug, Pipero, Polvo Blanco, Pony, Potato Chips, Powder, Powder Diamonds, Press, Prime Time, Primo, Product, Quill, Racehorse Charley, Rane, Raw, Ready Rock, Red Caps, Regular P, Rest in Peace, Roca, Rock, Rock Attack, Rocks of Hell, Rooster, Rox, Roxanne, Roz, Rush, Schmeck, Schoolboy, Schoolcraft, Scorpion, Scottie, Scotty, Scrabble, Scramble, Scruples, Serpico 21, 7-Up, Shabu, She, Sherm, Sightball, Slab, Sleet, Sleigh Ride, Smoke, Smoking Gun (with heroin), Snowball (with heroin), Snow Bird, Snowcone, Snow Seals (with amphetamine), Snow White, Society High, Soda, Space Base (crack mixed with PCP), Space Cadet (crack with PCP), Space Dust (crack with PCP), Speed, Speedball (with heroin), Speedboat (crack with PCP and marijuana), Square Time Bob, Squirrel (crack with PCP and marijuana), Star, Star Dust, Star-Spangled Powder, Stones, Studio Fuel, Sugar, Sugar Block, Sweet Stuff, Swell Up, T, Talco, Tardust, Teenager, Teeth, Tension, Thing, Tissue, Toot, Top Gun, Topo, Tornado, Toss Up, Tragic Magic (crack with PCP), Trails, Troop, Turkey, Tweaks, 24–7, 20 Rock, Ultimate, Wave, Whack, White Ball, White Dragon, White Ghost, White Girl, White Horse, White Lady, White Mosquito, White Powder, White Sugar, White Tor- nado, Whiz Bang, Wicky Stick (crack with marijuana and PCP), Wild Cat (with methcathinone), Wings, Witch, Wooly (crack with marijuana), Wrecking Crew, Yahoo, Yale, Yayoo, Yeaho, Yeah-O, Yeyo, Yimyom, Zip

Type: Stimulant (cocaine class). See page 17
Federal Schedule Listing: Schedule II (DEA no. 9041) USA Availability: Prescription
Pregnancy Category: C

Uses. The drug was first isolated from coca plants in the mid-1800s. Cocaine apparently functions as an insecticide in the plants, but the substance has had no commercial agricultural use for that purpose. Early medical applications included administration to treat addiction to alcohol and opiates, but persons addicted to those drugs did not better on cocaine. Like many stimulants, co- caine has anorectic (weight-reducing) properties that decline as usage stretches over time; but the drug’s main medical use has been as a local anesthetic, particularly in ear, nose, and mouth surgery. Experimental use as an antide- pressant has been unsuccessful. Cocaine has been used to treat tonsillitis, ear- ache, toothache, burns, skin rash, hay fever, asthma, hemorrhoids, nerve pain, nausea, and vomiting. It makes the body’s immune system more active. For medical purposes cocaine has been largely superseded by drugs having less potential for abuse, but it is still called an excellent anesthetic for nose and throat surgery, has been used for gynecological surgery in modern times, and still has ophthalmological use as eye drops, although the latter employment must be cautious in order to prevent corneal damage. Due to hazards of co- caine injections, since the 1920s medical usage of cocaine has been largely limited to topical (applying it directly to a body surface).

Cocaine 97

Like other stimulants, cocaine may improve mood, self-confidence, and so- ciability. Taking the drug for such purposes may be recreational or for self- medication of psychological distress; for example, a strong association exists between posttraumatic stress disorder and cocaine use. Cocaine can tempo- rarily enhance work performance whether the task be manual labor or intel- lectual concentration. A century ago railroad engineers, dock workers, and cotton pickers were reported to be using the drug for that purpose, and it also received experimental military use in that pre-amphetamine era. On an oc- casional basis cocaine can help accomplish intense intellectual effort, such as staying awake all night to finish a piece of writing, and on a regular basis, cocaine can help accomplish dull repetitive tasks requiring close mental atten- tion. As with other stimulants, steady use can eventually worsen work ability as a person’s physical reserves are exhausted and as a person becomes emo- tionally strung out.

For over a century the most popular ways of taking cocaine were by injec- tion or by inhaling the drug as a snuff. The latter technique inherently pro- duces sensations of lesser strength than injection does, but a person desiring more can simply inhale larger quantities of powder.

Drawbacks. Habitually inhaling cocaine powder can cause a runny or con- gested nose and nosebleeds. Too much inhalation can bring on nasal ulcers and in exceptional cases can kill tissue and pierce the cartilage in the middle of the nose. Snorting can cause headaches. Abuse can also damage muscles (including heart), kidneys, and liver. Cases of heart attack and stroke are known, as are cases of serious intestinal damage related to problems with blood flow. Preexisting asthma can be worsened. Rupture of pulmonary air sacs and lung collapse are possible, though uncommon, results from cocaine smoking. The drug may bring on a type of glaucoma.

Some undesired effects are similar to those of amphetamine abuse: peevish- ness, nervousness, combativeness, paranoia, insomnia, and (after a dose wears off) depression. Typical afflictions include repetitions in movement or speech. Males may engage in sexual intercourse far longer than usual. Abusers may cut themselves off from other persons and become suspicious of them. As- sorted hallucinations may occur, the classic one being “coke bugs” crawling under the skin. Psychological problems produced by unwise use of cocaine are so similar to those from other stimulants that some scientists believe sim- ilar mechanisms must cause the problems. Psychosis can be induced by co- caine but, as with other stimulants, generally does not continue after the drug use stops. Smoking cocaine can produce respiratory difficulties reminiscent of tobacco smoking—difficulties that develop faster than with tobacco because lungs must deal not only with the “air pollution” but with powerful drug effects as well. Particles of crack smoke floating in the air and landing on someone’s eye can damage the cornea.

The amount of drug needed to kill a person varies; depending on a person’s condition a dose that provides pleasure one day can kill on another. The same goes for persons sharing a supply: What satisfies one user can cause serious trouble for another. In rat experiments females are more sensitive to cocaine than males. Immediate problems in humans may include high blood pressure, irregular heartbeat, and seizures. The drug promotes rises in pulse rate and

98 Cocaine

body temperature, which can be problems if a person engages in strenuous physical activity such as wild dancing.

Abuse factors. Before the 1970s cocaine smoking was never popular because the necessary heat destroyed much of the drug’s potency. In that decade, however, the practice of freebasing cocaine began. That process allowed the drug’s potency to be retained when smoking it, thereby allowing a route of administration providing the same intense impact formerly available only through intravenous injection. Freebasing, however, involves volatile chemi- cals that can explode in a flash fire if they are mishandled. In the 1980s illicit chemists discovered a much safer way to modify cocaine into a smokable format. The resultant product was known as crack cocaine and became the most notorious illicit drug since heroin.

A few seconds after inhaling crack smoke a user can experience a sense of well-being and joy accompanied by what has been described as a total body orgasm, followed by a few minutes of afterglow.

Tolerance is reported. Debate exists about whether a cocaine addict expe- riences physical withdrawal symptoms upon giving up the drug. A consensus holds that any physical consequences caused by the initial phase of abstinence can be less serious than those that develop when withdrawing from opiates and far less serious than withdrawing from alcohol or barbiturates.

Drug interactions. Cocaine masks some effects of alcohol, encouraging drinkers to ingest larger quantities of beverages. Alcohol’s effects are longer lasting than cocaine, however, so a person functioning adequately under both drugs can suddenly become very drunk as the cocaine intoxication ends. If that transition happens while a person is operating dangerous machinery (such as a car), for example, the consequences may be disastrous. Cocaine’s influence on the heart and liver seem increased by alcohol. Mazindol boosts the elevation that cocaine causes in pulse rate and blood pressure and makes those changes last longer. Mice experiments indicate possible fatal interaction if a cocaine-using asthmatic is treated with aminophylline (a combination of ethylenediamine and theophylline). Cocaine abusers also tend to be extra sus- ceptible to the benzodiazepine class of depressant drugs. In animal experi- ments caffeine and nicotine boost cocaine effects. Naloxone, a drug used to counteract opiate actions, can boost cocaine effects in humans. For many years some medical practitioners have mixed adrenalin with topical applications of cocaine in order to make anesthetic effects last longer. The reason adrenalin interacts in that way with cocaine is unclear, and the custom is disputed. What works when applying cocaine to a body surface for anesthesia does not nec- essarily work in other contexts. Seeking to stretch out effects of recreational cocaine with various substances can be so unsuccessful as to require hospi- talization for unexpected interactions. In some manipulations of a rat experi- ment the tricyclic antidepressant amitriptyline reduced cocaine actions.

Cancer. Cocaine’s potential for causing cancer is uncertain.

Pregnancy. The drug’s potential for causing birth defects is uncertain. Some animal experiments produce birth defects; some do not. In the 1980s and 1990s cocaine was widely reported to have devastating impact on mental ability of infants whose mothers used the drug during pregnancy. Scientists have been unable to verify those reports. Evidence is growing that offspring tend to

Cocaine 99

perform at the lower end of the normal range, but pregnant women who use cocaine also typically use hefty amounts of tobacco cigarettes and beverage alcohol while failing to get proper nutrition and prenatal care. Such confound- ing factors hinder scientists’ ability to measure what cocaine does to a fetus, although persistent investigators are beginning to separate cocaine’s influence from other factors. Even so, despite excellent theoretical reasons to suspect that cocaine damages fetal development, those suspicions have not been con- firmed. Nonetheless, cocaine is not considered safe for a pregnant woman to use. Apparently cocaine enters human milk and can be passed to infants via that route. A case report tells of an infant hospitalized for cocaine overdose received from the mother’s milk.

Additional scientific information may be found in:

Brain, P.F., and G.A. Coward. “A Review of the History, Actions, and Legitimate Uses of Cocaine.” Journal of Substance Abuse 1 (1989): 431–51.

Gay, G.R., et al. “Cocaine: History, Epidemiology, Human Pharmacology, and Treat- ment. A Perspective on a New Debut for an Old Girl.” Clinical Toxicology 8 (1975): 149–78.

Johnson, B., et al. “Effects of Acute Intravenous Cocaine on Cardiovascular Function, Human Learning, and Performance in Cocaine Addicts.” Psychiatry Research 77 (1998): 35–42.

Lester, B.M., L.L. LaGasse, and R. Bigsby. “Prenatal Cocaine Exposure and Child De- velopment: What Do We Know and What Do We Do?” Seminars in Speech and Language 19 (1998): 123–46.

Magura, S., and A. Rosenblum. “Modulating Effect of Alcohol Use on Cocaine Use.” Addictive Behaviors 25 (2000): 117–22.

Middleton, R.M., and M.B. Kirkpatrick. “Clinical Use of Cocaine. A Review of the Risks and Benefits.” Drug Safety: An International Journal of Medical Toxicology and Drug Experience 9 (1993): 212–17.

Rawson, R., et al. “Methamphetamine and Cocaine Users: Differences in Characteristics and Treatment Retention.” Journal of Psychoactive Drugs 32 (2000): 233–38. Siegal, H.A., et al. “Crack-Cocaine Users as Victims of Physical Attack.” Journal of the

National Medical Association 92 (2000): 76–82.
Siegel, R.K. “Cocaine and the Privileged Class: A Review of Historical and Contem-

porary Images.” Advances in Alcohol and Substance Abuse 4 (1984): 37–49.


Pronunciation: KOH-deen
Chemical Abstracts Service Registry Number: 76-57-3. (Phosphate hemihydrate

form 41444-62-6)

Formal Names: BRON, Methylmorphine

Informal Names: AC/DC, Barr, C, Captain Cody, Co-Dine, Cody, Coties, Cough Syrup, Down, Homebake, Karo, Lean, Lean & Dean, Nods, Schoolboy, Syrup, T-3s. With glutethimide: Doors & 4, 4 Doors, Hits, Loads, Packets, Pancakes & Syrup, Sets, 3s & 8s

Type: Depressant (opiate class). See page 22
Federal Schedule Listing: Schedule II, III, V controlled substance, depending on

product formulation (DEA no. 9050)
USA Availability: Prescription and nonprescription Pregnancy Category: C

Uses. Codeine was discovered in 1832 by French chemist Pierre-Jean Robi- quet. Typically it is derived from the more potent drug morphine, which, depending on dosage route (oral, injection), is considered about 3 to 12 times stronger than codeine. After codeine is administered, body chemistry trans- forms it back into morphine; thus employer drug screens on someone who used a codeine cough remedy can be positive for morphine. Basically codeine is a prodrug, a substance having little medicinal effect itself but that the body transforms into a useful drug—in this case, morphine. Although scientists have long believed that codeine’s therapeutic effects come from morphine, as the twenty-first century began, one group of researchers reported that persons whose bodies cannot properly convert codeine into morphine can nonetheless experience medical benefit from codeine itself.

Codeine is administered for sedation and to stop diarrhea, coughs, and pain. The substance is considered one of the best cough medicines, although re- search in the 1990s indicated the drug has little ability to control coughs from colds. Some people take the drug regularly to diminish chronic pain. One study of the drug’s ability to ease pain after tonsillectomy found its effective- ness comparable to morphine, but another tonsillectomy study found codeine no more effective than acetaminophen (Tylenol and similar products). Re- search examining pain from a wide variety of causes, ranging from cancer to backache, found no more discomfort relief from a combination dose of codeine

Codeine 101

and acetaminophen than from combining hydrocodone and ibuprofen. Such findings probably indicate simply that various kinds of pain relievers work adequately for various discomforts, with codeine often being as good as the other drugs.

Some regular codeine users take it to reduce anxiety, and some simply find the substance’s effects pleasant. A clinical test of codeine found no antide- pressant action, but people who use codeine for a long time tend to be de- pressed and may be taking that drug to medicate themselves for depression— so if they have access to antidepressants they may have less interest in co- deine. Codeine cough syrups may include stimulants and other ingredients that persons find pleasant, increasing the syrups’ appeal.

Drawbacks. Codeine can promote sleepiness, abdominal cramps, constipa- tion, urinary retention, nausea, and breathing impairment. A case report tells of a massive dose followed by several days of hallucinations and paranoia in a person already prone to psychiatric problems. After taking a dose, people should avoid operating dangerous machinery until they know the drug is not hindering their ability to do so. When 70 professional army drivers in Finland were tested in a driving simulator after taking 50 mg of codeine, they ran off the roadway more frequently than when they were under the influence of alcohol. Elderly persons who take codeine have an increased likelihood of hip fracture, presumably because the substance makes them woozy and more likely to fall. Codeine has been known to cause pancreatitis, particularly if the victim’s gallbladder has been surgically removed, but this effect is considered unusual. Medical personnel refrain from administering the drug through in- travenous injection because that route can lower blood pressure and blood oxygen to fatal levels.

In two studies researchers found that people taking codeine felt few sen- sations from the drug and had normal performance on assorted tests of phys- ical and mental functioning. Those findings, however, may be related to dosages given by experimenters; higher dosages might well produce different results.

Abuse factors. Codeine abuse can be troublesome enough that persons need treatment to break the addiction. Some cases have required hospitalization. Nonetheless, prevalence of codeine addiction was disputed in 1989 by two authorities who carefully examined past reports of addiction: Little scientific research had been done on the topic, and most had involved persons already addicted to morphine. As morphine addicts will use codeine as a stopgap to hold off a withdrawal syndrome when their main drug is unavailable, their responses to codeine are not necessarily representative of a general popula- tion’s reactions. In addition, codeine cough syrups may contain a substantial percentage of alcohol, so heavy use of such a product can involve a further confounding factor of alcoholism. The 1989 authorities concluded that verifi- able accounts of people being addicted primarily to codeine (rather than mainly to some other drug, with codeine on the side) were unusual.

Dependence with codeine can develop; withdrawal symptoms are like those of morphine withdrawal, but milder. A study of rheumatism patients receiv- ing codeine found that quite a few needed higher doses to control pain as

102 Codeine

months went by, but the increase was caused by decline of their physical condition rather than development of tolerance.

The same study noted that almost no patients abused the drug, and of those few who did, all abused other substances as well. That finding is consistent with many observations of other drugs having abuse potential; only a small minority of users misuse them, and this minority is prone to problems with more than one substance. People having a bad relationship with codeine tend to have bad relationships with alcohol, marijuana, and (less commonly) her- oin. One study found that almost half the patients requesting treatment for codeine cough syrup addiction engaged in sexual conduct putting them at risk for AIDS, conduct illustrating a multiproblem lifestyle in which codeine abuse was simply one aspect. Background checks of deceased Los Angeles– area codeine abusers revealed almost 66% had attempted suicide, had a prior overdose on some drug, had been hospitalized for psychiatric problems, had been in physical fights, and had an alcohol problem (87% had an alcohol- related arrest record). So codeine may be only one of several problems in such lives.

Not all drug abuse is illicit. Sometimes people develop an abusive relation- ship with a drug that is supplied to them through legitimate medical channels. Swedish researchers compared the use of codeine in that country to the use of propoxyphene, an opioid related to methadone. Those investigators found that doctors in two of Sweden’s largest cities typically tended to prescribe codeine to middle-aged females and that in one of those cities codeine was used the most in poor areas of town and was often associated with taking benzodiazepines frequently (in experiments the benzodiazepine diazepam lengthened the time that a codeine dose lasted, while codeine interfered with diazepam—suggesting that a codeine user would have to take more diazepam to get benzodiazepine sensations, consistent with the Swedish findings of in- creased benzodiazepine consumption among codeine users). Those kinds of codeine usage characteristics were not found for propoxyphene in the Swedish research even though both drugs would have opiate-type effects; the differ- ence in usage suggests that physicians’ customs may have been promoting codeine abuse.

In drug abuse treatment programs codeine has been used successfully to shift addicts from other opiates—so successfully that one group of researchers suggests that codeine maintenance programs might be an alternative to meth- adone maintenance, particularly because codeine produces fewer unwanted effects than methadone.

Drug interactions. The antidepressants fluoxetine (Prozac) and paroxetine interfere with the body’s transformation of codeine into morphine; therefore, persons taking those antidepressants are considered less likely to develop co- deine abuse (because they would experience fewer effects from codeine). Al- though codeine is weaker than morphine, similarities between the two drugs mean that interactions occurring with morphine can be expected to occur with codeine.

Cancer. Laboratory tests find no evidence that the drug causes cell muta- tions that might lead to cancer. Experimenters gave codeine to rats and mice for two years and looked for evidence of cancer caused by the drug but found

Codeine 103

none. Although no direct observations have noted codeine causing cancer in rats or mice, computer analysis of data from some experiments indicates that the drug may cause cancer in rodents. The human body produces very small amounts of codeine naturally, and researchers suspect this naturally occurring codeine may deter development of lung cancer; but those natural processes do not mean that doses of the drug would help prevent cancer.

Pregnancy. Whether codeine causes birth defects is unknown. It produced no evidence of malformations when given to pregnant rats and rabbits. Co- deine reduced fetal weight in mice and hamsters in one experiment but did not increase the normal rate of defects in mice, nor was a statistically signif- icant change in malformation rate observed in hamsters. Investigators running another mice experiment, however, concluded that codeine does cause as- sorted malformations. Researchers seeking evidence about various human birth defects examined medical records of 100 to 199 women who used a cough remedy containing codeine and found that none of the offspring had any of the congenital abnormalities being investigated. Suspicion exists that codeine may cause cleft palate and cleft lip in humans, but birth defects are considered unlikely if the drug is used during pregnancy. A pregnant woman who takes codeine can produce an infant who is dependent on that drug and who undergoes a withdrawal syndrome upon birth.

Codeine passes into the milk of nursing mothers, but researchers find its level and that of its metabolite morphine to be acceptable if the woman is using codeine moderately. Nonetheless, nursing mothers are advised to avoid codeine because mechanisms that break down codeine in the body are incom- pletely formed in newborns, causing them to react more strongly to the drug than older children or adults.

Additional scientific information may be found in:

Eggen, A.E., and M. Andrew. “Use of Codeine Analgesics in a General Population. A Norwegian Study of Moderately Strong Analgesics.” European Journal of Clinical Pharmacology 46 (1994): 491–96.

Mattoo, S.K., et al. “Abuse of Codeine-Containing Cough Syrups: A Report from In- dia.” Addiction 92 (1997): 1783–87.

Romach, M.K., et al. “Long-Term Codeine Use Is Associated with Depressive Symp- toms.” Journal of Clinical Psychopharmacology 19 (1999): 373–76.

Rowden, A.M., and J.R. Lopez. “Codeine Addiction.” DICP: The Annals of Pharmaco- therapy 23 (1989): 475–77.

Sproule, B.A., et al. “Characteristics of Dependent and Nondependent Regular Users of Codeine.” Journal of Clinical Psychopharmacology 19 (1999): 367–72.


Pronunciation: dee-ee-tee
Chemical Abstracts Service Registry Number: 61-51-8 Formal Names: Diethyltryptamine
Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7434) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. In rats DET actions resemble some of bufotenine’s, but DET effects in humans are likened to those of mescaline and LSD. Volunteers report major changes in body perception, such as feeling porous or having an empty chest or absent hands. Sometimes users feel they are outside of their bodies. Hal- lucinations may seem real; typically they are visual, but sometimes sounds and smells are perceived as well. Users have reported that faces of individuals around them look different, taking on a masklike or caricature quality. Barriers between senses may erode, for example, allowing sounds to be seen. Altered perception of time is common. Perception of space can also change; a room’s size may appear to grow, with walls getting further away or becoming curved, or motionless objects may appear to keep coming closer. Typically conscious- ness becomes fuzzy, with persons reporting they feel partially asleep.

Reactions to such experiences differ. A researcher who engaged in self- experimentation, once a more common procedure in science but now uncom- mon, reported that his mood flipped back and forth between happiness and anxiety. He also reported temporary autism while intoxicated by the drug. Another self-experimenting scientist noted a need to avoid interacting with people. A group of artists and professional colleagues of researchers who wanted to explore creative possibilities with the drug were ecstatic about what happened to them. Some had spiritually moving experiences; afterward some felt impelled to begin creating artwork they had never attempted before. The substance can promote meditation, allowing repressed concerns to emerge. For that reason the drug was considered to have potential in psychotherapy. One research team reported examples of reticent schizophrenics becoming communicative while under DET’s influence, revealing honest information that benefitted therapy. In a setting where users feel safe they may become more sensitive to one another’s emotions and have genial interactions.

DET 105

Drawbacks. If persons want to stay in control of what happens to them, they may become upset if they are unable to stop DET’s effects. One group of volunteers found DET unpleasant, and some said the experience was so negative that they would depart the research center if a repeat performance was expected. These were unemployed laborers who had no particular interest in the drug. Some users in another study compared the experience to delirium caused by typhus or pneumonia. DET typically raises blood pressure, causes dizziness and perspiration, and may cause tremors and burning sensations. Rapid heartbeat has been reported. In addition to those symptoms, schizo- phrenics have routinely experienced shakiness, nausea, and vomiting. Some persons feel agitated and have a need to move around. The drug makes people more open to suggestion and therefore more susceptible to exploitation. In a research environment, normal subjects often become suspicious of persons managing the experiment. Performance declines on tests of reaction time and intelligence. A technically accomplished artist drew with less proficiency dur- ing DET intoxication, but at the time she seemed unaware of decline in per- formance. After the drug has worn off, users may feel a little depressed and suffer from headache; they may be tired but have difficulty sleeping. These problems clear up in a day’s time.

Abuse factors. Not enough scientific information to report about tolerance, dependence, withdrawal, or addiction.

Drug interactions. Not enough scientific information to report. Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

Bo ̈szo ̈rme ́nyi, Z. “Creative Urge as an After Effect of Model Psychoses.” Confina Psy- chiatrica 3 (1960): 177–26.

Bo ̈szo ̈rme ́nyi, Z., P. De ́r, and T. Nagy. “Observations on the Psychotogenic Effect of N-N Diethyltryptamine, a New Tryptamine Derivative.” Journal of Mental Science 105 (1959): 171–81.

Sza ́ra, S. “The Comparison of the Psychotic Effect of Tryptamine Derivatives with the Effects of Mescaline and LSD-25 in Self-Experiments.” In Psychotropic Drugs, ed. S. Garattini and V. Ghetti. New York: Elsevier, 1957. 460–67. Sza ́ra refers to DET as T-9.

Sza ́ra, S., et al. “Psychological Effects and Metabolism of N,N-Diethyltryptamine in Man.” Archives of General Psychiatry 15 (1966): 320–29.


Pronunciation: DEK-stroh am-FET-uh-meen

Chemical Abstracts Service Registry Number: 51-64-9. (Sulphate form 51-63-8)

Formal Names: Adderall, Amsustain, Biphetamine, D-Amphetamine, Dexamphet- amine, Dexedrine, Dexidrine, DextroStat, Sympamin

Informal Names: Beans, Black Beauties, Brownies, Christmas Trees, Dexies, Fast- balls, Orange Hearts, Oranges, Purple Hearts

Type: Stimulant (amphetamine class). See page 12 Federal Schedule Listing: Schedule II (DEA no. 1100) USA Availability: Prescription
Pregnancy Category: C

Dextroamphetamine is often called amphetamine. To reduce potential con- fusion, remember that in this book “amphetamine” refers to a class of stim- ulants, and “dextroamphetamine” refers to a specific drug in that class.

Uses. The substance stimulates the central and sympathetic nervous systems and is comparable to methamphetamine. Dextroamphetamine is typically used to treat narcolepsy, to treat attention deficit hyperactivity disorder (ADHD) in adults and children, and to help reduce a person’s weight—in rhesus monkey experiments it is one of the most effective appetite suppres- sants. Some use has been made to help epileptics. The drug can be given in combination with scopolamine as an anti–motion sickness medicine; astro- nauts have used this combination during missions in outer space and consider it effective.

Dextroamphetamine has been found more effective than standard antide- pressants in alleviating depression among HIV (human immunodeficiency vi- rus) patients and can also increase their energy. The drug has successfully treated depression among non-HIV hospital patients and among other persons as well. The drug has helped restore physical vigor and positive mental out- look to institutionalized elderly persons, so that older individuals who had been unable to take care of themselves were able to go home. Experimenters in the 1970s and 1990s found that the drug could accelerate work rate without multiplying mistakes in performing tasks. Those laboratory results cannot be extrapolated to the workplace in general but nonetheless remind us of the original welcome that employers gave to the first amphetamines. Dextroam- phetamine can help persons maintain satisfactory job performance while being

Dextroamphetamine 107

deprived of sleep. In the Persian Gulf War of 1991, U.S. aviators used the drug. Some pilots called the substance crucial for top performance of respon- sibilities. Outside evaluation concluded that efficiency and safety improved when pilots were under the drug’s influence. Athletic performance may be enhanced by the drug, but amphetamine class substances are generally banned by sports regulatory authorities.

Drawbacks. Tests on healthy volunteers found that taking enough dextro- amphetamine to produce euphoria was also enough to produce mania. The drug may cause stroke and is normally avoided if patients have heart disease, hardening of the arteries, high blood pressure, glaucoma, hyperthyroidism, restlessness, and former or current drug abuse. Heart trouble has been attrib- uted to several years’ abuse of the drug, and brain damage has been noted.

Abuse factors. Lack of dependency has been noted among juveniles receiv- ing medical doses of dextroamphetamine. Another study found that adults with medical authorization to use dextroamphetamine for obesity or depres- sion often found it no more appealing than a placebo. These results are con- sistent with the fact that any drug’s potential for abuse depends on the needs it satisfies in a user; if a medical need is the only one satisfied, then the person will have no interest in continuing the drug once the affliction is cured. Among persons inclined toward abuse, that inclination can be increased by taking dextroamphetamine with morphine. Those two substances can cancel out some of each other’s unpleasant physical sensations while retaining the psychological pleasures of both drugs. Abusers may interpret the situation as “gain without pain,” but combining stimulants with depressants can give the human body quite a beating. Moreover, researchers find that abusers can ac- quire tolerance to the psychological effects of dextroamphetamine while effects on blood pressure remain strong. Therefore, boosting the dose to maintain the level of psychic high may pose as much danger to a habituated user as to someone unaccustomed to the drug.

Drug interactions. Although the antimania medicine lithium reduces central nervous system stimulation caused by amphetamine, experiments have not shown lithium reducing either mania or heart rate and blood pressure in- creases caused by dextroamphetamine. Dextroamphetamine is to be avoided if persons have taken a monoamine oxidase inhibitor (MAOI—in some anti- depressants and other medicine) within the past 14 days. Particular hazard arises when combining an MAOI and dextroamphetamine while eating foods containing tyramine. Such foods include beer, some wines, cheese, chocolate, bananas, raisins, avocados, salami, and soy sauce. Although an experimental study found that dextroamphetamine could enhance the beneficial effects of MAOIs, using the two drugs together can be fatal. Tricyclic antidepressants make a dose of dextroamphetamine last longer and can increase amphetamine blood levels produced by dextroamphetamine.

Although extrapolation of animal studies to human conditions must always be cautious, it is known that dextroamphetamine’s effects become stronger in rats if they take caffeine at the same time. Rat and human experiments also indicate that dextroamphetamine will improve pain relief provided by mor- phine. Animal experiments indicate that dextroamphetamine interferes with alcohol absorption, suggesting that achieving alcohol intoxication might re-

108 Dextroamphetamine

quire a dextroamphetamine user to drink more than normal. Upon taking dextroamphetamine, tobacco cigarette smokers use more cigarettes and report greater pleasure from smoking.

Combining marijuana smoking with dextroamphetamine does not seem to affect physical coordination (walking and the like) more than just using mar- ijuana alone. Each of those two drugs raises heart rate and blood pressure but do not seem to have a multiplier effect when used together—the increase in cardiac effects is simply the amount caused by dextroamphetamine plus the amount caused by marijuana; one does not make cardiac effects of the other more potent.

Cancer. Potential for causing cancer is unknown.

Pregnancy. As with many drugs, effect on fetal development is unknown. One instance of serious birth defects is reported from a woman who used dextroamphetamine in the first trimester, but the meaning of that one instance is uncertain because she also used lovastatin (a drug for reducing cholesterol in persons at serious risk of heart attack), and lovastatin by itself is considered highly dangerous to fetal development. A statistical association has been re- ported between maternal dextroamphetamine use and infant heart defects. Dextroamphetamine has been prescribed for use in pregnancy without ap- parent ill effect on infants but is considered potentially hazardous. Possible consequences merit full discussion between doctor and pregnant patient.

Combination products. Adderall contains several active ingredients: dextro- amphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate USP, and amphetamine sulfate USP (the latter substance formerly marketed as Benzedrine).

Biphetamine, like other dextroamphetamines, is medically used to treat obe- sity, narcolepsy, and ADHD. Biphetamine is used recreationally to boost men- tal quickness and physical activity and to create euphoria. The compound can facilitate hallucinations, raise blood pressure, and prevent sleep.

Dexedrine’s oral capsule is designed to deliver some of the drug immedi- ately, followed by gradual delivery of the remaining drug. Capsule and tablet products both contain “inactive” ingredients. In this context “inactive” means an ingredient that does not promote a drug’s medical purpose, not that the ingredient has no pharmaceutical effect. Inactive ingredients in the tablet in- clude FD&C Yellow No. 5 (tartrazine), a substance to which some persons are allergic, particularly if they are abnormally sensitive to aspirin. Their reactions can include bronchial asthma. When used against ADHD in children Dexe- drine can curtail growth, but that effect is believed to be temporary. Dexedrine can raise body temperature. Experimenters found that the product can allow satisfactory performance by airplane pilots on continuous simulator flight duty for 64 hours straight without sleep.

DextroStat tablets include FD&C Yellow No. 5 (tartrazine). Additional scientific information may be found in:

Brauer, L.H., J. Ambre, and H. De Wit. “Acute Tolerance to Subjective But Not Car- diovascular Effects of D-Amphetamine in Normal, Healthy Men.” Journal of Clin- ical Psychopharmacology 16 (1996): 72–76.

Caldwell, J.A., et al. “Efficacy of Dexedrine for Maintaining Aviator Performance dur-

Dextroamphetamine 109

ing 64 Hours of Sustained Wakefulness: A Simulator Study.” Aviation, Space, and

Environmental Medicine 71 (2000): 7–18.
Domino, E.F., et al. “Effects of D-Amphetamine on Quantitative Measures of Motor

Performance.” Clinical Pharmacology and Therapeutics 13 (1972): 251–57. Emonson, D.L., and R.D. Vanderbeek. “The Use of Amphetamines in U.S. Air Force Tactical Operations during Desert Shield and Storm.” Aviation, Space, and Envi-

ronmental Medicine 66 (1995): 260–63.
Graybiel, A. “Space Motion Sickness: Skylab Revisited.” Aviation, Space, and Environ-

mental Medicine 51 (1980): 814–22.
Griffith, J.D., et al. “Dextroamphetamine.” Archives of General Psychiatry 26 (1972): 97–

Jacobs, D., and T. Silverstone. “Dextroamphetamine-Induced Arousal in Human Sub-

jects as a Model for Mania.” Psychological Medicine 16 (1986): 323–29.
Jasinski, D.R., and K.L. Preston. “Evaluation of Mixtures of Morphine and D- Amphetamine for Subjective and Physiological Effects.” Drug and Alcohol Depen-

dence 17 (1986): 1–13.
Ward, A.S., et al. “Effects of D-Amphetamine on Task Performance and Social Behavior

of Humans in a Residential Laboratory.” Experimental and Clinical Psychophar- macology 5 (1997): 130–36.


Pronunciation: dex-troh-meth-OR-fan

Chemical Abstracts Service Registry Number: 125-71-3

Formal Names: Benylin, Cosylan, Creo-Terpin, Demorphan Hydrobromide, Dex- ylets, Drixoral, DXM, Medicon, Mediquell, MorphiDex, Pertussin CS, Robitussin-DM

Informal Names: Bromage, Brome, Cough Syrup, Dex, Dextro, DM, Drix, K (with alcohol), Mega-Perls, Pole (with heroin), Polo (with heroin), Robe, Robo, Rojo, Sky, Syrup, Triple C, Tussin, Velvet

Type: Depressant (opioid class). See page 22 Federal Schedule Listing: Unlisted
USA Availability: Nonprescription Pregnancy Category: C

Uses. This cough and cold medicine has been used in the United States since the 1950s. Because the drug is an opiate analogue and is related to levor- phanol, for convenience this book lists dextromethorphan as an opioid. Nal- oxone, a chemical used to provoke withdrawal symptoms in persons who have dependence with opiates and opioids, can bring forth those symptoms in addicts who have switched from methadone to dextromethorphan. That finding is consistent with dextromethorphan being an opioid; nonetheless, the substance is not generally classified as an opioid.

The drug resembles codeine but is considered weaker in humans, although a cat experiment measured dextromethorphan as three times stronger than codeine. Body processes break down dextromethorphan into other substances including dextrorphan.

Urinalysis comparing the amounts of dextromethorphan and its break- down product dextrorphan can identify a person’s susceptibility to lung can- cer. Case reports tell of dextromethorphan’s success in treating infants’ brain seizures. One experiment found the substance to be a useful supplement in treating older epileptics, but another study detected no improvement. Parkin- son’s disease patients have shown encouraging response to treatment with the drug, but using it against Huntington’s disease and Lou Gehrig’s disease has brought disappointment. Animal research suggests that the substance may be useful in treating stroke. A mice experiment in France tested whether dextro- methorphan can protect against the effects of the chemical warfare agent so-

Dextromethorphan 111

man, but the results were negative. A U.S. Army experiment with guinea pigs also found dextromethorphan to have little value as protection against soman poisoning.

Dextromethorphan is considered ineffective as a general pain reliever but does reduce certain kinds of pain: Experiments show the drug can relieve pain from diabetes, and researchers speculate that the drug may also provide sim- ilar benefit to AIDS (acquired immunodeficiency syndrome) sufferers.

Drawbacks. Most persons find the drug unpleasant if the medically rec- ommended dosage is exceeded, with unwanted effects such as easy excitabil- ity, memory trouble, nausea, itching, interference with male sexual function, slurred speech, trouble with thinking, and difficulty with moving arms and legs. Some persons become tired and woozy even on normal doses. Nonethe- less, one study of cough medicines found that volunteers preferred dextro- methorphan to other remedies that were effective, leading the researchers to speculate that the drug was providing pleasure unrelated to effectiveness in relieving cough. Indeed, some users feel more sociable and report euphoria and hallucinations. Cases of mania are known, likened to the kind of stereo- typical behavior popularly associated with PCP. In one instance, the com- pound allowed a lawyer to work industriously for weeks with little sleep, followed by mental collapse requiring hospitalization. This individual had engaged in manic episodes and drug abuse in the past, however. A patient in another mania case report also had a medical history of drug abuse. Persons without such a history may well be susceptible to manic reactions from over- use of dextromethorphan, but the examples just cited raise the question of whether persons prone to drug abuse are particularly susceptible.

Investigators examining dextromethorphan’s potential for treating juvenile bacterial meningitis called off the experiment when patients began developing diabetes after receiving high doses of the drug (possibly because of action on the pancreas inhibiting insulin production), and reports exist about other in- stances of juveniles developing diabetes when being treated with the com- pound.

Abuse factors. Accounts of persons abusing dextromethorphan began ap- pearing in science journals during the 1960s. In the 1990s news media reports described the substance as popular among teenagers, who sometimes referred to this drug use as “robo-copping.” Usage by persons of that age group is not limited to the United States. For example, authorities in Korea have expressed concern about fatal overdoses among young illicit users, particularly when they combine dextromethorphan with another drug to intensify effects.

In the 1960s human addiction to dextromethorphan was dismissed as highly unlikely. Subsequently, researchers who documented behavior of rats exposed to drug combinations concluded that dextromethorphan has abuse potential. Human addiction has indeed been reported, although this is described as un- usual. Scientists have not found dependence or withdrawal symptoms. A rat study determined that dextromethorphan can reduce alcohol withdrawal symptoms, and experiments with rats and mice show that dextromethorphan can reduce morphine withdrawal symptoms. One human study found that dextromethorphan by itself did not relieve methadone abstinence, but differ- ent research shows that in combination with other substances dextromethor-

112 Dextromethorphan

phan can relieve abstinence symptoms experienced by heroin addicts. Such results do not demonstrate whether dextromethorphan has cross-tolerance with all the drugs just named, allowing it to be substituted for any of them; their withdrawal syndromes all include elements mimicking the common cold and flu, and dextromethorphan may simply be able to relieve flulike symp- toms regardless of cause.

Rats that dose themselves with intravenous cocaine have shown less interest in that drug after receiving dextromethorphan, but the meaning of that re- duced interest is unclear: Does dextromethorphan promote abandonment of drug use, or do the animals find dextromethorphan so preferable that cocaine cannot compete?

Drug interactions. Dextromethorphan can boost pain relief actions of mor- phine, allowing patients to use less of that opiate. Research has also found that dextromethorphan does not boost euphoria or dependence produced by morphine, leading one investigator to conclude that morphine’s illicit attrac- tions are not increased by dextromethorphan.

Dangerous interactions may occur if dextromethorphan is taken along with MDMA, with monoamine oxidase inhibitors (MAOIs, found in some antide- pressants and other medicine), or with serotonin uptake reinhibitors (a type of antidepressant). When taken with dextromethorphan the latter substances could provoke the “serotonin syndrome,” a potentially fatal emergency in- volving muscle tremors, heartbeat and blood pressure abnormalities, changes in mental state, and loss of consciousness. In rats the drug reduces effects produced by PCP. Dextromethorphan can cause false positives for PCP in urine tests, but an experiment failed to produce positives for opioids.

Cancer. Not enough scientific information to report.

Pregnancy. The drug has been widely used for decades without report of congenital malformations. After chicken embryo experiments in the 1990s sug- gested that dextromethorphan might cause birth defects, a study in Canada compared women who used the drug during pregnancy with those who did not and found no increase of congenital defects in the drug group. A study looking for birth malformations in Spain found none that could be attributed to dextromethorphan and concluded that normal medical used of the drug did not produce birth defects. Those negative findings have not surprised experts familiar with drawbacks in using chicken embryos to test for birth defects; chicken development can be harmed by conditions having no effect on humans, and chicken embryo tests are no longer accepted as indicating human risk of birth defects. Several human studies, however, have found a slight increase in risk of birth defects among pregnant women using dextro- methorphan. The risk is close to negligible, but, as one authority points out, that is not the same as zero risk. The small chance can be reduced to zero by avoiding the drug during pregnancy.

Additional scientific information may be found in:

Darboe, M.N. “Abuse of Dextromethorphan-Based Cough Syrup as a Substitute for Licit and Illicit Drugs: A Theoretical Framework.” Adolescence 31 (1996): 239–45. Einarson, A., D. Lyszkiewicz, and G. Koren. “The Safety of Dextromethorphan in Preg-

nancy: Results of a Controlled Study.” Chest 119 (2001): 466–69.

Dextromethorphan 113

Hinsberger, A., V. Sharma, and D. Mazmanian. “Cognitive Deterioration from Long- Term Abuse of Dextromethorphan: A Case Report.” Journal of Psychiatry and Neuroscience 19 (1994): 375–77.

Mart ́ınez-Frias, M.L., and E. Rodr ́ıguez-Pinilla. “Epidemiologic Analysis of Prenatal Exposure to Cough Medicines Containing Dextromethorphan: No Evidence of Human Teratogenicity.” Teratology 63 (2001): 38–41.

Pender, E.S., and B.R. Parks. “Toxicity with Dextromethorphan-Containing Prepara- tions: A Literature Review and Report of Two Additional Cases.” Pediatric Emer- gency Care 7 (1991): 163–65.

Polles, A., and J.L. Griffith. “Dextromethorphan-Induced Mania.” Psychosomatics 37 (1996): 71–74.

Rammer, L., P. Holmgren, and H. Sandler. “Fatal Intoxication by Dextromethorphan: A Report on Two Cases.” Forensic Science International 37 (1988): 233–36.


Pronunciation: deks-troh-MOHR-a-meyed
Chemical Abstracts Service Registry Number: 357-56-2. (Tartrate form 2922-


Formal Names: Alcoid, Dauran, Dimorlin, Jetrium, Linfadol, Moramide, Narcolo, Palfium, Troxilan

Type: Depressant (opioid class). See page 24 Federal Schedule Listing: Schedule I (DEA no. 9613) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This drug was first identified in the 1950s. It has no officially sanc- tioned medical role in the United States but is used elsewhere for pain control in conditions such as kidney stone attacks, cancer, surgery, or injury. A case report tells of a person who used this drug to diminish pain during self- mutilation. Dextromoramide can provide relief when standard opiates fail. Although generally classified as an opioid (a synthetic chemical) the drug is produced from unripened opium seeds and is 2 to 70 times stronger than morphine, depending on the animal species being tested and the effect being measured. Dextromoramide acts quickly; authorities disagree on how long its effects last.

Drawbacks. Unwanted effects can include nausea, vomiting, perspiration, rapid pulse, breathing impairment, urinary difficulty, lowered body temper- ature and blood pressure, and dizziness. Compared to morphine, dextro- moramide is less likely to cause constipation or sleepiness. Euphoria can occur. Persons taking dextromoramide are generally warned against driving cars or running other dangerous machinery. A case report mentions a drug abuser’s serious, but curable, heart damage caused by injecting crushed oral tablets of dextromoramide.

Abuse factors. Dextromoramide is chemically related to methadone, and some researchers believe that dextromoramide could be a useful supplemental drug for addicts being treated in methadone maintenance programs. Mor- phine and dextromoramide have enough cross-tolerance to prevent morphine withdrawal symptoms. Dextromoramide itself is addictive; around 1990 a sur- vey of 150 methadone patients in London found that 7 were being treated for

Dextromoramide 115

dextromoramide addiction. At one time some medical observers doubted that dextromoramide is addictive, but negative results in their research were prob- ably due to the medical context in which the drug was being used. In rats the development of dextromoramide tolerance is so much slower than with mor- phine that one group of investigators doubted the phenomenon was really occurring. Researchers have disagreed about how fast tolerance appears in humans, but it does occur, as does dependence. Disagreement about how quickly tolerance emerges in humans may be related to which drug effects are being examined; tolerance does not necessarily develop to all of a drug’s ef- fects at the same rate. For example, tolerance to pain relief properties might emerge at a different point of treatment than tolerance to nausea or sleepiness caused by a drug.

Drug interactions. Taking this drug with antihistamines or depressants (such as alcohol) can be risky. Monoamine oxidase inhibitors (MAOIs, found in some antidepressants and other medicine) are particularly dangerous to take with dextromoramide. Persons with breathing difficulty or poor thyroid activity should be careful about taking this drug.

Cancer. Not enough scientific information to report.

Pregnancy. The drug produces massive birth defects in mice, but its ability to cause human malformations at normal medical dosage levels is unknown. Dextromoramide has been used to ease childbirth, but if pregnant women receive the drug shortly before giving birth, their infants may have trouble breathing. One medical authority has called the substance too dangerous to use during labor. Dextromoramide passes into milk of nursing mothers.

Additional scientific information may be found in:

De Vos, J.W., et al. “Craving Patterns in Methadone Maintenance Treatment with Dex- tromoramide as Adjuvant.” Addictive Behaviors 24 (1999): 707–13.

Jurand, A., and Martin, L.V. “Teratogenic Potential of Two Neurotropic Drugs, Halo- peridol and Dextromoramide, Tested on Mouse Embryos.” Teratology 42 (1990): 45–54.

La Barre, J. “The Pharmacological Properties and Therapeutic Use of Dextromora- mide.” Bulletin on Narcotics 11, no. 4 (1959): 10–19.

Newgreen, D.B. “Dextromoramide: Review and Case Report.” Australian Journal of Pharmacy 61 (1980): 641–44.


Pronunciation: dex-TROR-fan
Chemical Abstracts Service Registry Number: 125-73-5 Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Unlisted

Uses. This substance is closely related to levorphanol and can produce a false positive for levorphanol in drug screen tests. The human body will trans- form part of a dextromethorphan dose into dextrorphan. The same trans- formation occurs in rats; when comparing results in males and females, researchers found that a given amount of dextrorphan lasts twice as long in female rats.

Dextrorphan can fight coughs and reduce epileptic seizures, although test results differ about how well it diminishes seizures. Mice research has found that the drug helps mice recover from strokes, and in humans the drug ap- pears useful for treating minor strokes. Some research indicates that the sub- stance has potential for treating various human neurological afflictions, but such potential has yet to be fulfilled. A rat experiment found dextrorphan ineffective in preventing brain damage caused by the chemical warfare agent soman. A rat study testing dextrorphan’s potential as an antidote for meth- cathinone poisoning had limited success.

Drawbacks. Unwanted side effects may include nausea, vomiting, sleepi- ness, high or low blood pressure, uncontrollable eye movement, and halluci- nations. Rat experiments show that high enough does can impair memory and learning. When one group of researchers tested dextrorphan’s ability to pre- vent some types of brain damage, the scientists found instead that dextror- phan caused damage in rats.

Abuse factors. At one time dextrorphan was a Schedule I substance, but eventually it was removed from any schedule of controlled substances. Such a journey is most unusual; assorted drugs have been moved from one schedule to another over the years, but the direction is almost always to put the drugs under more controls rather than fewer. Scientists describe dextrorphan as pro- ducing effects similar to PCP. At sufficiently high levels, dextrorphan can make people feel as if they are intoxicated with alcohol.

Drug interactions. Dextrorphan has reduced cocaine effects in mice. Cancer. Not enough scientific information to report.
Pregnancy. After male mice received dextrorphan in an experiment, they

Dextrorphan 117

produced offspring having lower weight, delays in maturation, and abnormal swimming behavior. Whether the drug passes into a human fetus or the milk supply of a nursing mother is unknown.

Additional scientific information may be found in:

Aylward, M., et al. “Dextromethorphan and Codeine: Comparison of Plasma Kinet- ics and Antitussive Effects.” European Journal of Respiratory Diseases 65 (1984): 283–91.

Dematteis, M., G. Lallement, and M. Mallaret. “Dextromethorphan and Dextrorphan in Rats: Common Antitussives—Different Behavioural Profiles.” Fundamental and Clinical Pharmacology 12 (1998): 526–37.

“Safety, Tolerability and Pharmacokinetics of the N-Methyl-D-Asparate Antagonist Ro- 01-6794/706 in Patients with Acute Ischemic Stroke.” Annals of the New York Academy of Sciences 765 (1995): 249–61, 298.

Schutz, C.G., and M. Soyka. “Dextromethorphan Challenge in Alcohol-Dependent Pa- tients and Controls.” With reply by Drystal and Petrakis. Archives of General Psychiatry 57 (2000): 291–92.

Szekely, J.I., L.G. Sharpe, and J.H. Jaffe. “Induction of Phencyclidine-Like Behavior in Rats by Dextrorphan But Not Dextromethorphan.” Pharmacology, Biochemistry, and Behavior 40 (1991): 381–86.


Pronunciation: dye-AZ-e-pam

Chemical Abstracts Service Registry Number: 439-14-5

Formal Names: Alupram, Atensine, Diastat, Diazemuls, Evacalm, Solis, Stesolid, Tensium, Valium, Valrelease, Vival

Informal Names: Blues, Drunk Pills, Ludes, Mother’s Little Helper, V, Val Type: Depressant (benzodiazepine class). See page 21
Federal Schedule Listing: Schedule IV (DEA no. 2765)
USA Availability: Prescription

Pregnancy Category: D

Uses. By the end of the twentieth century diazepam was one of the best- known antianxiety agents in America. Other medical uses of this fast-acting and long-lasting drug include treatment of insomnia, migraine, facial pain, muscle spasms, convulsions, vomiting, malaria, rattlesnake bite, alcohol and heroin withdrawal syndromes, cardiac difficulty created by cocaine, and mus- cle stiffness from tetanus and other causes. In children the drug is used to combat seizures caused by fever. Diazepam is commonly administered to calm patients just before surgery. The body converts the drug into other chemicals, including temazepam and oxazepam.

Drawbacks. Unwanted actions of diazepam include weariness and weak- ness and occasionally headache, dizziness and vertigo, nausea, fuzzy or dou- ble vision, urinary control problems, and depressed mood. A case report tells of the drug bringing on an attack of gout. Diazepam is not recommended for persons with acute narrow-angle glaucoma.

The compound can make users tired and impair vigilance, judgment, re- action times, and movement. A person using diazepam should be cautious about operating dangerous machinery; simulated driving tests demonstrate reduced ability after a dose. The drug can cause memory problems. A study of newborn rats receiving the drug found that it slowed learning, but their learning capacity was normal even though the rats needed more time to learn something. Diazepam can interfere with the ability to recognize an angry ex- pression on someone’s face—a disability with distinct potential for social con- sequences—and a laboratory experiment demonstrated the drug’s ability to make people more aggressive if they are provoked.

Diazepam is given to treat epileptic seizures, but long-term use can increase

Diazepam 119

epileptic seizures. Among epileptics the drug can also cause status epilepticus, a potentially fatal condition in which seizures occur back to back.

Injecting diazepam into an artery is perilous. This mishap has been known to occur even when medical professionals administer the drug, and most rec- reational users lack training in anatomy. This mistake can cause gangrene, leading to amputation of appendages. Intravenous injection of diazepam can stop breathing and heart action; when administering the drug intravenously hospitals are prepared for such emergencies, but most street users are not. Intravenous injection can also lower muscle strength and blood pressure. In a small percentage of human volunteers (5% or less), rectal administration has produced euphoria, breathing difficulty, skin rash, runny nose, or diarrhea.

Diazepam is one of the few drugs that can cause flat brain wave readings in a living person. Such readings are a classic sign of death, and medical personnel seeing such readings might decide to stop efforts that are keeping a patient alive.

Abuse factors. Among illicit drug users in the 1990s diazepam was the most common benzodiazepine. When researchers supplied recreational drug users with several benzodiazepine class substances, diazepam was rated as having the most abuse potential. In testing of the drug’s appeal, volunteers reported that the higher the dose, the higher the attractiveness. Researchers evaluating results of an experiment involving recreational drug users judged diazepam to be even more effective in producing pleasure than in producing medical effects.

In one experiment with recreational drug users over one third of them de- scribed diazepam’s effects as reminiscent of barbiturates, which produce ef- fects similar to alcohol. Perhaps such effects explain why tests of drug preference show diazepam to be popular among moderate alcohol drinkers. Research indicates that euphoria from diazepam is more likely in a person with a family history of alcoholism. Moderate drinkers find diazepam more appealing than light drinkers do, but that may be due less to alcohol per se than due to a personality that finds drugs generally attractive.

A rat experiment measured development of diazepam tolerance in those animals. Humans can develop dependence with diazepam, causing a with- drawal syndrome if dosage ceases all at once instead of gradually. Depending on how much of the drug has been used for how long, withdrawal symptoms can be mild or strong. Mild cases may simply involve trembling, reduced appetite, and trouble falling asleep. In bad cases a person can experience per- spiration, muscle cramps and tremors, vomiting, and convulsions. Sudden stoppage of long-term diazepam dosage can provoke seizures, so doses need to be tapered off instead.

Drug interactions. Alcohol and diazepam can boost each other’s actions. Diazepam effects can also be intensified by barbiturates, opiates, and mono- amine oxidase inhibitors (MAOIs—found in some antidepressants). Those in- teractions can be fatal. Effect of a diazepam dose can be lengthened by propoxyphene and by the ulcer drugs omeprazole and cimetidine. One study found that a dose tends to last for a shorter time among alcoholics. In a dog experiment phenobarbital decreased diazepam levels in the animals. In mice diazepam has boosted toxic effects from the cancer medicine ifosfamide. The

120 Diazepam

more tobacco cigarettes people smoke, the less drowsy diazepam makes them. Body weight also affects diazepam actions, with drug build-up and elimina- tion taking longer in bodies of fatter people. Experimenters have even found that drug effects can vary by time of day; at night diazepam prolongs the presence of an ibuprofen dose.

Cancer. Experimentation shows diazepam to have potential for causing cancer in mice, results causing researchers to suspect the same possibility in humans. Tests with rats, gerbils, and hamsters produced no cancer risk. Ex- amination of medical records from almost 13,000 diazepam users found no link to a higher cancer rate. Several other investigations found no connection between the drug and assorted human cancers, but results have been mixed on association with ovarian cancer.

Pregnancy. Hamsters receiving the drug during pregnancy can produce off- spring with cleft palate and other skull abnormalities. Similar results are seen in mice, particularly if cocaine is used as well. Chicken embryos exposed to diazepam develop malformations. Diazepam experiments with rats have re- sulted in fewer pregnancies and higher death rates for pups. Some rat exper- iments produce birth defects and some do not; size of dose may be important. If pregnant mice receive the drug, their male offspring may have difficulty with sexual functioning as adults. (In contrast, the drug is used for treating impaired male sexual functioning in humans.) Rodent offspring may suffer from compromised immune systems. They also may act more nervous than pups who lack fetal exposure, although rats that have no fetal exposure, but instead receive multiple doses soon after birth, act less uneasy in later life after dosage has stopped. A number of rodent studies find that prenatal ex- posure to diazepam may produce assorted behavioral effects that do not ap- pear until adolescence or adulthood. Those effects are measured by various tests (running mazes and the like) that are difficult to extrapolate to human experience, but the point is that diazepam’s effects may be unapparent in newborns and take years to emerge.

A study of 689 pregnant women taking assorted antidepressants was unable to attribute any birth defects to diazepam, and the same results came from a smaller study; but nonetheless the drug is suspected of causing malformations. Measurements from pregnant women indicate that diazepam passes to the fetus and builds up there; blood levels of the drug in newborns can be higher than the mother’s. Some researchers find that the drug slows fetal brain de- velopment. A case report notes severe multiple malformations in an infant whose mother used diazepam during pregnancy but does not establish cause and effect. Researchers tracked medical histories of several thousand women whose babies had major malformations and found an association between diazepam and cleft lip, the association becoming even stronger if women had smoked while taking diazepam during pregnancy. Additional research has associated diazepam with birth defects involving the heart, stomach obstruc- tion, and hernia. Association, however, does not prove cause and effect. In- deed, other research has found no association between diazepam and cleft lip or any other congenital malformation. One study found that newborns with fetal exposure to diazepam tend to weigh less than normal, but they soon gain weight and reach a normal level. Infants have exhibited withdrawal symptoms

Diazepam 121

if their mothers used diazepam during pregnancy; those symptoms may not appear immediately after birth.

Nursing mothers are advised to avoid the drug, which can continue to pass into breast milk long after drug use is halted. The drug can build up in babies, enough that they can be sedated by milk from mothers using diazepam, and the infants may lose weight while nursing.

Additional information. Methaqualone and diazepam each have the nick- name “Ludes,” but the drugs are different substances.

Additional scientific information may be found in:

Clarke, C.H., and A.N. Nicholson. “Immediate and Residual Effects in Man of the Metabolites of Diazepam.” British Journal of Clinical Pharmacology 6 (1978): 325–31.

Giri, A.K., and S. Banerjee. “Genetic Toxicology of Four Commonly Used Benzodiaz- epines: A Review.” Mutation Research 340 (1996): 93–108.

Gotestam, K.G., and B.E. Andersson. “Subjective Effects and Vigilance after Diazepam and Oxazepam in Normal Subjects.” Acta Psychiatrica Scandinavica 19, no. 274 (1978, Suppl.): 117–21.

Griffiths, R.R., et al. “Comparison of Diazepam and Oxazepam: Preference, Liking and Extent of Abuse.” Journal of Pharmacology and Experimental Therapeutics 229 (1984): 501–8.

Griffiths, R.R., et al. “Relative Abuse Liability of Diazepam and Oxazepam: Behavioral and Subjective Dose Effects.” Psychopharmacology (Berlin) 84 (1984): 147–54.

Juergens, S. “Alprazolam and Diazepam: Addiction Potential.” Journal of Substance Abuse Treatment 8 (1991): 43–51.

Sutton, L.R., and S.A. Hinderliter. “Diazepam Abuse in Pregnant Women on Metha- done Maintenance. Implications for the Neonate.” Clinical Pediatrics 29 (1990): 108–11.

Willumeit, H.P., H. Ott, and W. Neubert. “Simulated Car Driving as a Useful Technique for the Determination of Residual Effects and Alcohol Interaction after Short- and Long-Acting Benzodiazepines.” Psychopharmacology, no. 1 (1984, Suppl.): 182–92.


Pronunciation: dye-eth-ill-PROH-pee-on
Chemical Abstracts Service Registry Number: 90-84-6. (Hydrochloride form 134-


Formal Names: Adiposan, Amfepramone, Anfamon, Apisate, Bonumin, Brendalit, Dietic, Dietil-Retard, DIP, Dobesin, Frekentine, Lineal-Rivo, Linea-Valeas, Li- pomin, Liposlim, Magrene, Moderatan, M-Orexic, Nobesine, Nulobes, Prefa- mone, Propion, Regenon, Regibon, Slim-plus, Tenuate, Tenuate Dospan, Tepanil

Informal Names: Blues
Type: Stimulant (anorectic class). See page 15
Federal Schedule Listing: Schedule IV (DEA no. 1610) USA Availability: Prescription
Pregnancy Category: B

Uses. Humans find the drug’s effects similar to those of dextroamphetamine but at a weaker level. One experiment found dextroamphetamine 6 to 11 times stronger than diethylpropion when given orally, 10 to 20 times stronger when given by subcutaneous injection. Although diethylpropion was created in the 1920s, this amphetamine derivative was not marketed for weight loss until around 1960. The drug then achieved great popularity. Over 30 million per- sons around the globe had taken the drug by 1978. That year 1.5 billion pre- scriptions were written, but the number dropped to just one-fourth that amount by 1988 as the medical world became more aware of the drug’s draw- backs.

Occasional short-term usage rather than continual use has been recom- mended. The compound breaks up sleep and interferes with dreaming but has fewer stimulant effects than some other anorectics. Users feel less fatigue than with fenfluramine, and undesirable effects of diethylpropion disappear faster than those of fenfluramine when the drug is stopped. Studies of weight loss patients using diethylpropion found only trivial impact on heart rate or blood pressure, and the compound is considered a good choice for patients with high blood pressure.

Diethylpropion has been used experimentally to reduce craving for cocaine, with some success. Some researchers question that finding, however, pointing out that craving for cocaine diminishes in a hospital setting regardless of

Diethylpropion 123

whether patients receive diethylpropion or a placebo. In a two-week study, former crack cocaine users receiving diethylpropion showed no change in tests of thinking abilities. That result is interpreted as meaning that short-term use of diethylpropion may cause no measurable harm to brain function.

Another experimental use of the drug has been for relief of arthritis pain. Patients experienced increase of comfort but no increase in ability to use af- fected joints.

Drawbacks. Minor unwanted actions may include dizziness, dry mouth, and constipation. In a study of 132 patients taking the drug, about 3% had experiences such as euphoria, muscle tremors, or trouble with sleeping. As- sorted scientific reports indicate the drug rarely has untoward physical effects; the medical literature mentions an addict who ingested 30 to 100 times the recommended amount each day without major impact. Exceptions to the drug’s relative safety do occur. Diethylpropion is suspected of being involved in a case where someone suffered minor strokes (transient ischemic attacks), is suspected of contributing to a case of heart trouble, and is known to cause heart trouble if an overdose is taken. A rare affliction ascribed to the drug is overdevelopment of the vestigial male mammary glands.

The drug may bring on psychosis, especially when taken along with a mon- oamine oxidase inhibitor (MAOI, found in some antidepressants and other medicine). One user felt under assault from persons using mental telepathy; another heard voices; another thought a television set was observing her; an- other began worrying about someone using the “evil eye” to kill a child. In some cases those problems ceased after the diet drug stopped; in others the affliction reappeared. A therapist reporting on the latter type of cases sus- pected that the persons would have developed psychosis regardless of whether they used diethylpropion. The typical sufferer is a female 25 to 40 years old, leading a troubled life with a history of mental instability and drug abuse. Drugs abused by these women often include amphetamines, an im- portant factor because a former amphetamine abuser who later takes another stimulant can quickly shift back into the old abuse mode. Often such persons begin taking diethylpropion to help them lose weight but afterward continue taking it for pleasurable psychic effect. That special group’s experience, how- ever, is not commonplace among users in general.

Abuse factors. The drug’s amphetamine-type effects are strong enough to have produced an illicit market for diethylpropion in the 1960s, but large surveys determining levels of abuse for various drugs yielded no mention of diethylpropion during the drug’s peak of popularity in the mid-1970s. In that era analysis of 5,204 street drug samples found 1 containing diethylpropion. Because the compound is described as producing effects resembling those of amphetamine, diethylpropion is not recommended for persons who have suf- fered from psychological illness or drug abuse. Binge abusers report that pleasant sensations can be obtained for one to three days, but then nervous- ness and restlessness predominate if dosing continues. Tolerance develops to the drug’s stimulant actions.

Drug interactions. Experiments with mice show that alcohol and diethyl- propion produce more locomotor activity than either drug alone. Researchers in Brazil speculate that combining the two substances may increase other stim-

124 Diethylpropion

ulation sensations, perhaps explaining why using alcohol and anorectic drugs together is allegedly so popular in that country. How popular is that practice? In the latter 1980s the total distribution of diethylpropion and other anorectics was compared to Brazil’s population, yielding enough drugs to supply a daily dose to about 1.4% of the population that could afford to buy it, which is the same as saying 0.7% of that wealthier population could be taking two doses a day. The percentage of users becomes one third of those totals if doses are divided among the entire population rather than just among those with enough money to buy the drugs. By using a survey other researchers mea- sured use of anorectics as totaling 1.3% of the population in one area of south- ern Brazil in 1994, confined mostly to women from higher classes using the drugs under medical prescription. Those percentages lump together usage of diethylpropion with other anorectics, so usage of diethylpropion would be a fraction of those percentages. And recreational usage of diethylpropion to- gether with alcohol would be smaller yet.

Cancer. The drug’s potential for causing cancer is unknown.

Pregnancy. Tests with rabbits, mice, and rats produced no birth defects. A case in which a pregnant woman taking diethylpropion gave birth to a mal- formed infant raised fear that it may cause fetal damage, but studies of preg- nant women taking the drug attribute no birth defects to it. Nonetheless, potential for human birth defects is unknown. The drug passes into breast milk.

Additional scientific information may be found in:

Bolding, O.T. “Diethylpropion Hydrochloride: An Effective Appetite Suppressant.” Current Therapeutic Research: Clinical and Experimental 16 (1974): 40–48.

Carney, D.E., and E.D. Tweddell. “Double Blind Evaluation of Long Acting Diethyl- propion Hydrochloride in Obese Patients from a General Practice.” Medical Jour- nal of Australia 1 (1975): 13–15.

Carney, M.W.P., and M. Harris. “Psychiatric Disorder and Diethylpropion Hydrochlo- ride.” Practitioner 223 (1979): 549–52.

Cohen, S.D. “Diethylpropion (Tenuate): An Infrequently Abused Anorectic.” Psycho- somatics 18 (1977): 28–33.

“Diethylpropion Psychosis.” Medical Journal of Australia 2 (1970): 1052–53.
Glazer, G. “Long-Term Pharmacology of Obesity 2000: A Review of Efficacy and

Safety.” Archives of Internal Medicine 161 (2001): 1814–24.
Hoffman, B.F. “Diet Pill Psychosis: Follow-up after 6 Years.” Canadian Medical Associ-

ation Journal 129 (1983): 1077–78.
Silverman, M., and Ronald O. “The Use of an Appetite Suppressant (Diethylpropion

Hydrochloride) during Pregnancy.” Current Therapeutic Research: Clinical and Ex- perimental 13 (1971): 648–53.


Pronunciation: dye-high-droh-KOH-deen

Chemical Abstracts Service Registry Number: 125-28-0

Formal Names: BRON, DHC Continus, Drocode, Fortuss, Paracodin, Synalgos

Type: Depressant (opiate class). See page 22

Federal Schedule Listing: Schedule II, III, or V, depending on product formulation (DEA no. 9120)

USA Availability: Prescription and nonprescription

Uses. Cough suppression is a standard medical use for dihydrocodeine, and it can also improve sleep in chronic coughers by reducing the number of times that coughing wakes them. Although a dose may briefly impede breathing, in a successful experiment the drug improved breathing in persons having chronic airflow obstruction, allowing them to engage in more exercise such as walking. The compound has also helped respiration of emphysema patients. Dihydrocodeine has allowed persons with chronic heart failure to become more physically active. The substance is a standard pain reliever but has been found ineffective in helping some kinds of discomfort from surgical and dental procedures, and excessive amounts of the drug can have the paradoxical effect of increasing pain. Dihydrocodeine has at least the same pain relieving strength as codeine, perhaps more. Morphine is considered about seven times stronger than dihydrocodeine.

Drawbacks. Typical unwanted effects include sleepiness, nausea, and con- stipation. Euphoria, dizziness, and abnormal dreams are occasionally re- ported. Excessive dihydrocodeine dosage can cause muscle damage that is known to clear up if the drug is discontinued. Hallucinations may occur. An unusual case report tells of a person developing Alice in Wonderland Syn- drome and Lilliputian hallucinations after routinely drinking a dihydroco- deine cough syrup for several years. In the Alice Syndrome people may see real objects as far smaller than they actually are; the Lilliputian situation (named for an episode in Gulliver’s Travels) involves seeing tiny imaginary objects. Such conditions have also been associated with migraine, fevers, and mononucleosis. In the apparently drug-induced case just mentioned, Lillipu- tian hallucinations persisted despite psychiatric treatment.

Abuse factors. Although dihydrocodeine addiction rarely arises from med- ical use, tolerance and dependence can develop if a person uses the substance

126 Dihydrocodeine

long enough. Drug maintenance programs, in which addicts are weaned off one drug of abuse and switched to one that treatment authorities consider preferable, have used dihydrocodeine to switch addicts from heroin and other opiates. Those programs have also used methadone and dihydrocodeine to substitute for each other: Methadone addicts have been switched to dihydro- codeine and vice versa, substitution indicating that drug abusers find the two substances to be similar. Body chemistry converts dihydrocodeine into dihy- dromorphine, a Schedule I controlled substance. Although an illicit market exists for dihydrocodeine, some physicians believe illegal diversion of pre- scriptions is discouraged by the nature of the drug: Dissolving oral tablets for injection is difficult, and intravenous injection typically produces discontent- ment rather than euphoria.

Drug interactions. The drug may boost actions of the anti–blood clotting medicine warfarin.

Cancer. Not enough scientific information to report.

Pregnancy. Many pregnant women have used dihydrocodeine with no ap- parent harm to fetal development. Nonetheless, the compound is not recom- mended during pregnancy, and excessive quantities can produce an infant who is dependent at birth. Although researchers are uncertain if the substance passes into breast milk, they believe the amount would be too small to no- ticeably affect nursing infants.

Additional scientific information may be found in:

Frame, J.W., et al. “A Comparison of Ibuprofen and Dihydrocodeine in Relieving Pain Following Wisdom Teeth Removal.” British Dental Journal 166 (1989): 121–24.

Johnson, M.A., A.A. Woodcock, and D.M. Geddes. “Dihydrocodeine for Breathlessness in Pink Puffers.” British Medical Journal 286 (1983): 675–77.

Marks, P., H. Ashraf, and T.R. Root. “Drug Dependence Caused by Dihydihydroco- deine.” British Medical Journal 1 (1978): 1594.

Palmer, R.N., et al. “Incidence of Unwanted Effects of Dihydrocodeine Bitartrate in Healthy Volunteers.” Lancet 17 (1966): 620–21.

Takaoka, K., and T. Takata. “ ‘Alice in Wonderland’ Syndrome and Lilliputian Hallu- cinations in a Patient with a Substance-Related Disorder.” Psychopathology 32 (1999): 47–49.

Wotherspoon, H.A., G.N. Kenny, and C.S. McArdle. “Analgesic Efficacy of Controlled- Release Dihydrocodeine. A Comparison of 60, 90 and 120 Mg Tablets in Cold- Induced Pain.” Anaesthesia 46 (1991): 915–17.


Pronunciation: dye-fen-OCK-see-lait
Chemical Abstracts Service Registry Number: 915-30-0. (Hydrochloride form


Formal Names: Diarphen, Eldox, Logen, Lomotil, Lonox, Protector, Reasec, Re- tardinr, Topergan

Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II or V, depending on product formulation

(DEA no. 9170)
USA Availability: Prescription and nonprescription Pregnancy Category: C

Uses. Diphenoxylate was developed in the 1950s but did not see much use until the next decade. The drug is related to meperidine. When used alone at high dosage levels, diphenoxylate produces effects reminiscent of morphine, although pain relief capability is nil. Experimental rubbing of diphenoxylate on patches of psoriasis has helped that skin condition. The drug is a standard remedy for diarrhea and is commonly combined with atropine for that pur- pose. Another purpose of the combination format is to deter recreational use of the controlled substance, by forcing a would-be misuser to experience the simultaneous unpleasant actions of atropine (such as dry mouth, fever, excited behavior, and fuzzy eyesight).

Drawbacks. Diphenoxylate can reduce alertness and speed of movements, making operation of dangerous machinery (such as cars) inadvisable. Other effects of normal doses may include nausea, vomiting, dizziness, numbness, despondency, or euphoria. The drug should be avoided by persons who are prone to intestinal blockage because the compound can aggravate that condition. Pancreatitis is associated with the drug, but a cause and effect relationship is unconfirmed. Because diphenoxylate is available in a nonpres- cription format, some people do not realize how dangerous an overdose can be; breathing trouble leading to brain injury and death can occur; those con- sequences mostly involve accidental overdose in children. Overdose on the atropine component of a diphenoxylate combination product is also possible; atropine poisoning can include fever, agitation, irregularity in heartbeat and breathing, and psychosis involving hallucinations and delirium.

Abuse factors. Addiction to the diphenoxylate-atropine combination is un-

128 Diphenoxylate

usual, but a case report tells of someone who used dozens of tablets every day for years. Under medical supervision the individual gradually reduced and finally stopped dosage over a two-week period; dependence was only slight, with mild flulike symptoms. A case is also reported of a drug addict using diphenoxylate-atropine tablets to hold off withdrawal symptoms when the person’s abused drug was unavailable. Medical personnel have adminis- tered the diphenoxylate-atropine combination in order to wean addicts off methadone maintenance. When the combination was used in that context, recipients showed no signs of tolerance or addiction to it, an intriguing finding because that population of recipients would be particularly susceptible to such effects. Diphenoxylate has also been used to help addicts withdraw from heroin.

Drug interactions. The drug may interact dangerously with monoamine oxidase inhibitors (MAOIs, a component of some antidepressants and other medication). Tranquilizers, alcohol, or barbiturates should not be mixed with diphenoxylate.

Cancer. Diphenoxylate’s potential for causing cancer is unknown, although animal experiments with the drug have found no tendency for the disease to appear.

Pregnancy. Fertility of female rats was impaired when they were dosed daily throughout a three-litter cycle at 50 times the recommended human level. Litter sizes declined when the females daily received 10 times the human dose. Tests on rats, mice, and rabbits revealed no birth defects, but results were not conclusive. A small survey of human medical records found “no strong associations” between the drug and various congenital malformations, and associations are only an indication that further investigation is needed, not that a problem exists. Diphenoxylate’s effect on milk of nursing mothers is uncertain, but the atropine component in a diphenoxylate combination product does pass into the milk.

Additional information. Although difenoxin (CAS RN 28782-42-5) is avail- able as a pharmaceutical preparation, body chemistry also produces this sub- stance from a dose of diphenoxylate. By itself, difenoxin is a Schedule I substance illegal to possess under any circumstance (DEA no. 9168), officially classified as having no medical value. When combined with enough atropine sulfate, however, difenoxin is a Schedule IV prescription drug known as Lys- pafen and Motofen.

Difenoxin acts much like diphenoxylate and is used to treat diarrhea. Dan- gers are similar to diphenoxylate’s. A two-year experiment gave daily doses of difenoxin and atropine to rats and produced no evidence that the combi- nation causes cancer.

In rat experimentation the difenoxin-atropine combination (Pregnancy Cat- egory C) had only a weak impact on fertility, and no birth defects were at- tributed to the combination after being administered to rats and rabbits at levels that were dozens of times the amount recommended for humans. Preg- nant rats, however, did have longer labor and more stillbirths, and a higher percentage of their offspring died as newborns. The difenoxin-atropine com- bination is not recommended for pregnant women or nursing mothers.

Additional scientific information may be found in:

Diphenoxylate 129

Favin, F.D. “Chronic High-Dose Lomotil Abuse and Safe Withdrawal.” ASHP Midyear Clinical Meeting 26 (December 1991): 92D.

Ives, T.J. “Illicit Use of Diphenoxylate Hydrochloride to Prevent Narcotic Withdrawal Symptoms.” Drug Intelligence and Clinical Pharmacy 14 (1980): 715–16.

Kleinman, M.H., and D. Arnon. “Use of Diphenoxylate Hydrochloride (Lomotil) in the Management of the Minor Withdrawal Syndrome during Methadone Detoxifi- cation: Clinical Report.” British Journal of Addiction 72 (1977): 167–69.

Penfold, D., and G.N. Volans. “Overdose from Lomotil.” British Medical Journal 2 (1977): 1401–2.

Rumack, B.H., and A.R. Temple. “Lomotil Poisoning.” Pediatrics 53 (1974): 495–500. Whitehead, W.E., A. Wald, and N.J. Norton. “Treatment Options for Fecal Inconti-

nence.” Diseases of the Colon and Rectum 44 (2001): 131–42.


Pronunciation: dih-PIP-uh-nohn
Chemical Abstracts Service Registry Number: 467-83-4 Formal Names: Diconal, Piperidyl-Methadone, Wellconal Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule I (DEA no. 9622)
USA Availability: Illegal to possess
Pregnancy Category: None

Uses. Actions of this drug are similar to those of morphine. Dipipanone has no officially approved medical usage in the United States, but elsewhere it is used as a powerful pain reliever for conditions such as surgery and cancer. Some cancer patients prefer this drug for pain control. The compound can control coughs.

Drawbacks. Persons are supposed to avoid the drug if they suffer from low thyroid activity or enlarged prostate. Dipipanone can make people sleepy, and users are supposed to be cautioned about operating dangerous machinery. Volunteers in one experiment experienced lower alertness after taking dipi- panone, but other experiments found the substance to lack sedative action. Study does show that sedation can occur when dipipanone is given together with the antihistamine triprolidine. Dipipanone can cause headache, tremors, nausea, and vomiting, impair vision, interfere with breathing, make urination difficult, lower blood pressure, and reduce production of saliva. Seizures have been reported. Euphoria may occur. A case study notes delusions and hallu- cinations caused by the drug. Paranoia has occurred occasionally. A case re- port tells of serious colon difficulty occurring after someone injected three dissolved oral Diconal tablets, a combination product containing dipipanone and the antivomiting drug cyclizine, accompanied by drinking three liters of beer. Even in ordinary medical use, however, dipipanone can cause consti- pation and is supposed to be used cautiously if a person has bowel obstruc- tion.

Abuse factors. Dipipanone is related to methadone and can be substituted for assorted opioids. That property gave dipipanone a role in addiction treat- ment programs seeking to switch addicts to dipipanone. Tolerance and de- pendence can occur. Reportedly drug abusers find dipipanone more potent than heroin, and in combination with cyclizine, dipipanone reportedly can

Dipipanone 131

create a rush of enjoyment that some persons prefer over heroin. In the 1980s some British observers considered dipipanone abuse to be as much a problem as abuse of methadone and methylphenidate, with some addicts getting their supplies legally from doctors. Rather little has been heard about the substance since then, however.

Drug interactions. Dipipanone may interact badly with monoamine oxidase inhibitors (MAOIs), which are substances found in some antidepressants and other medication.

Cancer. Potential for causing cancer is unknown.

Pregnancy. Potential for birth defects is unknown. Authorities are uncertain whether the drug passes into a nursing mother’s milk, but they believe the level would be so low as to cause no harm to the infant. An infant can be born dependent on the drug if the mother has been using it during the final trimester of pregnancy.

Additional scientific information may be found in:

Bound, D., and S. Greer. “Psychotic Symptoms after Dipipanone.” Lancet 2 (1978): 480. Faull, C., et al. “Experience with Dipipanone Elixir in the Management of Cancer Re-

lated Pain—Case Study.” Palliative Medicine 8 (1994): 63–65.
Posner, J., et al. “Effects of an Opiate on Cold-Induced Pain and the CNS in Healthy

Volunteers.” Pain 23 (1985): 73–82.
Stewart, M.J., et al. “Forensic Toxicology in Urban South Africa.” Journal of Toxicology:

Clinical Toxicology 38 (2000): 415–19.
Telekes, A., et al. “Effects of Triprolidine and Dipipanone in the Cold Induced Pain

Test, and the Central Nervous System of Healthy Volunteers.” British Journal of

Clinical Pharmacology 24 (1987): 43–50.
Turnbull, A.R., and P. Isaacson. “Ischemic Colitis and Drug Abuse.” British Medical

Journal 2 (1977): 1000.


Pronunciation: dee-em-tee
Chemical Abstracts Service Registry Number: 61-50-7 Formal Names: Dimethyltryptamine, N,N-Dimethyltryptamine

Informal Names: AMT, Businessman’s LSD, Businessman’s Special, Business- man’s Trip, Cohoba Snuff, Disneyland, Disneyworld, Dmitri, Fantasia, 45 Min- ute Psychosis, 45 Minute Trip, Instant Psychosis, Psychosis

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7435) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. Various plants contain this chemical, and minute quantities are man- ufactured by body processes in mammals. The substance can also be made in a laboratory and is chemically similar to bufotenine. Grasses containing DMT can sicken and kill livestock.

Native peoples of the Amazon use snuffs and drinks containing DMT for religious purposes. Supposedly such drinks can give a person telepathy and other ESP (extrasensory perception) powers, but one researcher failed to achieve such states even though he used the drink 30 times while living among a native population for three years.

In rat experiments the animals acted as if DMT is similar to LSD. A human study found DMT to evoke visual and auditory hallucinations so intense that the volunteers lost contact with ordinary reality during the drug experience. The volunteers vacillated back and forth between euphoria and unease. In contrast, a different human study comparing DMT and delta-9- tetrahydrocannabinol (also called THC, the main active ingredient in mari- juana) found their actions to be equivalent. The finding was exceptional, however; most reports describe DMT as a potent hallucinogen with actions reminiscent of LSD or mescaline. Some people are said to become relaxed as DMT’s initial actions wear off.

One commonly mentioned DMT effect is awareness of elves, fairies, or some alien intelligence—encounters that users do not necessarily find pleasant. Some users say that time seems to slow. Most scientists seek explanations that do not require acceptance of alternative realities, because throughout the his- tory of science the simplest explanations tend to be correct. For example, time

DMT 133

may seem slower if many events crowd simultaneously on someone’s con- sciousness—an explanation that does not require time itself to alter. Likewise, industrious investigators have detected changes in the eye during DMT in- toxication, changes that the brain may interpret as light and that a person can “see” as hallucinations.

Drawbacks. While under DMT’s influence a person can experience memory trouble, shortened attention span, and altered perception of one’s body. Phys- ical effects may include dizziness, nausea, tingling, trembling, weakness, and breathing difficulty, along with higher body temperature, heart rate, and blood pressure. Reportedly a typical human-size dose per body weight is enough to kill a sheep.

Some researchers suspect that excessive natural production of DMT and related substances by a person’s body processes may be the cause of schizo- phrenia and other psychotic conditions. Research along that line has produced mixed results. One study found that DMT levels generally went up and down in psychiatric patients, depending on outbreaks of psychotic behavior and return to normalcy, but timing of the shifts did not always match changes in patients’ conditions. In addition, psychologically normal persons with liver disease can have DMT levels about as high as those found in schizophrenic individuals.

Abuse factors. Human experimentation has detected no development of tol- erance to DMT’s psychological effects. Tolerance to some physical actions (such as higher pulse rate) has been measured, but tolerance to increase of blood pressure has not been seen. Mice form a tolerance to DMT, and rats not only acquire a tolerance to DMT but have also exhibited cross-tolerance with LSD (meaning the drugs can be substituted for each other, in some ways at least). Humans have also shown partial cross-tolerance between those two drugs. Cats and monkeys fail to develop tolerance to various DMT effects (such as changes in appetite, behavior, and coordination) but apparently tol- erance can develop to other effects. Some researchers feel that DMT tolerance is an uncertain phenomenon at best.

Drug interactions. Not enough scientific information to report. Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

Fish, M.S., and E.C. Horning. “Studies on Hallucinogenic Snuffs.” Journal of Nervous and Mental Disease 124 (1956): 33–37.

Gillin, J.C., et al. “The Psychedelic Model of Schizophrenia: The Case of N,N- Dimethyltryptamine.” American Journal of Psychiatry 133 (1976): 203–8.

Riba, J., et al. “Subjective Effects and Tolerability of the South American Psychoactive Beverage Ayahuasca in Healthy Volunteers.” Psychopharmacology (Berlin) 154 (2001): 85–95.

Rosenberg, D.E., et al. “The Effect of N,N-Dimethyltryptamine in Human Subjects Tol- erant to Lysergic Acid Diethylamide.” Psychopharmacologia 5 (1964): 217–27.

Shulgin, A.T. “Profiles of Psychedelic Drugs—DMT.” Journal of Psychedelic Drugs 8 (1976): 167–68.

Strassman, R.J. “Human Psychopharmacology of N,N-Dimethyltryptamine.” Behav- ioural Brain Research 73 (1996): 121–24.

134 DMT

Strassman, R.J., et al. “Dose-Response Study of N,N-Dimethyltryptamine in Humans. II. Subjective Effects and Preliminary Results of a New Rating Scale.” Archives of General Psychiatry 51 (1994): 98–108.

Sza ́ra, S. “The Comparison of the Psychotic Effect of Tryptamine Derivatives with the Effects of Mescaline and LSD-25 in Self-Experiments.” In Psychotropic Drugs, ed. S. Garattini and V. Ghetti. New York: Elsevier, 1957. 460–67.


Pronunciation: dee-oh-bee
Chemical Abstracts Service Registry Number: 53581-53-6 Formal Names: 4-Bromo-2,5-Dimethoxyamphetamine Informal Names: Bob, Bromo-DMA, Bromo-STP, PBR Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7391)
USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This drug became available in the 1960s. It can produce hallucinations and affect interpretations of time and space. Some persons who thought they took LSD were actually on DOB. Research has found DOB effects to develop more gradually and to be more prolonged than those of LSD.

A chemist who knew he was taking pure DOB reported that a small dose brightened his perception of colors and created a mellow mood. Larger doses created muscle tremors and increased insight into psychological issues. The chemist recommended against attempting to drive a car while intoxicated. In a controlled experimental setting with volunteers interested in using the drug to gain better awareness of themselves, the drug stimulated thoughts, feelings, and physical senses. People became more articulate, saw new meaning in or- dinary experiences, and became more inclined to self-examination. In contrast to MDA experiences, the DOB volunteers showed less lethargy and were more interested in what was going on around them. No hallucinations oc- curred.

Drawbacks. In canines DOB can elevate body temperature and blood pres- sure. In humans DOB’s physical effects can include nausea, diarrhea, muscle spasms, blood vessel spasms, sensations of tingling and burning, impaired sense of touch, convulsions, and seizures. The drug may be safe from a tech- nical pharmaceutical standpoint because there is a huge difference between the size of a therapeutic dose and a lethal one, but the drug is so potent that small doses are known to kill. Effects may last for hours and suddenly inten- sify and become fatal. Characteristics of overdose can resemble those of am- phetamine, including fear and physical aggression. The medical literature includes a DOB case somewhat resembling ergotism (see ergot), resulting in the patient’s lower legs being amputated.

136 DOB

Abuse factors. Not enough scientific information to report.
Drug interactions. Alcohol may increase the strength of a DOB dose. Cancer. Not enough scientific information to report.
Pregnancy. Not enough scientific information to report.
Additional scientific information may be found in:

Buhrich, N., G. Morris, and G. Cook. “Bromo-DMA: The Australasian Hallucinogen?” Australian and New Zealand Journal of Psychiatry 17 (1983): 275–79.

Davis, W.M. “LSD or DOB?” American Journal of Psychiatry 139 (1982): 1649.
Delliou, D. “4-Bromo-2,5-Dimethoxyamphetamine: Psychoactivity, Toxic Effects and

Analytical Methods.” Forensic Science International 21 (1983): 259–67.
Shulgin, A.T., T. Sargent, and C. Naranjo. “4-Bromo-2,5-Dimethoxyphenylisopropylam- ine, a New Centrally Active Amphetamine Analog.” Pharmacology 5 (1971): 103–7. Toennes, S.W., et al. “Aufkla ̈rung eines unklaren neurologischen Syndroms durch tox- ikologische Untersuchungen [Explanation of an Unclear Neurological Syndrome by Toxicologic Investigation].” Deutsche Medizinische Wochenschrift 125 (2000):

900–902. (Abstract in English).


Pronunciation: dee-oh-em

Chemical Abstracts Service Registry Number: 15588-95-1

Formal Names: 4-Methyl-2,5-Dimethoxyamphetamine

Informal Names: Serenity, Stop the Police, STP, Super Terrific Psychedelic, Too Stupid to Puke, Tranquility

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7395) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This substance was a classic of the 1960s drug scene, where it was likened to LSD and nicknamed STP for “Serenity, Tranquility, and Peace” and apparently performed as advertised. Because of the nickname initials some persons have confused the drug with a motor oil additive called STP, but they are different substances.

DOM is a powerful drug, 50 to 100 times stronger than mescaline, to which DOM is chemically related. Rats respond to DOM and mescaline in similar ways. Chemically DOM is not only related to mescaline but also to amphet- amine, and an experiment using low dosages of DOM found that the drug had a typical stimulant effect of improving performance on simple learning tasks.

Psychological and hallucinogenic effects depend on size of dose. As the size increases, so do intensity and longevity of effects. Many reports of alleged DOM experiences exist, but typically we do not know if the illicit substance really was DOM. One person who did ingest the real thing described hallu- cinations, brightened mood, more awareness of colors, more enjoyment of music and sex, and various insights into personal issues facilitated by the drug. Volunteers who received DOM in a formal experiment also experienced improved spirits and insights, but the amount of DOM was not enough to produce hallucinations. Results from another experiment showed increased awareness of emotion and thoughts, leading researchers to conclude that the substance might be useful in psychotherapy. In still another experiment psy- chological effects included disturbed perceptions of time and space, a sensa- tion of voices being distant, echoing sound, seeing sound as light, seeing

138 DOM

ordinary movement as stroboscopic jerkiness, seeing surfaces moving sinu- ously, and feeling like one was no longer located in one’s body.

Drawbacks. An experiment documented physical sensations that included warmth, tingling, dizziness, nausea, tremors, rapid heartbeat, impaired move- ment, coughing, sweating, and lack of hunger. Insomnia has also been re- ported. In rats DOM can raise body temperature and lower appetite.

Supposedly effects from a single dose can last for three days, but in a group of 25 volunteers who took substantial doses, only 2 persons experienced effects lasting past the day of the experiment, and none had any effects on the second day afterward. Some users who expect the drug to act like LSD have not realized that DOM effects take longer to develop, and after waiting the amount of time they would wait for LSD actions to begin, those persons have taken more DOM in a mistaken belief that the original amount was not enough. The result can be an overdose emergency. Achieving such an over- dose apparently takes dedication; one estimate puts DOM’s safety index at 10,000 (meaning a person would have to take 10,000 times the amount of a standard effective dose in order to be poisoned). Some investigators wonder if previous use of psychoactive drugs makes people more sensitive to DOM, thereby making overdose easier.

Abuse factors. Tolerance can develop.
Drug interactions. Not enough scientific information to report. Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

Hollister, L.E., M.F. Macnicol, and H.K. Gillespie. “An Hallucinogenic Amphetamine Analog (DOM) in Man.” Psychopharmacologia 14 (1969): 62–73.

Ropero-Miller, J.D., and B.A. Goldberger. “Recreational Drugs: Current Trends in the 90s.” Clinics in Laboratory Medicine 18 (1998): 727–46.

Shulgin, A.T., T. Sargent, and C. Naranjo. “4-Bromo-2,5-Dimethoxyphenyliso- propylamine, a New Centrally Active Amphetamine Analog.” Pharmacology 5 (1971): 103–7.

Snyder, S.H., L.A. Faillace, and H. Weingartner. “DOM (STP), a New Hallucinogenic Drug, and DOET: Effects in Normal Subjects.” American Journal of Psychiatry 125 (1968): 357–64.

Snyder, S.H., L. Faillace, and L. Hollister. “2,5-Dimethoxy-4-Methyl-Amphetamine (STP): A New Hallucinogenic Drug.” Science 158 (1967): 669–70.


See also Marijuana

Pronunciation: droh-NAB-i-nol
Chemical Abstracts Service Registry Number: 1972-08-3 Formal Names: Delta-9-Tetrahydrocannabinol, Marinol, THC Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule III (DEA no. 7369)
USA Availability: Prescription
Pregnancy Category: C

Uses. This is a pure form of THC, the main active ingredient found in the Schedule I substance marijuana. Dronabinol can be obtained from marijuana or manufactured synthetically. Compared to infrequent marijuana users, fre- quent marijuana users are better at identifying whether they have received dronabinol or a placebo.

Dronabinol is used to reduce nausea in persons undergoing cancer che- motherapy and to stimulate appetite in AIDS (acquired immunodeficiency syndrome) patients. Alzheimer’s patients who received experimental drona- binol showed improved appetites and reduction of behavior associated with the disease. Research indicates that the drug may widen airways, a help to persons suffering from breathing difficulty. Experimental success has also been achieved in treating spasticity, reducing not only that affliction but its associated rigidity and pain. Research has also examined whether dronabinol may work as a cough medicine. Human testing shows that oral dosage of dronabinol’s active ingredient THC can help reduce pain.

Drawbacks. Dronabinol can redden eyes and accelerate or slow heartbeat. Sometimes users feel faint upon suddenly standing up. Many of marijuana’s actions are experienced with dronabinol: euphoria, hallucinations, more acute- ness in physical senses, altered time perception, memory trouble, confusion, and drowsiness. Not everyone finds marijuana actions to be pleasant, and some nausea patients find those effects so unpleasant that they would rather forgo the dronabinol and endure the nausea. Some other effects associated with marijuana have not been observed with medical use of dronabinol, such as trouble with thinking skills and lack of ambition.

Abuse factors. Tolerance occurs to some of the drug’s actions but not to appetite stimulation. Dependence is reported, with withdrawal symptoms in-

140 Dronabinol

cluding sleeping difficulty, peevishness, fidgeting, perspiration, runny nose, appetite loss, and loose bowel movements. In one study withdrawal symp- toms lasted three days and gradually cleared up over that time. Addiction is uncommon. No one in a five-month study, including persons who had pre- viously abused other drugs, began abusing dronabinol; nor did any of these persons exhibit changes of personality or changes of ability to function in society. An effort to discover evidence of illicit use in San Francisco found none. Apparently persons interested in recreational effects of dronabinol pre- fer marijuana.

Drug interactions. Animal experimentation has found that dronabinol substantially increases the pain relieving qualities of codeine, heroin, hydro- morphone, meperidine, methadone, morphine, and oxymorphone. The an- tinausea drug prochlorperazine appears to reduce the unwanted marijuana actions of dronabinol.

Cancer. Dronabinol’s potential for causing cancer is unknown. The Ames test, a standard laboratory procedure for detecting cancer-causing potential, revealed none.

Pregnancy. No birth defects have been attributed to dronabinol in mice and rat experiments, although more pregnancy failures occurred. THC passes from a pregnant animal into the fetus. Pregnant women are advised to be cautious with the drug. It passes into milk of nursing mothers, and levels in milk are higher than in the mothers’ bloodstream.

Additional scientific information may be found in:

Beal, J.E., et al. “Long-Term Efficacy and Safety of Dronabinol for Acquired Immuno- deficiency Syndrome–Associated Anorexia.” Journal of Pain and Symptom Man- agement 14 (1997): 7–14.

Calhoun, S.R., G.P. Galloway, and D.E. Smith. “Abuse Potential of Dronabinol (Mari- nol).” Journal of Psychoactive Drugs 30 (1998): 187–96.

Devine, J.W., L.A. Mahr, and C.R. Rieck. “Effectiveness of Delta-9- Tetrahydrocannabinol in Chemotherapy-Induced Nausea and Vomiting.” Jour- nal of the Iowa Pharmacy Association 54 (1999): 22–24, 47–50.

Gonzalez-Rosales, F., and D. Walsh. “Intractable Nausea and Vomiting Due to Gastro- intestinal Mucosal Metastases Relieved by Tetrahydrocannabinol (Dronabinol).” Journal of Pain and Symptom Management 14 (1997): 311–14.

Haney, M., et al. “Abstinence Symptoms Following Oral THC Administration to Hu- mans.” Psychopharmacology 141 (1999): 385–94.

Kirk, J.M., and H. de Wit. “Responses to Oral Delta-9-Tetrahydrocannabinol in Fre- quent and Infrequent Marijuana Users.” Pharmacology, Biochemistry, and Behavior 63 (1999): 137–42.

Struwe, M., et al. “Effect of Dronabinol on Nutritional Status in HIV Infection.” Annals of Pharmacotherapy 27 (1993): 827–31.

Wright, P.L., et al. “Reproductive and Teratologic Studies with DELTA-9- Tetrahydrocannabinol and Crude Marijuana Extract.” Toxicology and Applied Pharmacology 38 (1976): 223–35.


See also Ma Huang

Pronunciation: e-FED-rin (also pronounced EF-uh-dreen)
Chemical Abstracts Service Registry Number: 299-42-3. (Hydrochloride form 50-

98-6; sulfate form 134-72-5)

Formal Names: Broncholate Syrup, Elsinore, Kie Syrup, Letigen, Marax, Pretz-D, Primatene, Rynatuss

Informal Names: Chinese Speed, Herbal Ecstasy, Herbal XTC Type: Stimulant (amphetamine class). See page 12
Federal Schedule Listing: Unlisted
USA Availability: Varies by state and by product formulation Pregnancy Category: C

Uses. Although natural products containing the drug have a long history, ephedrine was not isolated from ma huang until the 1880s. Ephedrine is found in other plants as well. It can be refined from plants or synthesized in a lab- oratory. Despite ma huang’s familiar use as a medicinal herb, Western med- icine did not accept ephedrine until the 1920s. Ephedrine has found usage in standard medicine, alternative medicine, and recreation. Responding to a sur- vey, 14 companies reported they sold the equivalent of 425 million individual doses in 1995, 976 million in 1997, and 3 billion in 1999.

Some early uses have since become outmoded, such as against leprosy and whooping cough. Weight loss experiments have found ephedrine, alone or in combination with caffeine or aspirin, to be more effective than placebos and also more effective than dexfenfluramine (see fenfluramine). A study found ephedrine useful in helping heavy smokers to reduce the number of cigarettes they consume. Standard medicine has also exploited ephedrine’s urinary re- tention effect to help incontinent persons. The drug has been employed against asthma, runny noses, narcolepsy, painful menstruation, and depression.

In alternative medicine ephedrine is marketed for losing weight, increasing muscle mass, facilitating intellectual concentration, and promoting vigor. A scientific study found that ephedrine in combination with caffeine (but not by itself) significantly improves endurance in physical exercise. Many sports or- ganizations ban use of ephedrine by athletes.

Although not a true amphetamine, ephedrine has qualities reminiscent of that stimulant class and has been commonly used to manufacture illicit meth-

142 Ephedrine

cathinone and methamphetamine. Indeed, ephedrine’s chemical relationship to amphetamine and methamphetamine is so close that urine tests can mis- identify ephedrine as those drugs. In an experiment where people received a substance without knowing what it was, ephedrine produced the same phys- ical and mental effects as phenmetrazine, methylphenidate, dextroampheta- mine, and methamphetamine. Ephedrine’s legal status was in flux as this book was written: Depending on the federal or state jurisdiction, ephedrine might be Schedule IV or a freely available unscheduled substance; commerce as a medical drug might be legal, but commerce as a raw chemical might be a crime.

Drawbacks. Amphetamine was designed in a laboratory to provide a sub- stitute for ephedrine because of the latter’s drawbacks. A double dose of ephedrine can be poisonous, in comparison to other drugs with the same therapeutic effects but that require 10 or 20 times the regular dose to become severely toxic. For that reason many physicians prefer to avoid prescribing ephedrine.

Ephedrine can cause skin rash, nausea, diarrhea, constipation, hepatitis, rise in body temperature, jitteriness, insomnia, hyperactivity, irregular heartbeat, high blood pressure, heart attack, stroke, seizures, kidney stones, visual and auditory hallucinations, and paranoid psychosis. Ephedrine can worsen mus- cle tics; animal experimentation shows the drug causing brain damage that can lead to the tics seen in Parkinson’s disease. During strong physical exer- tion, such as bodybuilding, ephedrine may increase danger of heart attack. Suspicion exists that persons who stop taking ephedrine may be more sensi- tive to it if they start using the drug again.

Many reports of adverse events come from cases in which a person was using ephedrine diet supplements commonly found in health food stores. Per- haps people regard such products as inherently “healthy” and fail to realize that an ephedrine food supplement can produce a drug overdose or be haz- ardous if used moderately but for too long.

The U.S. Food and Drug Administration (FDA) became particularly alarmed at the prevalence of medical problems developed by young healthy users, and regulatory efforts were increasing when this book was written. Some scientists say the FDA’s concerns are unfounded and that many physical problems after ephedrine ingestion derive from a person’s prior medical history or massive overdose. Nonetheless, the FDA believes that ephedrine may harm people who already have the following conditions: prostate trouble, psychological afflictions (including depression and nervousness), high blood pressure, dia- betes, glaucoma, and ailments of thyroid, kidney, or heart.

Alcohol is an ingredient in some ephedrine inhalers and can influence read- ings in breathalyzer tests for drunk driving. That problem can be avoided by a 15-minute wait between using the inhaler and administering a test.

Abuse factors. Historically ephedrine has seldom been abused, but in the 1990s it was cited as growing in popularity among youths, as a recreational stimulant with euphoric and aphrodisiac effects. Such characteristics have al- lowed illicit dealers to market ephedrine falsely as cocaine, methampheta- mine, and MDMA. Some cocaine users find ephedrine less satisfying but still a satisfactory substitute. Reports of ephedrine addiction exist.

Ephedrine 143

Drug interactions. Caffeine boosts ephedrine’s power and can transform a normal dose into a dangerous one. Aspirin and yohimbine (from yohimbe) may also strengthen some ephedrine effects. Dangerous interactions can occur with monoamine oxidase inhibitors (MAOIs, typically antidepressants). Less serious adverse effects may occur if ephedrine is taken with the antiasthma medicine theophylline.

Cancer. The FDA has noted research indicating that substances like ephed- rine may promote lung cancer, especially among tobacco smokers.

Pregnancy. Safety for use during pregnancy is unestablished. The drug is known to raise fetal heart rate, and fetal blood levels can reach about 70% of the pregnant woman’s blood level of ephedrine. The drug is transferred to breast milk in sufficient quantity to affect nursing infants, making them grouchy and interfering with their sleep. Chicken experiments with ephedrine produce defects in embryos, but such testing is considered inconclusive re- garding human impact. Rabbit experiments find a mix of ephedrine, theoph- ylline, and phenobarbital to cause birth defects similar to those observed in the child of a woman who took that drug combination while pregnant. The same drug combination is suspected in another birth defect case. Although a study of 373 human pregnancies found no malformations attributable to ephedrine even when used in the first trimester, the drug is associated with a small increase in likelihood of birth defects and is not recommended for use during pregnancy.

Additional information. Many nonprescription remedies for common colds include pseudoephedrine (CAS RN 345-78-8), which is related to ephedrine and has similar effects, both desired and undesired. Depending on actions being measured, pseudoephedrine may have from 25% to 50% of ephedrine’s strength. Pseudoephedrine can be used to make methamphetamine and meth- cathinone.

Pseudoephedrine is believed to promote a dangerous bowel disease called ischemic colitis, particularly in women around the time they go into meno- pause. A case report indicates that taking pseudoephedrine with serotonin reuptake inhibitor antidepressants may create a medical emergency called “se- rotonin syndrome.” Typical signs of that condition are hyperactivity, con- fusion, nervousness, vomiting, fast heartbeat, excessive body temperature, shivering, tremors, weakness, or losing consciousness. Caution is advised about using pseudoephedrine shortly after receiving vaccinations, which tem- porarily increase body temperature. Nonetheless, in the 1980s research on more than 100,000 individuals using prescription pseudoephedrine found no hospitalizations caused by the drug.

Influence on fetal development is uncertain, although pseudoephedrine is suspected of causing birth defects when used in the first trimester. The drug is known to accelerate fetal heartbeat but has no particular effect on fetal blood flow, nor does the substance seem to hinder passing nutrients and gases be- tween woman and fetus. Although excreted into human milk, the amount of excretion is so slight as to be considered safe for infants of nursing mothers.

Additional scientific information may be found in:

“Adverse Events Associated with Ephedrine-Containing Products—Texas, December 1993–September 1995.” Morbidity and Mortality Weekly Report 45 (1996): 689–93.

144 Ephedrine

Astrup, A., et al. “The Effect and Safety of an Ephedrine/Caffeine Compound Com- pared to Ephedrine, Caffeine and Placebo in Obese Subjects on an Energy Re- stricted Diet. A Double Blind Trial.” International Journal of Obesity and Related Metabolic Disorders 16 (1992): 269–77.

“Dietary Supplements Containing Ephedrine Alkaloids; Proposed Rule.” Federal Reg- ister 62 (1997): 30677–724.

Gruber, A.J., and H.G. Pope, Jr. “Ephedrine Abuse among 36 Female Weightlifters.” American Journal on Addictions 7 (1998): 256–61.

James, L.P., et al. “Sympathomimetic Drug Use in Adolescents Presenting to a Pediatric Emergency Department with Chest Pain.” Journal of Toxicology. Clinical Toxicol- ogy 36 (1998): 321–28.

Pipe, A., and C. Ayotte. “Nutritional Supplements and Doping.” Clinical Journal of Sport Medicine 12 (2002): 245–49.

Whitehouse, A.M., and J.M. Duncan. “Ephedrine Psychosis Rediscovered.” British Jour- nal of Psychiatry 150 (1987): 258–61.


Pronunciation: UR-guht

Chemical Abstracts Service Registry Number: 12126-57-7

Formal Names: Claviceps purpurea

Informal Names: Cockspur Rye, Hornseed, Mother of Rye, Muttercorn, Smut Rye, Spur Kernels, Spurred Rye

Type: Hallucinogen. See page 25
Federal Schedule Listing: Unlisted
USA Availability: Nonprescription natural product Pregnancy Category: None

Uses. The history of ergot is composed of madness and disfiguring disease but might still be an obscure footnote to medicine except for the discovery of a related chemical in the 1930s called LSD. That link brought modern attention to a normally inconspicuous natural product. Ergot comes from a rather fishy- smelling fungus growing on improperly stored grain (typically rye). In cool and damp conditions ergot is also found on various grains and grasses in the field. This happens around the world; in the 1990s Iowa’s barley crop suffered infection. Ergot chemicals are also found in morning glory seeds. Although ergot is typically an unwanted contamination in grain, sometimes the fungus is deliberately cultivated to be harvested for pharmaceutical purposes.

Ergot is a traditional treatment to reduce menstrual blood flow and bleeding after childbirth. The substance promotes contractions of the uterus, and the raw product has been used for centuries as an aid to birthing. Unskilled ad- ministration, however, can rupture the uterus. In more recent times ergono- vine (CAS RN 129-51-1) has been isolated from ergot as the active chemical for promoting childbearing. Chemicals from ergot can induce abortions in cows and sheep, but reports conflict on whether ergot has this effect on hu- mans. One authority notes that such attempted use can kill the pregnant woman. Ergot preparations are still used as a fallback if no other drug pro- vides sufficient aid in childbirth, but they are generally avoided in modern obstetrics.

Ergotamine, a substance derived from ergot, is used to treat migraine head- ache. Raw ergot is not used for that purpose because the unprocessed natural product would have too many unwanted effects, making the headache cure worse than the disease. Ergot chemicals have also been used to treat meno-

146 Ergot

pause and for experimental treatment of patients suffering from Parkinson’s disease and from mental deterioration associated with old age, including Alz- heimer’s disease. After volunteers took an ergot drug called co-dergocrine they were stimulated and did better than normal on tests of thinking, deci- sions, and physical movement. That finding is not surprising, given that LSD is related to ergot and can act as a powerful stimulant.

Drawbacks. Entire communities have been devastated when residents ate food contaminated with ergot. Such outbreaks of ergotism come in two vari- eties, convulsive and gangrenous. Both can occur simultaneously. The gan- grenous kind is characterized by weeks of severe burning pain in appendages, sometimes called St. Anthony’s Fire or Holy Fire. The convulsive kind can involve dizziness, ringing in the ears, tingling fingers, hallucinations, vomit- ing, convulsions, delirium, and a sensation that vermin are crawling under- neath the skin. Ergotism incidents occurred in Ethiopia in the 1970s, in India during the 1950s, in Russia during the 1920s, and in the United States during the 1800s. Some authorities argue that convulsions and hallucinations caused by ergot were responsible for the Salem witchcraft accusations in colonial America during the 1600s. Such instances are good examples of why herbal medicine authorities recommend avoiding the natural product.

Ergot constricts blood vessels in fingers and toes, enough that repeated use can cause gangrene. Extreme human cases can kill substantial portions of entire limbs; the same result was seen in cows that grazed in an ergot- contaminated pasture and in cattle that ate contaminated feed. Less serious unwanted effects can include nausea, vomiting, chest pain, itching, weak legs, and numb fingers. Extended dosage can cause difficulty in movement, impair vision by damaging blood vessels in the eye, and produce inability to use words.

Ergotamine can cause heart trouble and gangrenous ergotism. Rat tests show that a wide variety of health problems are caused by chronic consump- tion of ergocryptine, an ergot chemical.

Abuse factors. Not enough scientific information to report about tolerance, dependence, withdrawal, or addiction. Deliberate consumption of the natural product is probably rare.

Drug interactions. Ergot problems can be exacerbated by caffeine, by to- bacco cigarettes, by the HIV/AIDS drug ritonavir, and possibly by the anti- depressant fluoxetine (Prozac). A case report relates instances of bad reactions occurring when people used ergot products along with “beta blockers,” a type of drug that is typically prescribed for heart problems.

Cancer. In 1990 a World Health Organization study reported that no infor- mation was available on ergot’s potential for causing cancer. Research pub- lished in 1976, however, said that ergotamine and two other ergot chemicals did not cause cell mutations in mice and hamsters (mutations can indicate potential for cancer).

Pregnancy. Using ergot during pregnancy and nursing is considered haz- ardous. Ergot chemicals consumed by a pregnant cow can pass into the fetus and also appear in the cow’s milk. In pigs ergot can interfere with reproduc- tion and milk supply. Ergotamine is known to cause human fetal stress, is known to cause birth defects in animals, and is suspected of causing birth

Ergot 147

defects in humans. Pregnant women who took drugs in unsuccessful suicide attempts were the subjects of a study that tentatively concluded that ergota- mine did not cause congenital malformations, but the researchers felt they needed more data to be sure. Other investigators have noted reports of er- gotamine birth defects consistent with reduced blood flow (a known action of ergot preparations), but those reports have not been scientifically confirmed. Clinical observations have noted that when nursing mothers use ergotamine in the first week after birth, their infants show normal milk consumption and normal weight gain during that week. Ergot passes into human milk, however, and instances have been noted of infants poisoned from ergot in the milk.

Bromocriptine and cabergoline, drugs related to ergot, have been used in circumstances when milk production needs to be suppressed in women who have recently given birth. Cabergoline has been used experimentally to treat pituitary cancer and Parkinson’s disease, and in certain circumstances the drug should increase female fertility, but scientists are unsure about its po- tential for causing birth defects. Cabergoline experiments with rabbits and mice did not produce malformations. A study of pregnant women who used cabergoline found several instances of birth defects, but no more than would be expected if the drug had not been used. Congenital malformations among offspring were noted in another set of pregnant women who used the drug, but researchers reported no conclusion on the drug’s role.

Additional scientific information may be found in:

Hofmann, A. “Historical View on Ergot Alkaloids.” Pharmacology 16 (1978, Suppl. 1): 1–11.

Merhoff, G.C., and J.M. Porter. “Ergot Intoxication: Historical Review and Description of Unusual Clinical Manifestations.” Annals of Surgery 180 (1974): 773–79. Moir, J.C. “Ergot: From ‘St. Anthony’s Fire’ to the Isolation of Its Active Principle,

Ergometrine (Ergonovine).” American Journal of Obstetrics and Gynecology 120

(1974): 291–96.
Van Dongen, P., and A. De Groot. “History of Ergot Alkaloids from Ergotism to Er-

gometrine.” European Journal of Obstetrics and Gynecology and Reproductive Biology

60 (1995): 109–16.
Woolf, A. “Witchcraft or Mycotoxin? The Salem Witch Trials.” Journal of Toxicology.

Clinical Toxicology 38 (2000): 457–60.


Pronunciation: ess-TA-zoh-lam
Chemical Abstracts Service Registry Number: 29975-16-4 Formal Names: ProSom
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2756) USA Availability: Prescription
Pregnancy Category: X

Uses. Estazolam’s main medical uses are for relaxing muscles, fighting con- vulsions, and inducing sleep. The compound can also reduce anxiety in in- somniacs but is not intended for long-term use against insomnia. Estazolam has been used successfully to treat auditory hallucinations and to improve the general mental state of schizophrenics. The drug is considered more potent than diazepam. Insomnia studies show estazolam to be about 15 times stronger than flurazepam.

Drawbacks. Estazolam may, at inappropriate times, make people light- headed or sleepy and interfere with movement. Constipation and dry mouth are common. Even at high doses the drug’s hindrance of respiration is of no concern in persons who breathe normally but might be troublesome for per- sons who have impaired breathing—although experimental results have been reassuring even for that population. A rebound effect can occur when people stop taking the drug for insomnia, meaning that sleep disturbance temporarily becomes worse than it was before treatment. In one study the most common adverse effect was feeling tired the day after using the drug. Other volunteers have experienced lower mental acuity and pulse rate 10 hours after taking the drug, even after getting a good night’s sleep.

Abuse factors. Withdrawal symptoms are usually minor if a person takes estazolam long enough to produce dependence, but unusual reports exist of delirium and dangerous seizures during withdrawal.

Drug interactions. Estazolam actions can be boosted by alcohol, barbitu- rates, opiates, antihistamines, and monoamine oxidase inhibitors (MAOIs— found in some antidepressants). Cigarette smoking can shorten the time that an estazolam dose lasts.

Cancer. Long-term experiments with rats and mice found no sign that es- tazolam causes cancer. Potential for causing human cancer is unknown.

Estazolam 149

Pregnancy. A rat experiment produced no change in fertility. Estazolam is known to cause human birth defects, and pregnant women are never sup- posed to take the drug. Analysis of milk from nursing rats shows that esta- zolam and its breakdown products can pass into milk.

Additional scientific information may be found in:

Astrup, C., and L. Vatten. “Effect of the Benzodiazepine Derivative Estazolam in Schizophrenia.” Biological Psychiatry 19 (1984): 85–88.

Cohn, J.B. “Hypnotic Efficacy of Estazolam Compared with Flurazepam in Outpatients with Insomnia.” Journal of Clinical Pharmacology 31 (1991): 747–50.

“Estazolam—A New Benzodiazepine Hypnotic.” Medical Letter on Drugs and Therapeu- tics 33 (1991): 91–92.

Lingjaerde, O. “Effect of the Benzodiazepine Derivative Estazolam in Patients with Auditory Hallucinations. A Multicentre Double-Blind, Cross-Over Study.” Acta Psychiatrica Scandinavica 65 (1982): 339–54.

Pierce, M.W., V.S. Shu, and L.J. Groves. “Safety of Estazolam. The United States Clinical Experience.” American Journal of Medicine 88, no. 3A (1990): 12S–17S.

Rosen, R.C., et al. “Psychophysiological Insomnia: Combined Effects of Pharmacoth- erapy and Relaxation-Based Treatments.” Sleep Medicine 1 (2000): 279–88. Vogel, G.W., and D. Morris. “The Effects of Estazolam on Sleep, Performance, and

Memory: Long-term Sleep Laboratory Study of Elderly Insomniacs.” Journal of Clinical Pharmacology 32 (1992): 647–51.


Pronunciation: eth-KLOR-vih-nahl
Chemical Abstracts Service Registry Number: 113-18-8
Formal Names: Arvynol, ECV, Ethylchlorovinyl, Placidyl, Serensil Informal Names: Green Weenies
Type: Depressant. See page 19
Federal Schedule Listing: Schedule IV (DEA no. 2540)
USA Availability: Prescription
Pregnancy Category: C

Uses. Insomnia is the main medical condition treated by this drug, although it has also been used as a tranquilizer. The compound has been used to assist pain relief, on the theory that its calming and sleep-inducing qualities can allow pain relievers to work better. Although ethchlorvynol is considered safe for adults under medical supervision, ordinarily medical personnel are not supposed to dose children with ethchlorvynol, as adequate testing of impact on juveniles has not been done. Normally the drug is not supposed to be used for more than one week, as longer dosage increases risk of adverse effects.

The substance was introduced in the 1950s and is considered old-fashioned. It has mostly been superseded by newer pharmaceuticals that are more effec- tive and that have fewer adverse effects.

Drawbacks. Because the drug makes people sleepy, they should avoid run- ning dangerous machinery (such as motor vehicles) while under the influence. Symptoms of ethchlorvynol intoxication are similar to those of alcohol intox- ication. The drug can cause nausea and vomiting, dizziness, and fainting. Con- fusion, stammering, intense headache, and general loss of vigor have also been reported. Intravenous abuse of the drug has caused vomiting, low blood pres- sure and body temperature, liver damage, fluid buildup in the lungs, and coma.

Persons suffering from porphyria should avoid ethchlorvynol. Porphyria is a body chemistry disease that can cause sudden violent outbursts, and the disease can be promoted by ethchlorvynol. The substance should also be avoided by people who experience “paradoxical reactions” to barbiturates or alcohol. A paradoxical reaction is an effect opposite from the expected one— for example, barbiturates causing hyperactivity rather than mellowness. In an

Ethchlorvynol 151

unusual accident the drug squirted into someone’s eyes and seriously injured the corneas. One capsule format of an ethchlorvynol preparation called Pla- cidyl includes FD&C Yellow No. 5 (tartrazine), which can cause asthma at- tacks in some people.

Abuse factors. A case report indicates that tolerance may develop, but the indication was complicated by influence from the patient’s thyroid disease. Another case report tells of the opposite effect, with a person becoming so sensitive to the drug that a trivial dose put him into a coma for a week. Experts generally feel, however, that tolerance is a more typical development. Taking the drug long enough to produce dependence can also produce slurred speech, amnesia, discoordination, tremors, eyesight difficulty, and facial numbness. The drug has a withdrawal syndrome that may not start until days after dosage suddenly stops. Withdrawal may include the dependence symp- toms just noted, plus excitability, convulsions, delirium, hallucinations, ner- vousness, and loss of normal emotional reactions. Delirium tremens can occur. Standard treatment involves temporary reinstatement of the drug followed by tapering off doses, but phenobarbital has enough cross-tolerance to substitute for this purpose. Typically such detoxification is delicate enough to require hospitalization. In 1981 U.S. Supreme Court Justice William Rehnquist was reported to be so dependent upon medically prescribed ethchlorvynol that his mind was clouded while undergoing withdrawal in a hospital. A case report tells of someone who had months of hallucinations requiring weeks of hos- pitalization while trying to cope with ethchlorvynol withdrawal complicated by alcohol use. Alcohol abusers may find ethchlorvynol attractive. Medical authorities have noted close similarities between symptoms of dependence and withdrawal evoked by alcohol and ethchlorvynol.

Drug interactions. Individuals are not supposed to use ethchlorvynol along with other depressants (including alcohol and barbiturates) or with mono- amine oxidase inhibitors (MAOIs, included in some antidepressants and other medication). Delirium has occurred in persons who take ethchlorvynol along with the tricyclic antidepressant amitriptyline hydrochloride, and caution is advised about taking other tricyclic antidepressants along with ethchlorvynol. Ethchlorvynol may interact with medications given to prevent blood clots. In animals injected with THC, the main active component of marijuana, ethchlor- vynol becomes more potent than usual.

Cancer. Rat experiments using many times the recommended human dose of ethchlorvynol have yielded no evidence that the substance causes cancer. In contrast, mice experiments indicate (but have not confirmed) a cancer- causing potential. In the body the drug converts into other chemicals; results from laboratory testing have yielded mixed results concerning their cancer- causing potential.

Pregnancy. The drug is associated with fetal and newborn death in rat ex- periments. In one experiment using the drug on pregnant rats, offspring appeared normal but behaved abnormally and showed body chemistry ab- errations. Effects on human pregnancy are uncertain. The substance passes into a human fetus, and in dogs the fetal blood level reaches the same strength as the maternal level. A baby born to a woman using the drug showed with-

152 Ethchlorvynol

drawal symptoms; in an infant these may include abnormal reflexes, ner- vousness, and peevishness. Standard advice is to avoid ethchlorvynol during pregnancy. Although the drug’s presence in milk of nursing mothers is un- clear, the potential hazard of dosing infants through the milk makes nursing inadvisable.

Additional scientific information may be found in:

Flemenbaum, A., and B. Gunby. “Ethchlorvynol (Placidyl) Abuse and Withdrawal (Re- view of Clinical Picture and Report of 2 Cases).” Diseases of the Nervous System 32 (1971): 188–92.

Garetz, F.D. “Ethchlorvynol (Placidyl). Addiction Hazard.” Minnesota Medicine 52 (1969): 1131–33.

Heston, L.L., and D. Hastings. “Psychosis with Withdrawal from Ethchlorvynol.” Amer- ican Journal of Psychiatry 137 (1980): 249–50.

Kripke, D.F., P. Lavie, and J. Hernandez. “Polygraphic Evaluation of Ethchlorvynol (14 Days).” Psychopharmacology (Berlin) 56 (1978): 221–23.

Kurt, T.L., G. Reed, and R.J. Anderson. “Pulmonary Edema after Intravenous Ethchlor- vynol (Placidyl).” Veterinary and Human Toxicology 24 (1982, Suppl.): 76–78.

Marshall, E. “Rehnquist’s Drug Dependence Poses Dilemma.” Science 215 (1982): 379–80.

Yell, R.P. “Ethchlorvynol Overdose.” American Journal of Emergency Medicine 8 (1990): 246–50.


Pronunciation: EE-thur

Chemical Abstracts Service Registry Number: 60-29-7

Formal Names: Diethyl Ether, Diethyl Oxide, Ethoxyethane, Ethyl Ether, Ethyl Ox- ide, Sulfuric Ether

Informal Names: Anesthesia Ether, Sweet Vitriol Type: Inhalant. See page 26
Federal Schedule Listing: Unlisted

USA Availability: Some sales of the chemical are restricted because it can be used for manufacturing controlled substances

Uses. Although the substance has been available for hundreds of years it was not used as a drug until the nineteenth century began. The compound relaxes muscles and increases blood sugar levels. For decades it was a stan- dard anesthetic but has been superseded by chemicals that work faster, that are better tolerated by patients, and that are less of a fire hazard. Nonetheless, knowledgeable medical personnel can use ether safely without complicated equipment, and the drug remains common where high-tech medical facilities are not common or nonexistent. In liquid form ether is used medically to clean skin surfaces before putting on adhesive tape and is used to help take off adhesive tape.

The gas format is used recreationally (sometimes along with chloroform), but drinking liquid ether is a more common recreational usage. Effects of drinking are similar to those produced by alcohol but appear faster and last briefly. People feel stimulated and confused, may experience euphoria and hallucinations, may have difficulty walking, and sometimes pass out. Ether drinking is associated with Ireland, where the custom was adopted in re- sponse to temperance movement restrictions on alcohol’s availability in the 1800s. Ether drinking has been known in other European countries also, as well as the United States. In America during the 1800s ether was drunk on occasions ranging from a professional medical society meeting to weddings and quilting bees. Such a range indicates wide social acceptance of the prac- tice. The substance was considered less harmful than alcohol. While using ether, nineteenth-century writer and physician Oliver Wendell Holmes made notes about spiritual insight that he felt was opening to him with the drug’s help, but afterward he found the notes to be gibberish.

154 Ether

Drawbacks. Lighter doses of the gas stimulate breathing, but larger doses depress it. The gas irritates airways. At higher doses pulse rate and blood pressure decline. A serious unwanted effect can be a fatal convulsion. Using ether as a beverage can cause headache, increase salivation, irritate the pas- sageway from mouth to stomach (resulting in vomiting), and produce heavy flatulence. In liquid form the substance can irritate skin and be absorbed through it.

Ether is highly flammable, and various regulations govern medical usage to reduce chances of ignition. These rules even control types of clothing worn by caregivers and types of linen used on carts, lest a static electricity spark create an explosion. Ether vapor is heavier than air and can accumulate in depressions such as the area of a pillow around a patient’s head, making ignition all the more catastrophic. Stories are told of ether drinkers being killed when lighting a tobacco pipe or while indulging too close to an open flame. Even releasing ether fumes from the mouth toward a lit fireplace was consid- ered a hazard to avoid, lest ether ignition flash back and down a person’s throat.

Abuse factors. Some accounts describe ether usage as potentially addictive. Drug interactions. Not enough scientific information to report.
Cancer. Laboratory tests indicate ether may have potential for causing can-

cer, but whether the substance produces the disease in animals is unknown. Pregnancy. The drug has caused congenital malformations and fetal death in experiments on chicken embryos, but impact on humans is unclear. Women with industrial exposure are somewhat more likely to suffer spontaneous abortion. Ether passes from a pregnant woman into the fetus, but neither chronic exposure nor acute medical exposure is known to cause birth defects.

Nursing infants seem unharmed by milk from women using ether. Additional information. “Petroleum ether” and the drug ether are different

Additional scientific information may be found in:

Connell, K.H. “Ether Drinking in Ulster.” Quarterly Journal of Studies on Alcohol 26 (1965): 629–53.

Nagle, D.R. “Anesthetic Addiction and Drunkenness: A Contemporary and Historical Survey.” International Journal of the Addictions 3 (1968): 25–39.

Strickland, R.A. “Ether Drinking in Ireland.” Mayo Clinic Proceedings 71 (1996): 1015.


Pronunciation: eth-ill-EHS-treh-nol
Chemical Abstracts Service Registry Number: 965-90-2 Formal Names: Duraboral, Maxibolin, Orabolin, Orgabolin Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA control no. 4000) USA Availability: Prescription

Uses. Researchers have given the substance to children who needed im- provement in appetite. In places where the drug is illegal for agricultural use, some stockmen occasionally use it illegally to promote cattle growth.

Ethylestrenol has been used to help normalize blood disorders, including low white blood cell levels caused by leukopenia and conditions involving unwanted blood clotting. Experiments indicate that heart attack patients may gain particular benefit from blood actions of the drug. It has also worked as an experimental treatment for hemophilia. The drug can reduce purpura (pur- ple blotches caused by blood leaking just below the skin). Ethylestrenol has been used experimentally to treat frostbite, and case reports note success in using ethylestrenol to help treat a painful ulcerative skin disease called livedo vasculitis and another called atrophie blanche, but experiments with a similar affliction had mixed results. Persons suffering from rheumatoid arthritis and from Raynaud’s disease, an ailment involving poor blood circulation in fingers and toes, have improved while taking ethylestrenol. The drug has also been used to treat Behcet’s syndrome, another disease involving problems in blood circulation. Mice experiments using ethylestrenol show limited success in treating symptoms of the skin disease lupus erythematosus and also Sjo ̈gren’s syndrome, an immune system disease that includes destruction of the salivary glands and sweat glands.

Drawbacks. Among anabolic steroids ethylestrenol is considered to have few masculinizing effects, and it also helps maintain normal functioning of female organs. Nonetheless, in women the drug can cause acne, increase facial hair, and produce hoarseness that can transform into permanent deepening of the voice. The substance can bring on premature sexual development in boys and girls. In sexually mature females ethylestrenol can disrupt or even halt menstrual periods. Men can become less fertile. The substance promotes fluid and salt retention, which can aggravate assorted medical conditions. The

156 Ethylestrenol

drug is not recommended for men suffering from breast or prostate cancer. The substance can worsen porphyria, a disease that can make people violent and sensitive to light. Ethylestrenol has been used to help short youths grow taller but if used incorrectly may instead terminate bone growth, preventing young users from attaining the full adult stature that they would otherwise have achieved. Effective usage to promote height requires careful medical su- pervision.

Abuse factors. Some bodybuilders use ethylestrenol in hopes of promoting muscle mass even though the substance is banned by international athletic organizations.

Drug interactions. Rats that receive ethylestrenol are better able to survive massive exposure to meprobamate or nicotine and high exposure to the in- secticides paraoxon and parathion. Ethylestrenol also makes rats act less af- fected by LSD. Ethylestrenol can counteract anesthesia actions of barbiturates, diminish ulcers caused by the pain reliever indomethacin, and reduce conse- quences of vitamin D overdose.

Cancer. Not enough scientific information to report.

Pregnancy. Pregnant women and nursing mothers are supposed to avoid ethylestrenol. In rat experiments the drug masculinized female fetuses.

Additional scientific information may be found in:

Chakrabarti, R., and G.R. Fearnley. “Phenformin Plus Ethylestrenol in Survivors of Myocardial Infarction: Three-Year Pilot Study.” Lancet 2 (1972): 556–59.

Hecht, A. “Anabolic Steroids: Pumping Trouble.” FDA Consumer 18 (September 1984): 12–15.

Kawashima, K., et al. “Virilizing Activities of Various Steroids in Female Rat Fetuses.” Endocrinologia Japonica 24 (1977): 77–81.

Kerrebijn, K.F., and A. Delver. “Ethylestrenol (Orgabolin): Effects on Asthmatic Chil- dren during Corticosteroid Treatment.” Scandinavian Journal of Respiratory Dis- eases 68 (1969, Suppl.): 70–77.

Murchison, L. “Uses and Abuses of Anabolic Steroids.” Prescribers’ Journal 26 (1986): 129–35.

Van Puymbroeck, M., et al. “17alpha-ethyl-5beta-estrane-3alpha, 17beta-diol, a Biolog- ical Marker for the Abuse of Norethandrolone and Ethylestrenol in Slaughter Cattle.” Journal of Chromotography. B, Biomedical Sciences and Applications 728 (1999): 217–32.


Pronunciation: et-OR-feen
Chemical Abstracts Service Registry Number: 14521-96-1. (Hydrochloride form


Formal Names: Immobilon, M99

Informal Names: Elephant Juice

Type: Depressant (opiate class). See page 22

Federal Schedule Listing: Schedule I (DEA no. 9056). Hydrochloride form Sched- ule II (DEA no. 9059)

USA Availability: Illegal to possess except in hydrochloride form, which is pre- scription

Uses. This pain-relieving drug is derived from thebaine. In jurisdictions where etorphine is legal, it is used as a veterinary sedative. The substance is powerful. Depending on dosage method and animal species receiving the drug, its strength is estimated as anywhere from 10 times to 80,000 times that of morphine, so a person administering the drug must be skilled in order to avoid a serious overdose. The related Schedule II controlled substance dihy- droetorphine is also powerful—10 to 10,000 times stronger than morphine. Etorphine acts quickly. Veterinarians and naturalists use etorphine darts to knock down wild elephants and grizzly bears. Zoos utilize the drug on white rhinoceros, giraffes, and other animals when medical necessity requires them to be unconscious.

Human tests show that etorphine can relieve intense pain without causing unconsciousness. Tests using dihydroetorphine alone and in combination with acupuncture have found the drug to be safe and effective for easing labor pain in childbirth. The substance has relieved pain in cancer patients. Experiment- ers suspect that as well as being a more powerful pain reliever than morphine, dihydroetorphine may also be less likely to create dependence in a patient.

Opiates and other depressants normally interfere with physical perfor- mance. Administered in a particular way, however, etorphine reliably pro- duces a “paradoxical” effect (opposite to an expected effect) of increasing athletic performance by stimulating physical activity while reducing pain. Racehorses have been doped with the drug to make them run faster. Many lovers of the sport disapprove of the practice not only for its illegality but because the horse is harmed. Perhaps the most notorious incident occurred in

158 Etorphine

the late 1980s when Rocket Racer won the Perth Cup by eight lengths and continued running. The horse would not stop despite the jockey’s efforts; after nearly another lap around the track, the horse collapsed and died. Reportedly some human track competitors have used the same drug, accelerated their pace as a race progressed, and had difficulty stopping after crossing the finish line.

Drawbacks. In animal experiments dihydroetorphine interferes with the im- mune system, interference that may make infections more likely. Etorphine can send blood pressure up or down, reduce body temperature, and impair heartbeat and breathing. Impaired breathing is also an unwanted effect ob- served with dihydroetorphine, along with constipation, nausea, vomiting, diz- ziness, and drowsiness.

Although etorphine is a standard veterinary medicine, knowledgeable users treat it with great respect and keep an antidote on hand because accidental injection can be fatal. The drug may be absorbed though the skin, and supplies of etorphine are generally dyed red so users can readily tell if they have touched it (such as a smear across a shirt or hand). Swift administration of an antidote can prevent death.

The quantity needed to kill a person is so minute that its presence in a body can be difficult or even impossible to detect. Harmless chemicals added to a dose can make etorphine even harder to discover through laboratory tests. The drug has also attracted military attention as a possible chemical warfare agent.

Abuse factors. When humans in an experiment received etorphine they ex- perienced euphoria and described the drug as feeling like morphine. Research- ers who administered etorphine in that experiment concluded that the drug is likely to be abused. Misuse has been noted in China. Other investigators reached the same conclusion about dihydroetorphine from the way rats re- sponded to it. The U.S. Drug Enforcement Administration has ruled that dihy- droetorphine’s abuse potential is similar to heroin’s. The government of Hong Kong has noted dihydroetorphine’s lower price and less stringent control make it appealing to heroin addicts. Lawsuits against the tobacco industry unearthed documentation indicating one company considered the possibility that competitors might lace cigarettes with etorphine to add an addictive need that could not be satisfied by other brands, thereby coercing consumer loyalty to a particular product.

A mice study found no dependence at all after dihydroetorphine had been administered for six days, but rat and mice research demonstrates that dihy- droetorphine eventually produces enough dependence to cause withdrawal symptoms. Investigators have noted that rats act as if dihydroetorphine is a satisfactory substitute for heroin. Etorphine can prevent withdrawal symp- toms in morphine addicts, an action demonstrating cross-tolerance between the two drugs, but an etorphine dose holds off withdrawal symptoms for a shorter time than morphine would. In rhesus monkey experiments etorphine and dihydroetorphine are both cross-tolerant with morphine. In those same experiments, when dihydroetorphine dosage was suddenly stopped, few withdrawal signs appeared. Withdrawal symptom research on mice indicates that dihydroetorphine may do more than substitute for morphine: A dihy-

Etorphine 159

droetorphine dose may actually make morphine withdrawal symptoms go away, so further doses of either drug become unnecessary. Such a result would be inconsistent with what is known about opiate dependence, but dis- covery of new facts can change scientific understandings. Some researchers believe that etorphine and dihydroetorphine have potential for treating opiate addiction. Dihydroetorphine has been used for that purpose in China but seems to produce even stronger dependence among heroin addicts than meth- adone. So perhaps animal experiment findings that indicate low dependence potential in dihydroetorphine cannot be extrapolated to humans.

Drug interactions. Giving etorphine and morphine together increases pain relief in mice, while the etorphine does not seem to increase the strength of opiate dependence in the combination. Researchers speculate that the im- proved pain control might be great enough to allow much smaller doses of morphine in humans than would otherwise be needed, which in turn would greatly decrease the amount of dependence otherwise created by normal-size morphine doses.

Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

Firn, S. “Accidental Poisoning by an Animal Immobilizing Agent.” Lancet 2 (1973): 95–96.

“Immobilon: Curiously Strong.” Lancet 2 (1977): 178.
Jasinski, D.R., J.D. Griffith, and C.B. Carr. “Etorphine in Man. 1. Subjective Effects and

Suppression of Morphine Abstinence.” Clinical Pharmacology and Therapeutics 17

(1975): 267–72.
Marcoux, G.S. “Etorphine: A New Opiate of Abuse?” Canadian Journal of Psychiatry 41

(1996): 261.
“Schedule II Control of Dihydroetorphine under the Controlled Substances Act (CSA).”

Federal Register 65 (2000): 69442–43.


Pronunciation: fen-FLOO-ra-meen
Chemical Abstracts Service Registry Number: 458-24-2. (Hydrochloride form


Formal Names: Miniphage, Ponderal, Ponderax, Pondimin, Ponflural, Redux

Type: Stimulant (anorectic class). See page 15

Federal Schedule Listing: Schedule IV (DEA no. 1670). In 2002 federal authorities were planning to make the substance unscheduled.

USA Availability: Prescription Pregnancy Category: C

Uses. For convenience this drug is here classified as a stimulant simply because other anorectics controlled by the U.S. Drug Enforcement Adminis- tration are stimulants. Chemistry operates independently of classification schemes, however, and fenfluramine does not act like typical stimulants even though it is related to amphetamine. Fenfluramine can sedate users and has only modest influence on body temperature and blood pressure. Yet it also has characteristics of powerful stimulants: euphoria, hallucinations, paranoia. High doses can pep up a person rather than sedate. Fenfluramine can alter time perceptions and snap moods from one extreme to another. Some scien- tists classify it as a hallucinogen. Occasionally it can act as an aphrodisiac in females. Fenfluramine also lowers cholesterol levels.

In humans fenfluramine has been found effective for diminishing panic at- tacks but has had mixed success when used to treat obsessive behavior. Ex- perimental use against schizophrenia has been unsuccessful, with patients worsening under the drug regimen. Indeed, reports asked whether the drug might be inducing psychotic reactions. A four-week study found fenfluramine useful in improving the conduct of mentally retarded children suffering from attention deficit hyperactivity disorder (ADHD). A longer study (11 months) found the drug provided only limited help to autistic children, and a still longer study (27 months) found such long-term administration impractical due to unwanted effects and due to changes in the autistic children’s lives. A scientific review of such studies concluded that the drug’s potential nonethe- less merited further trials.

Fenfluramine is a drug of many effects, but medically its primary use has been for weight loss. Studies consistently indicate the drug’s effectiveness for

Fenfluramine 161

that purpose. One study found it comparable to dextroamphetamine in pro- ducing weight loss.

Drawbacks. Fenfluramine tends to dry out the mouth, a condition promot- ing tooth decay. Other unwanted actions can include headache, peevish feel- ings, dizziness, tiredness, nausea, vomiting, diarrhea, and frequent urination. Experience indicates that persons need to be weaned off the drug; cold turkey cessation can cause depression or even a medical emergency called “serotonin syndrome.” That syndrome may include hyperactivity, confusion, nervous- ness, vomiting, too-rapid heartbeat, excessive body temperature, shivering, tremors, weakness, or passing out.

Abuse factors. Experimental animals have shown little interest in receiving fenfluramine doses, a classic sign of small addiction potential. Human am- phetamine addicts have found fenfluramine to feel like a placebo.

Drug interactions. If the compound is taken along with migraine headache remedies or antidepressants (particularly monoamine oxidase inhibitors— MAOIs) serotonin syndrome can arise.

Researchers discovered that fenfluramine could be administered in combi- nation with phentermine, an anorectic that works in a different way. The combination became known as fen-phen (or phen-fen). Rat experiments showed that fen-phen reduces food intake far more than either drug can do alone, and experience confirmed the same kind of multiplier effect in humans. Such impact allows persons to take lower doses than would be necessary with either drug alone, thereby minimizing any undesired actions of the drugs. Phentermine counteracts fenfluramine’s common sedative quality, allowing users to function more normally.

Weight control is one of the most challenging conditions encountered by medical practitioners, and fen-phen became tremendously popular. One study found that almost 90% of 88 obesity patients taking fenfluramine or the closely related drug dexfenfluramine were also taking phentermine and that almost 33% of the 88 patients lacked obesity levels for which these or other anti- obesity drugs were an appropriate treatment.

Suddenly, after many years of wide use without much report of alarming adverse effects, in 1997 accounts began associating fenfluramine with rapidly developing fatal heart valve disorders. The U.S. Food and Drug Administra- tion asked the manufacturer to withdraw fenfluramine and dexfenfluramine from the market. In that litigious era the manufacturer instantly and volun- tarily complied. Hot debate then erupted in medical circles about whether heart disease was caused by fenfluramine, phentermine, or the two drugs in combination. Studies purported to confirm that the drugs alone or in combi- nation really did create heart valve affliction. Other research purported to find no evidence of the drugs’ involvement. Highly knowledgeable and distin- guished medical authorities took differing stances on the question and raged at one another in scientific journals. An issue also arose of whether fen-phen caused fatal pulmonary hypertension (high pressure in blood circulation to lungs), with researchers reminding fellow scientists that fenfluramine works in ways similar to the anorectic drug aminorex, which had been linked to pulmonary hypertension in the 1960s and was thereafter withdrawn from the market. Particular concern was expressed about fenfluramine’s impact on pul-

162 Fenfluramine

monary hypertension and edema among users living or traveling in high al- titudes. Phentermine is a monoamine oxidase inhibitor, and despite a lack of reports about acute adverse interaction with fenfluramine, some researchers noted that a more chronic interaction could cause the kind of heart and pul- monary damage that was appearing. Researchers began reporting organic brain damage from fenfluramine and dexfenfluramine in animal experiments. Investigators now noticed many instances of psychiatric disturbance among persons taking fenfluramine and noted that the disorders implied organic brain damage. The drug was also linked to human angina pectoris (a fright- ening sensation of pain and suffocation typically caused by insufficient oxygen supply to the heart) and to a case of a gangrenous condition resulting in amputation of fingers. As time passed, evidence appeared that the heart valve and pulmonary hypertension disorders could stabilize and even improve after patients stopped taking fen-phen. Scientific debate continues about fenflura- mine’s role in heart ailments and pulmonary hypertension.

Despite the beating that fen-phen took from the news media and from many scientists, researchers remain curious about whether the drug combination still has a role in medicine. Even though fenfluramine can cause depression, in- terest arose in possible psychotherapeutic uses. As the twenty-first century began, experimenters reported that fen-phen can ease withdrawal from co- caine. Rat experiments find that fen-phen reduces alcohol intake and elimi- nates alcohol withdrawal symptoms, findings that may be relevant to treatment of alcoholism. Indeed in 1995 one medical practitioner reported suc- cess in treating alcohol and cocaine addicts with fen-phen, sometimes substi- tuting pemoline for phentermine.

Cancer. Not enough scientific information to report.

Pregnancy. Experimenters who gave fenfluramine to pregnant mice found no measurable effect on fetal development and no effect on offspring’s ability to perform in learning tests. For primates evidence exists that the drug passes into the fetus and reaches high levels there. The combination fen-phen has not seemed to harm human fetal development.

Additional information. Dexfenfluramine (CAS RN 3239-44-9) is a stereoi- somer of fenfluramine, meaning the two molecules have the same chemical formula and the same atomic bonds, but the molecules look different (as a person’s left and right hands look different even though both have the same components). Studies comparing the two drugs find little or no difference in effect, although dexfenfluramine was introduced with the hope that it had fewer unwanted actions than fenfluramine when used for weight loss. A re- port praising dexfenfluramine characterized its weight loss capability as equal- ing that produced by the antidepressant fluoxetine (Prozac) or by a combination of ephedrine and caffeine. Diarrhea is noted as a dexfenflura- mine effect, and concern arose that the drug can aggravate glaucoma. De- pending on laboratory manipulations of circumstances, it can promote or diminish panic attacks.

Additional scientific information may be found in:

Davis, R., and D. Faulds. “Dexfenfluramine. An Updated Review of Its Therapeutic Use in the Management of Obesity.” Drugs 52 (1996): 696–724.

Fenfluramine 163

Griffith, J.D., J.G. Nutt, and D.R. Jasinski. “Comparison of Fenfluramine and Amphet- amine in Man.” Clinical Pharmacology and Therapeutics 18 (1975): 563–70.

Gross, S.B. “Appetite Suppressants and Cardiac Valvulopathy. Current Clinical Per- spectives.” Advance for Nurse Practitioners 7 (1999): 36–40.

McCann, U.D., V. Eligulashvili, and G.A. Ricaurte. “Adverse Neuropsychiatric Events Associated with Dexfenfluramine and Fenfluramine.” Progress in Neuro- psychopharmacology and Biological Psychiatry 22 (1998): 1087–102.

McCann, U.D., et al. “Brain Serotonin Neurotoxicity and Primary Pulmonary Hyper- tension from Fenfluramine and Dexfenfluramine: Systematic Review of the Ev- idence.” Journal of the American Medical Association 278 (1997): 666–72.

Schiller, N.B. “Fen/Phen and Valvular Heart Disease: If It Sounds Too Bad to Be True, Perhaps It Isn’t.” Journal of the American College of Cardiology 34 (1999): 1159–62. Vivero, L.E., P.O. Anderson, and R.F. Clark. “A Close Look at Fenfluramine and Dex-

fenfluramine.” Journal of Emergency Medicine 16 (1998): 197–205.
Wellman, P.J, and T.J. Maher. “Synergistic Interactions between Fenfluramine and Phentermine.” International Journal of Obesity and Related Metabolic Disorders 23

(1999): 723–32.


Pronunciation: FEN-ta-nill

Chemical Abstracts Service Registry Number: 437-38-7. (Citrate form 990-73-8)

Formal Names: Actiq, Alfenta, Alfentanil, Duragesic, Durogesic, Innovar, Subli- maze, Sufenta, Sufentanil

Informal Names: Apache, Bear, China, China Girl, China Town, China White, Dance Fever, Fen, Friend, Goodfellas, Great Bear, He Man, Jackpot, King Ivory, Murder, Murder 8, Persian White, Poison, Synthetic Heroin, Tango & Cash, TNT

Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II (DEA no. 9801) USA Availability: Prescription
Pregnancy Category: C

Uses. Developed in Europe during the 1950s, this drug became available for medical use in the United States during the 1960s. It is also used in veterinary medicine, especially with cats. Depending on means of administration (injec- tion, oral) fentanyl can be 10 times stronger than morphine, and fentanyl citrate can be 8 to 100 times stronger. One report claims fentanyl is 40 times stronger than heroin.

Relieving cancer pain is a standard use for fentanyl. With cancer, the drug is normally given only when a patient is dying and unable to experience enough pain control from other opioids. Fentanyl does not necessarily reduce the amount of pain per se but can make people less aware of discomfort. The substance also has sedative actions and suppresses coughs. The drug has been used to help treat tetanus. Fentanyl can alter a person’s spirits, making some- one euphoric or provoking an opposite feeling of sadness and discontent. One dosage format is the fentanyl patch, allowing the drug to be absorbed through the skin.

Drawbacks. Patches are potent enough in themselves, but a case report tells of one drug abuser who decided to heat a patch and inhale the vapor; he instantly lost consciousness, but prompt attention by skilled medical personnel saved his life.

Fentanyl may cause serious and even fatal breathing difficulty, and this problem can still arise after the drug’s action has apparently lifted. Risk of that unwanted effect is heightened among “opioid naive” patients who have not developed tolerance to pain relief from other opioids; so because of the

Fentanyl 165

breathing hazard those opioid-naive patients often do not receive fentanyl. Nonetheless, it is sometimes used for childbirth, surgery, and dentistry and for persons suffering from lower back ache and pain in bones and joints. Physicians even give fentanyl to infants.

The drug can promote sleepiness and slow a person’s pulse rate, alertness, and physical motions. Such effects interfere with ability to operate automo- biles or machinery. Other unwanted actions include itching, constipation, urine retention, nausea and vomiting, increased blood pressure, and fainting upon standing up. Cases of muscle rigidity have been reported. Laboratory tests suggest fentanyl might worsen a body chemistry disease called por- phyria.

Fentanyl can provoke seizures in persons prone to such affliction. A drastic treatment for seizures is surgical removal of a brain lobe where seizures orig- inate, and instrument readings during the operation guide surgeons on how much of the brain to remove. Fentanyl is a standard surgical anesthetic, and one study found that the drug can temporarily create seizures in healthy por- tions of the brain, thereby misleading surgeons about how much they should remove.

Like many other drugs, fentanyl has stronger effects on older persons, and dosage should be adjusted accordingly.

Abuse factors. Tolerance and dependence can occur, with typical opioid withdrawal symptoms. Just three days of medical dosing can produce enough dependence to cause uncomfortable withdrawal upon sudden stoppage of the drug, an exceptionally short time compared to most opioids. Animal experi- ments indicate that buprenorphine can alleviate fentanyl withdrawal.

Drug interactions. Normally people should avoid fentanyl if they have taken monamine oxidase inhibitors (MAOIs—found in some antidepressants and other medicine) in the past two weeks, as MAOIs can greatly increase opioid actions. For the same reason, using fentanyl with other depressants (including alcohol) can be risky. Midazolam hydrochloride and fentanyl ap- pear to boost each other’s actions. The HIV/AIDS medicine ritonavir makes a fentanyl dose last longer.

Cancer. Whether fentanyl causes cancer is unknown, although laboratory tests with one version of the drug yielded no indication of cancer-causing potential.

Pregnancy. Rats receiving fentanyl have lower fertility rates and bring fewer pregnancies to term, compared to rats not receiving the drug, and those effects occurred at smaller doses than humans typically receive. When fentanyl citrate has been given to pregnant rats, birth defects in their offspring have not been attributed to the drug. Whether fentanyl causes congenital malformations in humans is unknown. An infant can be born with dependence if the mother has been using fentanyl. The drug passes into a nursing mother’s milk but not in amounts deemed harmful to an infant.

Additional information. Alfentanil (Schedule II, CAS Registry No. 71195- 58-9) is a derivative of fentanyl used for pain control and anesthesia. Effects last only a few minutes. Depending on dosage form, pain relief is 1 to 10 times stronger than morphine. When given to a pregnant woman alfentanil appar- ently passes into the fetus. The drug can produce muscle rigidity in infants.

166 Fentanyl

Sufentanil (Schedule II, CAS Registry No. 56030-54-7, citrate form 60561-17- 3) is a derivative of fentanyl used for pain control and anesthesia. It is 50 to 100 times stronger than morphine and is used to knock out wild animals. The drug takes effect faster than fentanyl but lasts a shorter time. Sufentanil can lower heart rate and blood pressure, create muscle rigidity, and cause typical unwanted opioid effects such as itching and vomiting. At normal doses su- fentanil can halt breathing, so medical personnel stand by to provide respi- ration assistance when they administer the drug. Laboratory and animal experiments indicate no potential for causing cancer. Tests with rats and rab- bits did not produce birth defects. Researchers examining the results when sufentanil is used in childbirth found no harm to mother or infant. Sufentanil is assumed to pass into the milk of nursing mothers, but the amount is as- sumed harmless to the infant.

Other fentanyl derivatives exist. They are used illicitly to experience heroin sensations and can be 1,000 times stronger than heroin.

Fentanyl has the same molecular formula as the Schedule I substance acetyl- alpha-methylfentanyl (DEA no. 9815), but the two drugs are different sub- stances.

Additional scientific information may be found in:

Baylon, G.J. “Comparative Abuse Liability of Intravenously Administered Remifentanil and Fentanyl.” Journal of Clinical Psychopharmacology 20 (2000): 597–606.

Henderson, G.L. “Designer Drugs: Past History and Future Prospects.” Journal of Fo- rensic Sciences 33 (1988): 569–75.

Patt, R.B., and L.A. Hogan. “Comment: Transdermal Fentanyl.” Annals of Pharmaco- therapy 27 (1993): 795–96.

Schneider, U., et al. “Effects of Fentanyl and Low Doses of Alcohol on Neuropsycho- logical Performance in Healthy Subjects.” Neuropsychobiology 39 (1999): 38–43.

Zacny, J.P., et al. “Subjective and Behavioral Responses to Intravenous Fentanyl in Healthy Volunteers.” Psychopharmacology (Berlin) 107 (1992): 319–26.


Pronunciation: flyoo-neye-TRAYZ-eh-pam
Chemical Abstracts Service Registry Number: 1622-62-4 Formal Names: Rohypnol

Informal Names: Candy, Circles, Darkene, Date Rape Drug, Drop Drug, Dulcitas, Forget Me Drug, Forget Pills, La Rocha, La Roche, Lunch Money Drug, Mexican Valium, Mind Erasers, Pappas, Pastas, Peanuts, Pingus, Potatoes, Remember All, Reynol, Reynolds, Rib, Roaches, Roachies, Roach-2, Roapies, Robinol, Robutal, Rochas, Rochas Dos, Roche, Roche Dos, Roches, Rochies, Rohibinol, Roofenol, Roofies, Ropanol, Ropers, Ropes, Rophies, Rophs, Rophy, Ropies, Roples, Ro- Shay, Row-Shay, R05-4200, R-25, R-2, Rubies, Ruffies, Ruffles, Trip & Fall, Whiteys, Wolfies

Type: Depressant (benzodiazepine class). See page 21
Federal Schedule Listing: Schedule IV (DEA no. 2763), but Schedule I in many

state schedules
USA Availability: Prescription where legal

Uses. This quick-acting and long-lasting drug is widely used around the world for legitimate medical purposes. Flunitrazepam is prescribed to treat insomnia and anxiety, to relax muscles, to stop convulsions, and to calm peo- ple. In the 1990s it was Western Europe’s most commonly prescribed calming and sleep-inducing medicine. The drug is administered to treat alcohol with- drawal syndrome, and experimental use in treating depression has found flu- nitrazepam promising. Some unauthorized use of the drug is believed to be for self-medication of depression and low self-esteem. The drug has special- ized usefulness in surgery as a medication given prior to administration of anesthesia, and its tendency to reduce pressure inside the eyeball can avert the rise caused by the anesthetic succinylcholine (important if patients are at risk for glaucoma). In hospice care where doses can be higher and more fre- quent than normal, flunitrazepam has reduced nausea and vomiting from can- cer chemotherapy.

Actions are similar to those of diazepam, but flunitrazepam is 7 to 10 times stronger. Nonetheless, compared to other benzodiazepine class drugs an over- dose of flunitrazepam does not seem more poisonous, nor does flunitrazepam appear more prone to cause medical crises.

Drawbacks. The drug may cause euphoria, raise self-esteem, and give a

168 Flunitrazepam

sense of power in users while at the same time decreasing fear. Such effects may promote violence in a person who is already prone to such conduct, particularly when the substance is combined with alcohol.

Users are sometimes unable to remember what happened while they were under flunitrazepam’s influence. Immediate effects aside, researchers have documented that people still experience trouble when doing laboratory mem- ory tests 10 hours after taking a medical dose of the drug, a dose that may be much lighter than some abusers take. Many other benzodiazepine class drugs cause memory trouble as well, although their effect is less publicized than flunitrazepam’s.

Flunitrazepam can slow reaction times, reduce ability to pay attention to tasks, and leave people too woozy and discoordinated to drive a car safely. Difficulty in driving has been demonstrated in simulations and in an instru- mented automobile actually driven for several miles the day after drivers took a nighttime dose. In experiments (including a test of potential drug effects on shift workers) people took various sleep aids at bedtime; flunitrazepam harmed persons’ ability to move their limbs the next day. Such effects appear to be dose-related; an experiment using much smaller doses found little or no impact on performance the next day. Large doses can cause breathing trouble. Injection can kill skin around the needle site.

Abuse factors. Abuse of the drug has become a concern among public health authorities in several countries. Under provisions of international treaties the federal government lists flunitrazepam as a Schedule IV controlled substance but has forbidden sale of this pharmaceutical in the United States. State gov- ernments have begun reclassifying the substance as Schedule I, certifying it as having no medical value and allowing anyone possessing it to be prose- cuted under state law.

In the 1990s law enforcement agencies declared flunitrazepam to be a date rape drug, allowing men to commit sexual assault against unresisting victims who have foggy or even no memory of the circumstances. In this regard the drug is little different from alcohol, though faster acting. In a survey of 53 women who willingly used flunitrazepam, 10% said they were afterward as- saulted physically or sexually. When 66 other “flunitrazepam users” described the tablet, many descriptions were of some other drug even though the people believed they had taken flunitrazepam. Untoward events may be real, but the identity of an involved drug may be less certain than law enforcement officials say. The U.S. Drug Enforcement Administration (DEA) says detection of fluni- trazepam is nearly impossible in rape cases because urine samples must be analyzed within 72 hours of ingesting flunitrazepam, making the drug’s prev- alence as a tool in sexual assault impossible to demonstrate. Nonetheless, the DEA describes the problem’s extent as serious. A student of the topic found that from 1994 to 1998 a nationwide total of “at least” 26 sexual assaults “po- tentially involved” the drug. One laboratory conducted a two-year study of 1,179 urine specimens from sexual assault victims in 49 states, specimens se- lected because of suspicion that some drug was involved—and thereby more likely to have positive results than if samples were chosen randomly from sex crime cases. The lab found 6 positive for flunitrazepam (0.5%), 97 (8%) positive for a benzodiazepine class substance (a category including many drugs other

Flunitrazepam 169

than flunitrazepam), 451 positive for alcohol, and 468 negative for any drug of abuse that was searched for. A two-year study of 2,003 urine samples from sexual assault victims believed to have ingested a drug found less than 2% containing flunitrazepam or GHB. The same study reported that as of 1999 utilization of those two drugs seemed to be waning. Flunitrazepam’s legal manufacturer has offered to provide free and definitive analysis of samples submitted by medical and law enforcement personnel. Researchers at the Uni- versity of Miami report that detection of flunitrazepam in urine samples is easy and that, in contrast to ambiguous results from sex crime investigations, flunitrazepam had been confirmed in “up to” 10% of drunk driving cases in 1995 and 1996 in Miami-Dade County, Florida, but plummeted after the drug became Schedule I under state law in 1997.

Despite hype about flunitrazepam, a review article published in 1997 noted absence of evidence that the substance’s actions differ from those of other drugs in the benzodiazepine class. Flunitrazepam is simply a very strong ben- zodiazepine, and its potency may have much to do with stories told about it. To produce similar drug effects, a small amount of flunitrazepam may be about equal to a large amount of some other benzodiazepine.

Tolerance can occur. A person’s body can develop dependence with fluni- trazepam, resulting in a withdrawal syndrome if dosage stops. Withdrawal symptoms are similar to those with other benzodiazepine class substances. Severe cases can include delirium, hallucinations, and seizures. When re- searchers cut off the drug supply to dependent monkeys they became agitated and peevish, had tremors and poor control of muscles, and sometimes vom- ited and ran a fever. Although flunitrazepam is much stronger than diazepam, a canine experiment found those two drugs roughly equivalent in ability to produce dependence. Flunitrazepam reduced the morphine withdrawal syn- drome in mice; if the same effect carries over to humans flunitrazepam might appeal to opiate addicts who have an unreliable supply of opiates. Surveys show flunitrazepam to be a favorite among opiate abusers, although among other people the substance seems no more attractive than other benzodiaze- pines.

Drug interactions. Alcohol and flunitrazepam boost each other’s actions. Some illicit drug users find flunitrazepam to be a pleasing addition to a dose of inferior heroin, and some find that flunitrazepam eases harsh effects from cocaine. However, using multiple illicit drugs, particularly if the combination tends to make the body produce opposite actions simultaneously, is an invi- tation to problems. Buprenorphine disrupts the body’s ability to break down flunitrazepam.

Cancer. Laboratory testing of the drug itself and of urine from rats and humans who have received doses indicates that flunitrazepam can induce gene mutations, a possible sign of cancer-causing potential.

Pregnancy. In pregnant women the drug passes into amniotic fluid and the fetal blood supply, although fetal levels are lower than maternal levels. Ex- cessive muscular motions have been observed in a fetus after the drug is administered to a pregnant woman. When given to infants the drug lowers their blood pressure (an effect noted in adults as well). Although the drug

170 Flunitrazepam

passes into breast milk, levels are considered too low to affect a nursing infant if a mother does not take the drug regularly.

Additional scientific information may be found in:

Anglin, D., K.L. Spears, and H.R. Hutson. “Flunitrazepam and Its Involvement in Date or Acquaintance Rape.” Academic Emergency Medicine 4 (1997): 323–26.

Calhoun, S.R., et al. “Abuse of Flunitrazepam (Rohypnol) and Other Benzodiazepines in Austin and South Texas.” Journal of Psychoactive Drugs 28 (1996): 183–89.

Daderman, A.M., and L. Lidberg. “Flunitrazepam (Rohypnol) Abuse in Combination with Alcohol Causes Premeditated, Grievous Violence in Male Juvenile Offend- ers.” Journal of the American Academy of Psychiatry and the Law 27 (1999): 83–99.

“Flunitrazepam Misuse and Abuse in South Africa.” South African Medical Journal 89 (1999): 1155.

Mattila, M.A., and H.M. Larni. “Flunitrazepam: A Review of Its Pharmacological Prop- erties and Therapeutic Use.” Drugs 20 (1980): 353–74.

Ott, H., et al. “Anterograde and Retrograde Amnesia after Lormetazepam and Fluni- trazepam.” Psychopharmacology Series 6 (1988): 180–93.

Waltzman, M.L. “Flunitrazepam: A Review of ‘Roofies.’ ” Pediatric Emergency Care 15 (1999): 59–60.

Woods, J.H., and G. Winger. “Abuse Liability of Flunitrazepam.” Journal of Clinical Psychopharmacology 17 (1997, Suppl. 2): S1–S57.


Pronunciation: floo-ok-see-MESS-ter-ohn
Chemical Abstracts Service Registry Number: 76-43-7
Formal Names: Androfluorene, Android-F, Halotestin, Ora-Testryl, Stenox Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000)
USA Availability: Prescription
Pregnancy Category: X

Uses. This compound became available in the 1950s. Standard medical uses in males include treatment for delayed puberty and underdeveloped male organs. Experiments demonstrate that fluoxymesterone can improve the growth, weight, and social interactions of boys having slow physical matu- ration. Compared to some other anabolic steroids, this drug has less tendency to promote masculine body signs (facial hair, deeper voice) in girls, and fluox- ymesterone has been used to nurture increased height in girls. The drug can be administered to treat female sexual dysfunction.

In women the drug is used to fight breast cancer by interfering with hor- mones that encourage the disease. Research has found fluoxymesterone effec- tive in reducing a cancer called myeloma and for counteracting anemia caused by myeloma. Mixed results have occurred when using the drug for correcting anemia associated with kidney failure. The substance has been a treatment for osteoporosis, a condition in which bones become susceptible to easy breakage, and for hereditary angioedema—an affliction that may involve throat swelling that interferes with breathing.

Although anabolic steroids have potential for preventing young users from achieving expected adult height, with fluoxymesterone that outcome does not occur among females suffering from Turner’s syndrome (the expected adult height in persons with this condition, however, is already short). Several stud- ies tracking boys using the drug under close medical supervision found adult height to be normal.

A research team studied effects on normal males who received doses three times a day for a three-month period. Little impact could be detected, although a few unwanted effects such as headaches occurred. Perhaps the most notable reported change was a 30% drop in triglyceride levels; excessive triglycerides are associated with heart attack and stroke.

172 Fluoxymesterone

Drawbacks. Another study using normal men measured a drop in their testosterone levels, an unsurprising finding as fluoxymesterone is supposed to replace testosterone. Extended usage may interfere with male sexual func- tion and fertility. General unwanted actions have included acne, itching, diz- ziness, nausea, vomiting, yellowish tinge to body color (an indication of jaundice), constipation, and frequent urination. Fluid retention can cause swelling. The drug may interfere with blood clotting and may reduce the amount of insulin needed by diabetics. The compound also can be harmful to a person who suffers from porphyria, an affliction that can involve violence and sensitivity to light. Fluoxymesterone can pass into a sexual partner, enough to affect that person. Because of that, barrier contraceptives are rec- ommended for sexually active fluoxymesterone patients and their partners.

The substance is banned from athletic competitions. Scientists have not con- firmed that the substance helps sport abilities, but nonetheless some body- builders use it. Supposedly the drug can increase strength without increasing weight, an important factor in some classes of sporting competition. Report- edly the substance promotes aggressiveness, enhancing its appeal to athletes who must physically attack opponents. Some athletic users describe the drug as unpleasant. Athletic abuse of fluoxymesterone is not necessarily limited to human competitions; concern exists that the substance may be given to race- horses.

Abuse factors. Not enough scientific information to report about tolerance, dependence, withdrawal, or addiction.

Drug interactions. In female breast cancer patients receiving levothyroxine to boost thyroid gland activity, fluoxymesterone can interact and elevate thy- roid activity too much. Experiments have administered fluoxymesterone in combination with other drugs to alter the mood of older persons exhibiting nervousness, irritation, and suspiciousness toward caregivers. One study re- ported no change; another reported substantial change; the difference may have involved what drugs were used in addition to fluoxymesterone, along with differing dosages.

Cancer. Laboratory tests have provided uncertain guidance on whether fluoxymesterone causes cancer. A case report mentions that two men devel- oped prostate cancer after receiving the drug to treat impotence; cause and effect were not asserted, but the coincidence was considered important enough to merit caution. Men with prostate cancer should avoid the drug. A case report mentions liver cancer developing in a patient undergoing fluoxymes- terone therapy for over four years, but again cause and effect were not claimed. A survey examined all reported deaths from hepatic angiosarcoma, a type of liver cancer, in the United States from 1964 to 1974; from the total of 168 cases, 1 was associated with taking fluoxymesterone. Once again, how- ever, “association” is not “cause.”

Pregnancy. In humans the compound may harm fetal development of fe- male sexual organs, introducing male characteristics. The drug is not recom- mended for pregnant women, but the substance has been used to control milk production. Fluoxymesterone passes into milk, and nursing mothers should avoid the drug.

Additional scientific information may be found in:

Fluoxymesterone 173

Dhillon, V.S., et al. “In Vitro and in Vivo Genotoxicity of Hormonal Drugs. VI. Fluox- ymesterone.” Mutation Research 342 (1995): 103–11.

Kirkland, R.T., and G.W. Clayton. “Growth Increments with Low Dose Intermittent Growth Hormone and Fluoxymesterone in First Year of Therapy in Hypopitu- itarism.” Pediatrics 63 (1979): 386–88.

Lenko, H.L., J. Maenpaa, and J. Perheentupa. “Acceleration of Delayed Growth with Fluoxymesterone.” Acta Paediatrica Scandinavica 71 (1982): 929–36.

Novak, E., et al. “Pharmacologic Evaluation of Fluoxymesterone in Normal Men.” Cur- rent Therapeutic Research: Clinical and Experimental 16 (1974): 251–260.

Strickland, A.L. “Long-Term Results of Treatment with Low-Dose Fluoxymesterone in Constitutional Delay of Growth and Puberty and in Genetic Short Stature.” Pe- diatrics 91 (1993): 716–20.


Pronunciation: flur-AZ-eh-pam
Chemical Abstracts Service Registry Number: 17617-23-1. (Hydrochloride form

Formal Names: Dalmane, Paxane
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2767) USA Availability: Prescription
Pregnancy Category: X

Uses. Flurazepam has become one of the most common benzodiazepine class compounds in medical use around the globe. One reason for its popu- larity is flurazepam’s high therapeutic index, meaning the dose needed for medical action is much smaller than a fatal dose, making accidental poisoning unlikely. Caregivers mainly use this long-acting drug to help people sleep, and it has been used experimentally to reduce sleepwalking.

Drawbacks. Flurazepam often leaves people groggy the next day, impairing their mental abilities (including memory and accuracy of perceptions). Such problems can decrease after weeks or months of using the drug, but in one experiment users never achieved normal performance while taking fluraze- pam. Researchers find that volunteers may be unaware of the trouble they are having. In contrast to those typical findings, experiments using healthy college students found no effect on performance the day after taking a nighttime dose of the drug.

Laboratory tests of users demonstrate impairment in reaction time, eye- hand coordination, making decisions, and maintaining attention. All those skills are relevant to operating an automobile. Twelve hours after taking a nighttime dose of flurazepam, volunteers drove a test vehicle. Researchers conducting the experiment concluded that such drivers were much more likely to have a road accident than controls who received a placebo. Bolder experi- menters had drivers take a car into actual traffic the day after ingesting flur- azepam, and drivers had trouble keeping the car aligned in the proper lane. An experiment using a driving simulator also showed people to have trouble driving the morning after using flurazepam.

Users tend to be more accident prone in general, not just behind the steering wheel of a car. A case report tells of a person’s muscular discoordination

Flurazepam 175

clearing up when he stopped taking flurazepam, and experimental work has documented the drug’s tendency to interfere with movement. In elderly per- sons that unsteadiness is associated with falls causing broken hips, and cau- tion is advised in prescribing flurazepam to older people. One factor with flurazepam problems experienced by the elderly is that, compared to younger persons, the elderly maintain higher levels of the drug in their bodies from a given dose.

Researchers find that the substance can help people shift their sleep sched- ules from night to daytime, while promoting good-quality rest, yet the drug still has hangover effects that degrade ability to function after awakening.

The drug can worsen verbal communication, causing voices to become in- distinct and grammar to become garbled. Studies measuring sleep-time breathing find that the drug can exacerbate respiration problems; in some experiments researchers concluded that the change has no practical effect on health, but medical literature notes an instance in which the drug’s influence on breathing did cause trouble for a sleeping person. In a mice experiment flurazepam lowered body temperature. In humans long-term use of the drug is suspected of causing hallucinations and confusion, and a case report exists of a single dose creating those symptoms along with euphoria. Investigators in the 1970s found mild euphoria to be a routine effect of flurazepam. Head- ache, low blood pressure, eyesight trouble, nausea, vomiting, and constipation can occur. A case report relates that a woman’s interest in sexual activity increased when she stopped taking flurazepam and diazepam. Flurazepam is believed to interfere with women’s ability to achieve a sexual orgasm.

Abuse factors. Tests with normal persons find that flurazepam has equal or less appeal compared to placebo. Medical authorities examining the drug in the 1970s concluded that it probably had little potential for abuse. Despite the drug’s apparent low appeal, it can create a physical dependence with a per- son’s body. Withdrawal symptoms can include peevishness, fidgeting, anxiety, sweating, tremors, high blood pressure, and intolerance to light and sounds. One longtime user of flurazepam and diazepam developed such a strong de- pendence with them that a severe withdrawal syndrome occurred when she suddenly halted dosage: cramps, stomach discomfort, nervous unease, sleep difficulty, and nightmares. Milder versions of such symptoms are reported if the original level of dependence is lighter. Symptoms can be avoided if flur- azepam usage is tapered off rather than stopped suddenly. Volunteers who received flurazepam in a long-term experiment consistently detected the dif- ference between the drug and a placebo, an ability causing investigators to conclude that users of flurazepam do not develop tolerance to the drug (tol- erance is a classic indicator of addictive potential). This conclusion is not ac- cepted by all experts, however, and some believe tolerance does occur.

Drug interactions. A catalepsy effect from marijuana may become stronger in mice if they also receive flurazepam, but the reason is unclear. Alcohol and flurazepam boost some of each other’s effects. Experimenters find that caffeine can lessen flurazepam’s adverse next-day effects on performance. The heart- burn medicine cimetidine lengthens the time that flurazepam’s metabolite de- salkylflurazepam stays in the body. In a monkey experiment, that metabolite

176 Flurazepam

produced performance deficiencies reminiscent of those seen in humans with flurazepam and also lowered inhibitions.

Cancer. No indication of a cancer-causing potential has emerged.

Pregnancy. Experiments with rats and rabbits produced no birth defects. Researchers tracking assorted birth defects examined medical records of 50 to 99 women who took flurazepam during pregnancy and found no malforma- tions in offspring. Nonetheless, birth defects are considered a serious risk from the drug, and pregnant women are advised to avoid it. Newborns from moth- ers using the drug may have “floppy infant syndrome” involving sedation, inferior muscle tone, breathing trouble, and poor feeding.

Additional scientific information may be found in:

Council on Drugs. “Evaluation of a New Hypnotic Agent—Flurazepam Hydrochloride (Dalmane).” Journal of the American Medical Association 218 (1971): 246.

De Wit, H., E.H. Uhlenhuth, and C.E. Johanson. “Lack of Preference for Fluraze- pam in Normal Volunteers.” Pharmacology, Biochemistry, and Behavior 21 (1984): 865–69.

“Flurazepam (Dalmane).” Medical Letter on Drugs and Therapeutics 17 (1975): 29–30. Judd, L.L., E. Ellinwood, and L.A. McAdams. “Cognitive Performance and Mood in Patients with Chronic Insomnia during 14-Day Use of Flurazepam and Mida-

zolam.” Journal of Clinical Psychopharmacology 10 (1990, Suppl.): S56–S67.
Juhl, R.P., V.M. Daugherty, and P.D. Kroboth. “Incidence of Next-Day Anterograde Amnesia Caused by Flurazepam Hydrochloride and Triazolam.” Clinical Phar-

macy 3 (1984): 622–25.
Mendelson, W.B., et al. “A Clinical Study of Flurazepam.” Sleep 5 (1982): 350–60. Wesnes, K., and D.M. Warburton. “A Comparison of Temazepam and Flurazepam in

Terms of Sleep Quality and Residual Changes in Performance.” Neuropsycho-

biology 11 (1984): 255–59.
Younus, M., and M.J. Labellarte. “Insomnia in Children: When Are Hypnotics Indi-

cated?” Paediatric Drugs 4 (2002): 391–403.


Pronunciation: FREE-on
Chemical Abstracts Service Registry Number: 11126-05-9 Type: Inhalant. See page 26
Federal Schedule Listing: Unlisted
USA Availability: Generally unrestricted
Pregnancy Category: None

Uses. Freon is most familiar as a component of refrigeration and air- conditioning systems. The compound is commonly used to clean metal, and other industrial uses exist as well. In past times freon was routinely used in pressurized aerosol spray cans, but that usage ended after scientists discov- ered that freon contributes to the destruction of the Earth’s ozone layer. Some persons have experienced hallucinations from inhaling freon vapor. A medical case report mentions that heavy polydrug abusers have used freon to expe- rience flashbacks of those experiences. Various chemical formulations of freon exist, some of which may have hallucinogenic effect, and some of which may not.

Drawbacks. Freon may produce lung spasms. The substance has caused high blood pressure, perhaps as a consequence of kidney damage resulting from the substance. Users have described accelerated heartbeat. Inhalation has also brought on a cardiac emergency called ventricular fibrillation, which is fatal without immediate medical intervention. Even if the person survives, most individuals do not receive sufficient help in time to prevent lasting brain injury from lack of oxygen. In one case a 15-year-old freon user not only experienced the heart emergency but suffered lung and muscle damage as well. Using enough freon in a closed space can be fatal due to oxygen star- vation. Inhalers have also reported injuries ranging from lacerations to a bro- ken neck when they lost consciousness and collapsed while sniffing freon; such harm may not be attributable to the substance itself but can be a con- sequence of using it.

Pressurized freon gas can be cold enough to cause frostbite. Case reports note cold damage to fingers, along with drooling caused by frostbite injury to lips, tongue, and inside of the mouth. One report described “notable defor- mation” of someone’s face; in another case, plastic surgery was necessary to reconstruct the damaged face of one recreational user.

178 Freon

Injection of freon is possible but seems to occur as industrial accidents to fingers rather than as an effort to obtain psychological effects. Upon injection, the gas, which has been under pressure in a container, is free to expand inside the body, producing uncomfortable results. Case reports indicate that victims fully recover.

Injury has also occurred from exposure to liquid freon, which is extremely cold and can cause severe frostbite. In one case, portions of a stomach died from freezing, causing holes that had to be surgically repaired. As with injec- tions, injuries from liquid freon seem to be industrial accidents rather than results of recreational use.

Abuse factors. Not enough scientific information to report about tolerance, dependence, withdrawal, or addiction.

Drug interactions. Not enough scientific information to report. Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

“Aerosols for Colds.” Medical Letter on Drugs and Therapeutics 15 (1973): 86–88.
Brady, W.J., Jr., et al. “Freon Inhalational Abuse Presenting with Ventricular Fibrilla-

tion.” American Journal of Emergency Medicine 12 (1994): 533–36.
Goldsmith, R.J. “Death by Freon.” Journal of Clinical Psychiatry 50 (1989): 36–37.
Lee, T., et al. “Oral Frostbite Secondary to Freon Propellant Abuse.” Journal of Toxicol-

ogy. Clinical Toxicology 34 (1996): 562.
Maxwell, J.C. “Deaths Related to the Inhalation of Volatile Substances in Texas: 1988–

1998.” American Journal of Drug and Alcohol Abuse 27 (2001): 689–97.
Wegener, E.E., K.R. Barraza, and S.K. Das. “Severe Frostbite Caused by Freon Gas.”

Southern Medical Journal 84 (1991): 1143–46.


Pronunciation: gas-uhl-EEN (also pronounced GAS-uhl-een)
Chemical Abstracts Service Registry Number: 8006-61-9. (Benzine form 86290-

Formal Names: Petrol, White Gasoline Type: Inhalant. See page 26
Federal Schedule Listing: Unlisted
USA Availability: Generally unrestricted Pregnancy Category: None

Uses. Inhaling gasoline fumes can produce effects that researchers liken to those of mescaline: euphoria, hallucinations, and distortions of sensory per- ception including sensations of revolving and floating. Some users experience feelings of increased power and reduced fear, effects that may encourage mis- chief from users who are already social outcasts.

Drawbacks. Sniffers have complained of tasting gasoline for days afterward. Other unwanted effects may include fear, lonely feelings, sleepiness, weak- ness, headache, poor appetite, nausea, too much salivation, breathing diffi- culty, dizziness, lightheadedness, ringing in the ears, and amnesia. Conflicting evidence exists about possible inhalation harm to kidneys in male rats and in humans, although the human risk is considered low to nonexistent. Case re- ports tell of muscle injury from inhaling gasoline. Nerve damage can arise, causing trouble in walking and other movements. Manic behavior and sei- zures are reported. As with most other inhalant abuse, sudden death can occur.

The human body reacts to gasoline vapor in the same way regardless of a person’s motive for inhaling it, and researchers have expressed concern about health hazards faced by automobile filling station attendants who receive long-term low-level exposure to gasoline fumes.

Fumes from other types of fuels can have similar actions. In a training ex- ercise JP-5 aviation fuel vapor leaked into the cockpit of a T-34C turboprop aircraft. One pilot gradually lost control proficiency, becoming euphoric and mirthful even though he was told an emergency had been declared. The other pilot was nauseated but managed to land the craft. Both had trouble walking, were weary, and had problems completing familiar written reports. The next

180 Gasoline

day the pilot who had been more severely affected had allergic symptoms (sneezing, nasal discharge, eyes watering and itching) and poor appetite.

Sniffing leaded gasoline is uncommon in the United States, as federal reg- ulations halted motor fuel sales of that substance (although the product was still available in Mexico and Canada in the 1990s). In addition to injury from gasoline the product can cause lead poisoning. Leaded gasoline damage to thinking ability has been documented: attention, learning, and memory. Rec- reational users of leaded gasoline may also suffer organic brain damage lead- ing to tremors, difficulty in moving arms and legs, personality change, psychosis, sleepiness, and dementia. Recovery may occur, but fatal outcome is possible. One study of persons hospitalized for chronic leaded gasoline sniff- ing in Australia noted a 40% death rate, but that was the death rate for persons so sick that they required hospital care, not for chronic leaded gasoline users as a whole. Persons with industrial exposure to leaded gasoline fumes have exhibited psychotic behavior, occasionally followed by death. Gasoline sold as a motor fuel may contain toluene or various other chemicals that are haz- ardous to breathe and that may account for some unwanted effects attributed to gasoline.

Injection of liquid gasoline for recreational purposes is disastrous; in Nazi Germany gasoline injection was an experimental method of execution. A case report about a drug abuser who survived gasoline injection noted nerve dam- age that reduced motion capability in the arm and hand. Drinking gasoline can also have serious medical consequences; one case report listed kidney and respiratory failure along with damage to liver and blood, accompanied by seizures.

Injury may occur by combining dangerous activity with impaired judgment during intoxication. Unconscious persons may let a gasoline container spill its flammable contents all over them. Recreational users have suffered major burns from ignition of vapor and liquid. Open flame is unnecessary; a static electricity spark can set off the gasoline. Inhaled gases can spread into other parts of the body besides the lungs, and fire from ignited gasoline vapor can instantly reach into the body’s interior with devastating consequences. One scientific journal article is entitled “Death Due to ‘Harakiri’ or Gasoline Fumes?”

Abuse factors. Gasoline gets little attention as a substance of abuse in the United States, but researchers in India studied nine teenage and younger per- sons who declared gasoline to be their top choice among recreational sub- stances. These users were all from lower social and economic backgrounds, and their fathers tended to be alcoholics. Authorities have described the prac- tice as more popular in rural American communities than in big cities. A study of the habit among Navajo teenagers found them doing poorly in school and prone to trouble with police, factors probably having nothing to do with ef- fects of the chemical but that indicate that gasoline misuse appeals to social misfits. Research in Australia and Canada has also linked the practice to in- dividuals experiencing personal and social discontent. The practice seems more prevalent among males than among females. Gasoline sniffing is often a social occasion rather than a solitary practice, suggesting that the custom has elements of promoting group identity and solidarity.

Gasoline 181

Development of dependence with gasoline is indicated by a withdrawal syndrome: dry mouth, watery eyes, sleeping difficulty, peevishness, problems in moving arms and legs.

Drug Interactions. Not enough scientific information to report.

Cancer. Some types of DNA damage indicate cancer-causing potential, and evidence of DNA damage has been detected in persons with workplace ex- posure to gasoline fumes. A large study examining medical records of 19,000 automobile service station attendants through a 20-year period found higher- than-normal rates of cancer in the nose, throat, lungs, and kidneys. Gasoline vapor is suspected of causing acute myeloid leukemia. Gasoline fumes cause cancer in animal experiments.

Pregnancy. Infants born to women who were recreational gasoline inhalers during pregnancy may exhibit improper muscle tension, head deformities, mental retardation, and other deficiencies, leading some researchers to suspect that gasoline causes birth defects.

Additional scientific information may be found in:

Beckmann, G., and G. Hauck. “Tod durch ‘Harakiri’ oder Benzindampfe? [Death due to ‘Harakiri’ or Gasoline Fumes?]” Archiv fu ̈r Kriminologie 154 (1974): 77–82.

Edminster, S.C., and M.J. Bayer. “Recreational Gasoline Sniffing: Acute Gasoline Intox- ication and Latent Organolead Poisoning. Case Reports and Literature Review.” Journal of Emergency Medicine 3 (1985): 365–70.

Maruff, P., et al. “Neurological and Cognitive Abnormalities Associated with Chronic Petrol Sniffing.” Brain 121 (1998): 1903–17.

Nurcombe, B., et al. “A Hunger for Stimuli: The Psychosocial Background of Petrol Inhalation.” British Journal of Medical Psychology 43 (1970): 367–74.

Poklis, A., and C.D. Burkett. “Gasoline Sniffing: A Review.” Clinical Toxicology 11 (1977): 35–41.

Seshia, S.S., et al. “The Neurological Manifestations of Chronic Inhalation of Leaded Gasoline.” Developmental Medicine and Child Neurology 20 (1978): 323–34.
Tolan, E.J., and F.A. Lingl. “ ‘Model Psychosis’ Produced by Inhalation of Gasoline

Fumes.” American Journal of Psychiatry 120 (1964): 757–761.
Valpey, R., et al. “Acute and Chronic Progressive Encephalopathy Due to Gasoline

Sniffing.” Neurology 28 (1978): 507–10.


Pronunciation: jee-eightch-bee
Chemical Abstracts Service Registry Number: 591-81-1. (Sodium salt form 502-


Formal Names: 4-Hydroxybutanoic Acid, Gamma Hydroxybutyrate, Gamma- Hydroxybutyric Acid, Sodium Oxybate, Sodium Oxybutyrate

Informal Names: Blue Verve, Cherry Menth, Cherry Meth, Easy Lay, Everclear, EZ Lay, Fantasy, G, Gamma Oh, GBH, Georgia Home Boy, Ghana Marijuana, Gib, Goop, Great Hormones at Bedtime, Grievous Bodily Harm, G-Riffick, Growth Hormone Booster, Jib, Jib Gamma, Lemons, Liquid E, Liquid Ecstasy, Liquid X, Max (combination with amphetamines), Mickey Finn Special, Natural Sleep- 500, Nature’s Quaalude, Organic Quaalude, Oxy-Sleep, Poor Man’s Heroin, Salty Water, Soap, Scoop, Somatomax, Somsanit, Vita-G, Water, Wolfies, Zonked

Type: Depressant. See page 19
Federal Schedule Listing: Schedule I (DEA no. 2010) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. Although GHB is commercially manufactured, it is also produced within the bodies of mammals where it may promote hibernation and help the brain to withstand deficient oxygen supply. The substance was once widely available as a nutritional supplement in health food stores. People consumed it in hopes that the product would promote fat reduction and mus- cle development. Human experiments confirm that the drug can increase the body’s levels of human growth hormone while the substance is circulating in the bloodstream, but the studies did not last long enough to show whether this GHB effect built muscles or reduced fat. The hope for muscle development has been tested in experiments with rats and dogs, but without success; the drug failed to increase the animals’ growth hormone levels.

Where this drug is legal, its main medical use is for anesthesia and for treating drug abuse patients. It has been used experimentally to study epi- lepsy, to reduce damage from exposure to nuclear radiation, and to treat fi- bromyalgia (a rheumatic disease causing weariness, muscle pain, and stiff joints). Some efforts to help schizophrenics with the substance have been suc- cessful; some have not. Experiments with hamsters indicate the drug may

GHB 183

have potential for reducing damage from bleeding. Animal experiments also suggest the drug may have potential in treating heart attack. Although GHB is a depressant that has been used successfully to treat insomnia, it has also been used to treat narcolepsy, a condition in which people have difficulty staying awake.

According to law enforcement authorities, rapists have exploited GHB’s sed- ative effect to make victims pliable. From 1996 to 1999 a total of 22 such reports reached the U.S. Drug Enforcement Administration. From 1996 to 1999 a group of 2,003 urine samples were compiled from victims across the United States in sexual assault cases where drugs were a suspected weapon used by the assailant. Analysis found GHB or flunitrazepam in fewer than 2%, and the number of instances declined in each passing year. At about the same time, a 26-month study collected 1,179 samples from sexual assault cases na- tionwide in which a drug was suspected of playing a role and found 4% to be positive for GHB.

Persons wanting GHB sometimes obtain GBL instead (gamma butyrolac- tone, nicknamed Blue Nitro Vitality or Firewater). The body converts a dose of GBL into GHB, so their effects are about the same. Products containing GBL can be poisonous, a fact that some drug abusers learn in dramatic ways.

Recreational users take GHB for euphoria and hallucinations, to increase sociability, to promote interest in sexual activity, and to lower inhibitions. One drug misuser who used GBL likened its effects to alcohol. GBL is also mar- keted as a mood elevator, a quality that some GHB users ascribe to that sub- stance as well. Researchers using various scientific measurements have confirmed that GHB promotes mental calmness but may simultaneously make a person feel discontented.

Drawbacks. Tests using medical-size doses (which may be smaller than ones taken by illicit users) reveal no impairment of mental or physical abilities; the researchers concluded that GHB does not hurt job performance or ability to drive a car. Nevertheless, GHB is suspected of causing an automobile driver to pass out, and the drug’s sleep-inducing properties make it inadvisable to use while operating dangerous machinery. Supposedly the drug causes am- nesia about events that occur while a person is intoxicated with the substance, although experiments using medical-size doses find no effect on short-term memory. A large-enough dose can slow heart rate and interfere with a per- son’s ability to move and make a person vomit and fall asleep. Breathing difficulty can occur. Seizures have been reported, but some authorities believe those reports have misidentified various muscle contractions as seizures. In monkeys the drug lowers body temperature. In rats that effect depends on a dose’s size, with small amounts raising body temperature and large amounts lowering it. An odd overdose effect has been observed in persons who tem- porarily stop breathing yet become violent despite that impairment. The drug reduces control of urination and defecation. Although GHB can cause blood to appear in urine, no damage to body organs has been observed. People can take medical doses for years without showing any psychotic symptoms.

Abuse factors. Experiments with monkeys show little abuse potential in the drug, but some medical personnel who treat drug abusers consider the po- tential to be high. GHB abusers, however, tend to have bad relationships with

184 GHB

other drugs as well, so using such a population to evaluate GHB’s particular abuse potential is treacherous.

GHB has been used successfully to reduce or even eliminate withdrawal symptoms in alcohol addicts. One alcohol withdrawal study found GHB as effective as diazepam, a standard drug given to aid alcohol withdrawal; in addition, GHB worked faster than diazepam at alleviating sadness, restless- ness, and anxiety among patients. GHB has also reduced craving for alcohol on a long-term basis. One group of researchers administering GHB for this purpose observed no troublesome unwanted effects, and barely 1% of patients began abusing GHB—a disturbing percentage in a general population but a very low rate for a drug addict population. Tightly controlled dispensing con- ditions, however, may be the reason for that low rate; abuse might be heavier among persons with ready access to the drug. GHB is cross-tolerant enough with heroin and methadone to diminish their withdrawal symptoms. Animal experiments have found modest cross-tolerance with morphine, dextroam- phetamine, and LSD.

In studies measuring GHB’s usefulness for treating narcolepsy, no tolerance was observed even though some patients had been taking the drug for up to nine years. Dispute exists about whether tolerance develops in nonmedical usage. GHB dependence can emerge after taking large doses for a long time. Diazepam can ease GHB withdrawal symptoms. Tremors, uneasiness, dif- ficulty with sleep, visual and auditory hallucinations, high blood pressure, faster heartbeat, sweating, nausea, and vomiting can be part of the withdrawal syndrome. Symptoms may last for over two weeks. GHB withdrawal can in- clude psychosis so severe that people have to be restrained, but how much of that reaction is caused by the drug and how much is caused by the individ- ual’s underlying personality may be unclear. Dosage affects severity of with- drawal, with heavy users having the most trouble.

Drug interactions. The HIV (human immunodeficiency virus) drugs saqui- navir and ritonavir can have serious and potentially fatal interactions with GHB. Simultaneous use of alcohol or other depressants with GHB increases risk of overdose. The drug has a high sodium content, which might be a problem for persons needing to limit their intake of sodium.

Cancer. Tests on rats and mice indicate GHB does not cause cancer.

Pregnancy. Whether the drug causes birth defects is unknown. It passes into the fetus if a pregnant woman takes a dose and can reduce fetal respiration. When the substance was still a legal medical drug, GHB was used as an aid to childbirth.

Additional scientific information may be found in:

“Adverse Events Associated with Ingestion of Gamma-butyrolactone—Minnesota, New Mexico, and Texas, 1998–1999.” MMWR. Morbidity and Mortality Weekly Report. 48 (1999): 137–40.

Bernasconi, R., et al. “Gamma-hydroxybutyric Acid: An Endogenous Neuromodulator with Abuse Potential?” Trends in Pharmacological Sciences 20 (1999): 135–41.

Dyer, J.E. “Gamma-hydroxybutyrate: A Health-Food Product Producing Coma and Seizurelike Activity.” American Journal of Emergency Medicine 9 (1991): 321–24.

Ferrara, S.D., et al. “Effects of Single Dose of Gamma-hydroxybutyric Acid and Lora-

GHB 185

zepam on Psychomotor Performance and Subjective Feelings in Healthy Vol-

unteers.” European Journal of Clinical Pharmacology 54 (1999): 821–27.
Galloway, G.P., et al. “Gamma-hydroxybutyrate: An Emerging Drug of Abuse That

Causes Physical Dependence.” Addiction 92 (1997): 89–96.
Hernandez, M., et al. “GHB-Induced Delirium: A Case Report and Review of the Lit-

erature on Gamma Hydroxybutyric Acid.” American Journal of Drug and Alcohol

Abuse 24 (1998): 179–83.
Li, J., S.A. Stokes, and A. Woeckener. “A Tale of Novel Intoxication: A Review of the

Effects of Gamma-hydroxybutyric Acid with Recommendations for Manage- ment.” Annals of Emergency Medicine 31 (1998): 729–36.


Pronunciation: gloo-TETH-ih-meyed
Chemical Abstracts Service Registry Number: 77-21-4 Formal Names: Doriden, Elrodorm, Noxyron

Informal Names: CB, CD, Ciba, D, Glue, Goofballs, Goofers. With codeine: Doors & 4s, Dors & 4s, 4 Doors, G & C, Hits, Loads, Packets, Pancakes & Syrup, Sets, Setups, 3s & 8s

Type: Depressant. See page 19
Federal Schedule Listing: Schedule II (DEA no. 2550) USA Availability: Prescription
Pregnancy Category: C

Uses. The substance became available in the 1950s as an alternative to bar- biturates. As a medicine this drug is mainly used to calm people and make them sleepy. It has also been used to help prevent jaundice in newborns and to reduce muscle tremors in adults. Glutethimide intoxication has been likened to that from alcohol or barbiturates.

Drawbacks. Glutethimide can have a rebound effect, meaning that if a per- son is taking the drug to combat anxiety or insomnia and stops taking it, those conditions can temporarily become worse than before. One study found that after several months the drug’s ability to induce sleep deteriorates so badly that users have more trouble falling asleep than insomniacs who don’t use any sleep-inducing drug.

A test of the drug’s influence on mental ability found little effect, but to- bacco smokers seemed to be affected more than nonsmokers. A test of skills related to automobile driving found little influence from glutethimide. The drug produced inconsistent results in another experiment measuring alertness, reaction time, and decision making. Those tests, however, involve normal doses during relatively brief time spans. Generally people are advised to be- come aware of how the drug affects them before attempting to run dangerous machinery. Long-term heavy abuse can reduce mental skills in ways that re- semble organic brain damage. Animal experiments suggest that the substance may worsen porphyria, a body chemistry disorder that can make a person violent. The drug can aggravate urinary tract blockage and should be used cautiously by persons with enlarged prostate. Eyesight difficulty and dry mouth are among typical unwanted effects.

Glutethimide 187

A severe overdose can produce what looks like skin burns, and muscle spasms or even convulsions may occur. Case reports note that long-term use of glutethimide can decrease a person’s calcium levels; one report tells of bones softening in a person who took the drug routinely for 10 years, and another report notes seizures occurring due to low calcium. The drug can also reduce a body’s supply of vitamin D. After a dozen years of daily glutethimide ingestion, one person had lost so much muscle control that speech was diffi- cult, unassisted walking was impossible, and control of urination and bowel movements was no longer possible. Similar case reports exist. Others, how- ever, mention persons who took the drug for years without noticeable ill ef- fect.

Abuse factors. Some illicit drug users take glutethimide with codeine. The combination supposedly produces a euphoria and stupor like heroin’s. Users of the combination report increased sociability and feelings of intellectual in- sight in discussions that were actually about nothing. The drug mix can se- riously impair breathing, and deaths are verified. Some of these deaths involve dosages of each drug that were theoretically safe, outcomes implying that glutethimide and codeine may boost each other’s actions. Users of the com- bination have experienced typical unwanted actions of both drugs in addition to headaches, grouchiness, tremors, cramps, and trouble sleeping.

Glutethimide tolerance and dependence can develop. Withdrawal has symptoms similar to those seen with barbiturates. Seizures are noted in case reports. Among persons taking medical doses of glutethimide for months, a withdrawal syndrome can include hallucinations, fever, delirium, and con- vulsions. Case reports tell of withdrawal experiences that included catatonia. For addiction treatment, phenobarbital can be substituted for glutethimide, and a person can then be gradually weaned off the phenobarbital.

Drug interactions. The drug reduces effectiveness of warfarin, a medicine that fights heart attack and stroke by reducing blood clotting. Glutethimide is also supposed to be avoided if someone is taking the anti-blood-clotting sub- stance coumarin. A U.S. Army aerospace test found that using alcohol with glutethimide did not harm breathing. That finding has rather narrow signifi- cance for most persons, but a more generally relevant finding came from an experiment showing that glutethimide raised blood alcohol levels of persons who had been drinking. Alcohol and glutethimide may be a mix to avoid. Antihistamines should be used cautiously with glutethimide. Animal experi- mentation shows that injection of marijuana’s main active component THC (tetrahydrocannabinol) increases the potency of glutethimide, thereby increas- ing risk of overdose.

Cancer. Not enough scientific information to report.

Pregnancy. Glutethimide is related to thalidomide, perhaps the most noto- rious pharmaceutical cause of human birth defects. In experimentation with rats and rabbits glutethimide did not produce physically apparent birth de- fects. The death rate among rabbit offspring was 6%, however, compared to a 2% rate among offspring with no fetal drug exposure—a rate three times higher for the glutethimide group than for the nondrug group. One experi- ment found the death rate of rats with prenatal glutethimide exposure to be three times that of rats with no drug exposure. Surviving rats with fetal ex-

188 Glutethimide

posure to glutethimide exhibit abnormal behavior, but their own offspring behave normally. Pregnant women have routinely received glutethimide for insomnia, nausea, and vomiting. Humans with sufficient fetal exposure may be born dependent on the drug. It has been used to ease labor. Nursing moth- ers who take the drug may have enough glutethimide in their milk to make their infants sleepy.

Additional scientific information may be found in:

Bender, F.H., J.V. Cooper, and R. Dreyfus. “Fatalities Associated with an Acute Over- dose of Glutethimide (Doriden) and Codeine.” Veterinary and Human Toxicology 30 (1988): 332–33.

DiGiacomo, J.N., and C.L. King. “Codeine and Glutethimide Addiction.” International Journal of the Addictions 5 (1970): 279–85.

Haas, D.C., and A. Marasigan. “Neurological Effects of Glutethimide.” Journal of Neu- rology, Neurosurgery, and Psychiatry 31 (1968): 561–64

Jones, A.H., and J.F. Mayberry. “Chronic Glutethimide Abuse.” British Journal of Clinical Practice 40 (1986): 213.

Kovacs, T. “[Acute Toxicological Cases during a Ten-Year Period in Our Clinic].” Orvosi Hetilap [Hungarian Medical Journal] 143 (2002): 71–76. Abstract in English. Mould, G.P., S.H. Curry, and T.B. Binns. “Interaction of Glutethimide and Phenobar-

bital with Ethanol in Man.” Journal of Pharmacy and Pharmacology 24 (1972): 894–

Reveri, M., S.P. Pyati, and R.S. Pildes. “Neonatal Withdrawal Symptoms Associated

with Glutethimide (Doriden) Addiction in the Mother during Pregnancy.” Clin-

ical Pediatrics 16 (1977): 424–25.
Shamoian, C.A. “Codeine and Glutethimide; Euphoretic, Addicting Combination.” New

York State Journal of Medicine 75 (1975): 97–99.


Pronunciation: hal-AZ-eh-pam
Chemical Abstracts Service Registry Number: 23092-17-3 Formal Names: Paxipam
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2762) USA Availability: Prescription
Pregnancy Category: D

Uses. Halazepam’s main medical usage is for reducing anxiety. Because the drug promotes drowsiness, it is sometimes prescribed to be taken at bedtime, aiding both sleep and calmness. One experiment found the compound to be more effective than clorazepate dipotassium in helping anxiety. Another study found that halazepam can diminish anxiety significantly on the very first day of administration. Halazepam is also used to treat symptoms of alcohol with- drawal and has had some experimental success in alleviating schizophrenic psychoses. Physicians have observed that halazepam can reduce stress and depression and can improve epilepsy. An experiment found that halazepam did not increase belligerence, unlike some benzodiazepine class drugs. Canine studies show that in the body the drug converts into nordiazepam and oxa- zepam, which are also metabolites of diazepam.

Drawbacks. The compound can reduce saliva output. With stronger dosages elderly persons sometimes experience difficulty in manual dexterity and other muscle control; during an experiment several elderly individuals fell. In cer- tain kinds of tests mice exhibit memory trouble after the drug is given.

Abuse factors. In an experiment some alcoholics had difficulty distinguish- ing halazepam from placebo, an outcome suggesting that the drug has low potential for abuse (as abusers of alcohol and other drugs should be particu- larly susceptible). Nonetheless, a person’s body can develop physical depen- dence with halazepam, which is a traditional sign of addictive potential. One group of researchers found withdrawal symptoms to be so mild, however, that a placebo could control them.

Drug interactions. The heartburn medicine cimetidine is suspected of inter- fering with halazepam’s effects.

Cancer. No cancer developed in rats and mice at daily dosage levels 5 to 50 times the maximum human dose.

190 Halazepam

Pregnancy. Experiments with rats and rabbits have produced no evidence that the drug causes birth defects.

Additional scientific information may be found in:

Fann, W.E., W.M. Pitts, and J.C. Wheless. “Pharmacology, Efficacy, and Adverse Effects of Halazepam, a New Benzodiazepine.” Pharmacotherapy 2 (1982): 72–79.
Fann, W.E., B.W. Richman, and W.M. Pitts. “Halazepam in the Treatment of Recurrent

Anxiety Attacks in Chronically Anxious Outpatients: A Double Blind Placebo Controlled Study.” Current Therapeutic Research: Clinical and Experimental 32 (1982): 906–10.

Griffiths, R.R., and B. Wolf. “Relative Abuse Liability of Different Benzodiazepines in Drug Abusers.” Journal of Clinical Psychopharmacology 10 (1990): 237–43.

“Halazepam (Paxipam)—Another Benzodiazepine.” Medical Letter on Drugs and Ther- apeutics 24 (1982): 50.

Jaffe, J.H., et al. “Abuse Potential of Halazepam and of Diazepam in Patients Recently Treated for Acute Alcohol Withdrawal.” Clinical Pharmacology and Therapeutics 34 (1983): 623–30.

Pecknold, J.C., et al. “Controlled Comparative Study of Halazepam in Anxiety.” Cur- rent Therapeutic Research: Clinical and Experimental 32 (1982): 895–905.


Pronunciation: HAIR-oh-in (also pronounced HEAR-oh-in) Chemical Abstracts Service Registry Number: 561-27-3
Formal Names: Acetomorphine, Diacetylmorphine, Diamorphine

Informal Names: Agua de Chango, AIP, Al Capone, Alquitran, Alquitranat, Am- sterdam Marble, Antifreeze, Aries, Aunt Hazel, Bad Seed, Ball, Ballot, Bart Simp- son, Beast, Big H, Big Harry, Birdie Powder, Black Pearl, Black Stuff, Black Tar, Blanca, Blanco, Blows, Blue Bag, Blunt, Bomb, Bombido, Bombita, Bombs Away, Bonita, Boy, Bozo, Brain Damage, Brea, Brick Gum, Broja, Brown, Brown Crystal, Brown Marijuana, Brown Rhine, Brown Sugar, Brown Tape, Bundle, Butu, Caballo, Caca, Calbo, Canade, Cap, Capital H, Carga, Carne, Chapopote, Charley, Chatarra, Cheese, Chicle, Chieva, China Cat, China White, Chinese Red, Chip, Chiva, Climax, Cocofan, Coffee, Cotics, Courage Pills, Crank, Crap, Crop, Crown Crap, Cura, Cut-Deck, Dava, Dead on Arrival, Deck (quantity), Deuce, Diesel, Dirt, DOA, Dog Food, Dogie, Doogie, Dooje, Doo- jee, Dooley, Dope, Dreck, Dr. Feelgood, Dugie, Duji, Dujie, Dust, Dyno, Dyno- Pure, Eighth, Estuffa, Ferry Dust, Flea Powder, Foil, Foo Foo Stuff, Foolish Powder, Fry Daddy (with crack), Furra, Galloping Horse, Gallup, Gamot, Gar- bage, Gato, George, Georgia Smack, Girl, Glacines, Glass, Gold, Golden Girl, Golpe, Goma, Good, Good & Plenty, Good H, Good Horse, Goofball (com- bination with cocaine), Gravy, H, H & C (with cocaine), H-Bomb (with MDMA), Hache, H Caps, Hairy, Hard, Hard Candy, Hard Stuff, Harry, Hazel, Heaven, Heaven Dust, Helen, Hell Dust, Henry, Hera, Hero, Heroina, Herone, Hero of the Underworld, Hessle, Him, Hombre, Hong-Yen, Horse, Horsebite, Hot Dope, HRN, Indian Pink, Iroini, Isda, Jee Gee, Jee Jee, Jerry Springer, Jive, Jive Doo Jee, Joharito, Jojee, Jones, Joy, Joy Flakes, Joy Powder, Junco, Junk, Kabayo, Karachi (with methaqualone and phenobarbital), Kompot, La Buena, LBJ, Lem- onade, Little Bomb, Load (quantity), Malaysian Pink, Manteca, Matsakow, Mayo, Mexican, Mexican Brown, Mexican Horse, Mexican Mud, Mojo, Mon- key Water, Moonrock (with crack cocaine), Morotgara, Mortal Combat, Mud, Murder 1 (with cocaine), Murotugora, Muzzle, Nanoo, New Jack Swing (with morphine), Nice & Easy, Noise, Nose, Nose Drops, Number 8, Number 4, Num- ber 3, Nurse, Ogoy, Oil, Old Steve, Orange Line, Pack, Pangonadalot, Para- chute (alone or with crack), P-Dope, Peg, Penang Pink, Perfect High, Perica, Perico, Persian, Persian Brown, P-Funk, Piedra, Poison, Polvo, Poppy, Powder, Predator, Preza, Primo (with cocaine), Pulborn, Punk Rocker (with assorted other substances), Pure, Quill, Racehorse Charlie, Ragweed, Rambo, Rane, Raw

192 Heroin

Fusion, Raw Hide, Ready Rock, Red, Red Chicken, Red Eagle, Red Rock, Red Rock Opium (with barbital, caffeine, and strychnine), Red Rum (with barbital, caffeine, and strychnine), Red Stuff (with barbital, caffeine, and strychnine), Reindeer Dust, Rhine, Rufus, Sack, Salt, Scag, Scat, Scate, Schmeek, SCOT, Scott, Scramble, Second to None, Shit, Shmeck, Shoot, Shoot-Up, Silk, Skag, Skid, Skunk, Sleeper, Slime, Smack, Smoke (with crack cocaine), Smoking Gun (with cocaine), Snow, Snowball (with cocaine), Speedball (with cocaine or methylphenidate), Spider Blue, Spike, Spoon (quantity), Stuff, Sugar, Sweet Dreams, Sweet Jesus, Sweet Stuff, Tar, Taste, Tecata, Thanie, Thing, Thunder, Tigre, Tigre Blanco, Tigre del Norte, Tits, TNT, Tongs, Tootsie Roll, Vidrio, Whack (with PCP), White, White Boy, White Girl, White Junk, White Lady, White Nurse, White Stuff, Whiz Bang (with cocaine), Wicked, Wings, Witch, Witch Hazel, Z (quantity), Zoquete

Type: Depressant (opiate class). See page 22
Federal Schedule Listing: Schedule I (DEA no. 9200) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. For most of the twentieth century drug addiction and heroin were synonymous in the United States; all substance abuse was assumed to lead to heroin. Only in the 1980s did heroin become displaced as the devil drug, supplanted in public fear and disapproval by cocaine. Being a Schedule I substance, heroin has no officially approved medical use in the United States.

Heroin is produced from morphine, and body chemistry converts a heroin dose back into morphine. Most users cannot detect a difference between those two substances. Depending on means of administration and the effect being measured, heroin is 1.5 to 8.0 times stronger than morphine and is used med- ically to suppress coughs and relieve pain in children and adults. One study of pain relief found heroin comparable to hydromorphone, a standard med- ication administered to fight severe pain. Physicians have judged heroin to be a safe anesthetic for use during childbirth, with no apparent ill effect on mother or child. The drug is also used to treat porphyria, a body chemistry disorder making people sensitive to light and occasionally making them vio- lent. Heroin users of both genders have reported increased sexual activity upon starting the compound, with decline in that activity as usage continues. That sequence would be consistent with the drug at first reducing psycholog- ical anxiety, an effect gradually evolving into indifference about the world. As noted below, heroin has hormonal actions that reduce male sexual activity.

Extrapolating from severity of withdrawal symptoms, any particular size heroin dose taken by intravenous injection is five times stronger than one taken by inhaling heated vapor (“chasing the dragon”). Other measurements show a dose to be four times more potent when taken intravenously instead of by inhaling powder.

Sometimes intravenous injection of heroin produces a rush of feeling lik- ened to a total body sexual orgasm. Heroin may allow some nonmedical users to experience euphoria, but more typically an intoxicating dose increases psy-

Heroin 193

chic distance between the user and the world, making reality seem unimpor- tant. Used in that way the drug is an escape—not into happiness but into emptiness. Someone intoxicated by a dose of heroin does not care what hap- pens any more. Lesser doses simply reduce tension, taking the edge off life’s stresses. People using lesser doses of heroin in that way may function more productively, or they may experience trouble because they feel confident enough to get into situations they would otherwise avoid.

Drawbacks. Classic unwanted heroin actions are nausea, vomiting, and con- stipation. Many other afflictions attributed to the drug actually come from adulterants in illicit supplies or from dosage techniques—such as addicts shar- ing the same hypodermic needle with one another, a custom promoting dis- eases ranging from hepatitis to AIDS (acquired immunodeficiency syndrome). Researchers find, however, that injectors of a heroin variety called “black tar” have an increased risk for botulism infection at the injection site, no matter how hygienic their equipment and technique. Injectors of any type heroin are more prone to all sorts of infections, and some researchers suspect that heroin impairs the immune system. Inhaling heated heroin vapor can rapidly pro- duce enough brain damage to cripple a person, although case reports indicate that partial recovery is possible. Inhaling either the vapor or powder can also cause breathing trouble, and injection can cause swift fluid buildup in the lungs. A study found reduced bone density in chronic male heroin users, making broken bones more likely, and researchers suspected the problem re- sulted from lower testosterone levels caused by heroin (a heroin action that is also known to reduce male sex drive). Apparently the bone density and testosterone problems can correct themselves if heroin use stops. Although stroke is an uncommonly reported outcome of heroin use, autopsy examina- tions of 100 heroin addict brains indicate that 5% to 10% of injectors suffer small strokes that may not cause the person to seek medical treatment but that may thereafter affect the person’s behavior. One experiment with heroin addicts found still another unwanted effect: Most of them see colors somewhat differently than nonusers do.

Abuse factors. All the above hazards are real, but experience also shows that addicts can take maintenance doses (enough to hold off withdrawal symptoms but not enough to get high) for years with no apparent ill effect. The behavior of people on a maintenance dose can be indistinguishable from someone using no drug at all; while on a maintenance dose of heroin ordinary middle-class persons can function well in all aspects of life at work and at home.1 Such factors are highly influenced by the legal setting of heroin use. When federal legislation outlawed the drug in the early twentieth century, the kinds of persons who took the drug changed, as did the common reasons for using the drug.

Achieving heroin addiction is normally a lengthy process; people do not become addicts instantly with a single dose. Indeed, persons can use heroin intermittently for years and not develop dependence, let alone develop a com- pulsion to take the drug. Someone with a fulfilling life is unlikely to become addicted even if heroin is used occasionally. In contrast, people with nothing to live for may find heroin to be the best part of their lives, a discovery leading to addiction.

194 Heroin

Breaking heroin addiction depends on the reason someone takes the drug. Severe withdrawal symptoms mimic influenza, but someone willing to put up with them for a couple of days can emerge with no more dependence on the drug. Physical dependence with heroin is a relatively trivial part of addiction. Few addicts take the substance simply to avoid the withdrawal syndrome. Instead, they take the drug to cope with assorted frustrations in life. If those frustrations are resolved, the heroin addiction will resolve. If those difficulties remain, heroin may remain the best way the addict knows to cope with them, and addiction will persist.2 Both heroin and tobacco can reduce stress, and if heroin users cut back on that drug, they often increase their cigarette con- sumption.

Although heroin is traditionally considered the final step in illicit drug use, with previous substances leading from one to another until the climax of her- oin is reached, scientific research does not support that scenario. Experienced drug users have typically used assorted substances over the years, but the “gateway” hypothesis in which one substance leads to another has been re- futed time and again. Nor is heroin necessarily the final stopping place for addicts. For example, research demonstrates that some heroin users move on to amphetamines as their main drug.

Drug interactions. Some persons use heroin and amphetamines together or heroin and cocaine together, a potentially fatal practice called speedballing, in order to get a variety of simultaneous drug sensations. Analysis of fatalities attributed to heroin suggests that alcohol increases risk of death.

Cancer. Whether heroin can cause cancer is unknown. One study found that cells of heroin addicts show chromosome damage that might promote cancer, but the damage becomes less over a period of months if addicts switch from heroin to methadone. Other research has found that intravenous heroin users are more likely to get cancer than the general population, but factors other than heroin may be involved.

Pregnancy. Although heroin usage apparently damages chromosomes, the damage may be from breakdown products rather than heroin itself. A study of several dozen infants found that those from heroin-using mothers had six or seven times the amount of chromosome damage found in infants from mothers who did not use the drug. This damage did not translate into con- genital malformations, however. Researchers have examined children born to women who abused heroin during pregnancy and found no indication that the drug causes birth defects. Infants may be smaller than normal upon birth, but heroin’s role is uncertain because the women tend to abuse additional drugs and engage in other conduct harmful to fetal development. Infants born to such mothers may have dependence with heroin and undergo withdrawal symptoms. Sudden infant death syndrome is more common in babies with fetal exposure to heroin than in babies without any illicit drug exposure, but researchers are uncertain whether the drug is a more important factor than overall home environment. Physical and mental development of children whose mothers used heroin during pregnancy is slightly slower than normal, an observation supported by findings in rat experiments. Examination of school-age boys who had fetal exposure to heroin finds them to be much like other children despite lower scores on various physical and psychological

Heroin 195

tests; one group of researchers noted that prenatal exposure to alcohol has much more impact than heroin, and another investigator noted that girls’ test scores were normal.

Among pregnant Australian women in drug treatment programs who use both heroin and methadone, infant mortality is higher than among women who only use methadone, but researchers believe the difference is not due to heroin but due to multiproblem lifestyles in which heroin is just one of many problems. This theme was also brought out by a study in Israel comparing children of parents who abused heroin and children of parents who did not, while at the same time comparing home environments. The investigators dis- covered that assorted problems suffered by children of heroin users had much more to do with general conditions at home than with any chemical influence of the drug on fetal development, a conclusion supported by still more Israeli research and consistent with findings by the U.S. National Institute on Drug Abuse and other researchers.

Breast-feeding by heroin-using mothers is considered safe for their infants. Passage of heroin into the milk is doubtful, and levels of heroin’s breakdown products (such as morphine) are low enough to avoid hazard.

Additional scientific information may be found in:

Cygan, J., M. Trunsky, and T. Corbridge. “Inhaled Heroin-Induced Status Asthmaticus: Five Cases and a Review of the Literature.” Chest 117 (2000): 272–75.

“Diamorphine.” In Therapeutic Drugs, ed. C. Dollery. 2d ed. New York: Churchill Liv- ingstone, 1999. D70–D75.

Ornoy, A., et al. “The Developmental Outcome of Children Born to Heroin-Dependent Mothers, Raised at Home or Adopted.” Child Abuse and Neglect 20 (1996): 385–96. Sawynok, J. “The Therapeutic Use of Heroin: A Review of the Pharmacological Liter-

ature.” Canadian Journal of Physiology and Pharmacology 64 (1986): 1–6. Schneider, J.W., and S.L. Hans. “Effects of Prenatal Exposure to Opioids on Focused Attention in Toddlers during Free Play.” Journal of Developmental and Behavioral

Pediatrics 17 (1996): 240–47.
Sneader, W. “The Discovery of Heroin.” Lancet 352 (November 21, 1998): 1697–99. Zuckerman, G.B., et al. “Neurologic Complications Following Intranasal Administra-

tion of Heroin in an Adolescent.” Annals of Pharmacotherapy 30 (1996): 778–81. Notes

1. P. Biernacki, Pathways from Heroin Addiction: Recovery without Treatment. Health, Society, and Policy series, ed. S. Ruzek and I.K. Zola (Philadelphia: Temple University Press, 1986), 6, 36, 55; T.S. Blair, “The Relation of Drug Addiction to Industry,” Journal of Industrial Hygiene 1 (October 1919): 288; Blum, “Student Characteristics and Major Drugs,” in R.H. Blum, et al., Students and Drugs: College and High School Observations, The Jossey-Bass Behavioral Science Series and the Jossey-Bass Series in Higher Edu- cation (published jointly) (San Francisco: Jossey-Bass, 1969), 77–78; I. Chein, et al., The Road to H: Narcotics, Delinquency, and Social Policy (New York: Basic Books, 1964), 358; T.D. Crothers, Morphinism and Narcomanias from Other Drugs (Philadelphia: W.B. Saun- ders and Company, 1902), 31 (Not all of the Crothers book has withstood later scientific advances); W.R. Cuskey, A.W. Klein, and W. Krasner, Drug-Trip Abroad: American Drug Refugees in Amsterdam and London (Philadelphia: University of Pennsylvania Press, 1972), 94–96; W.C. Cutting, “Morphine Addiction for 62 Years,” Stanford Medical Bul- letin 1 (August 1942): 39–41; T. Duster, The Legislation of Morality: Law, Drugs, and Moral

196 Heroin

Judgment (New York: The Free Press, 1970), 9, 117–28, 241; C.W. Earle, “The Opium Habit: A Statistical and Clinical Lecture,” Chicago Medical Review 2 (1880): 445; L.S. Goodman and A. Gilman, The Pharmacological Basis of Therapeutics, 2nd ed. (New York: The Macmillan Company, 1955), 242–44; N. Hentoff, A Doctor Among the Addicts (Chi- cago: Rand McNally, 1968), 43–44; L. Hutchins, et al., “A Two-Year Follow-Up of a Cohort of Opiate Users from a Provincial Town,” British Journal of Addiction 66 (1971): 129–40; Jaffe, “Drug Addiction and Drug Abuse,” in Goodman and Gilman, Pharma- cological 7th ed. (1985), 542, 547; Jaffe and Martin, “Opioid Analgesics and Antagonists,” in Goodman and Gilman, Pharmacological 7th ed. (1985), 498; L. Johnston, Drugs and American Youth (Ann Arbor, MI: Institute for Social Research, University of Michigan, 1973), 193, 218; J. Kaplan, The Hardest Drug: Heroin and Public Policy, Studies in Crime and Justice (Chicago: University of Chicago Press, 1983), 136; R. King, The Drug Hang- Up: America’s Fifty Year Folly (New York: W.W. Norton & Company, 1972), 18, 76; L. Kolb, Drug Addiction: A Medical Problem (Springfield, IL: Charles C. Thomas, 1962), 10– 11, 46, 57–58, 64, 104–5, 114; Mellinger et al., “Drug Use, Academic Performance, and Career Indecision: Longitudinal Data in Search of a Model,” in D.B. Kandel, ed., Lon- gitudinal Research on Drug Use: Empirical Findings and Methodological Issues (Washington, DC: Hemisphere Publishing Corporation, 1978), 167–69, 172–73; H.W. Morgan, Drugs in America: A Social History, 1800–1980 (Syracuse, NY: Syracuse University Press, 1981), 31; H.W. Morgan, Yesterday’s Addicts: American Society and Drug Abuse 1865–1920 (Nor- man: University of Oklahoma Press, 1981), 8; E.J. Morhous, “Drug Addiction in Upper Economic Levels: A Study of 142 Cases,” West Virginia Medical Journal 49 (July 1953): 189; J.A. O’Donnell, Narcotics Addicts in Kentucky, U.S. Public Health Service Publication No. 1881 (National Institute of Mental Health, 1969) [SuDocs FS2.22:N16/3], 56, 60, 79– 80, 94–98, 204, 211, 214, 217, 223–33, 241; S. Peele, with A. Brodsky, Love and Addiction (New York: Taplinger Publishing Company, 1975), 35; J.J. Platt and C. Labate, Heroin Addiction: Theory, Research, Treatment, Wiley Series on Personality Processes, A Wiley Interscience Publication (New York: John Wiley & Sons, 1976), 171; H.G. Pope, Jr., M. Ionescu-Pioggia, and J.D. Cole, “Drug Use and Life-Style among College Undergrad- uates: Nine Years Later,” Archives of General Psychiatry 38 (1981): 588–91; C. Raymond, “Researchers Say Debate over Drug War and Legalization Is Tied to Americans’ Cul- tural and Religious Values,” Chronicle of Higher Education 36 (March 7, 1990): A6–A7, A10–A11 (Craig Reinarman comments); “Report of Committee on the Acquirement of Drug Habits,” Proceedings of the American Pharmaceutical Association 51 (1903): 473; J. Rublowsky, The Stoned Age: A History of Drugs in America, Capricorn Books (New York: G.P. Putnam’s Sons, 1974), 138, 191; E.M. Schur, Narcotic Addiction in Britain and Amer- ica: The Impact of Public Policy (Bloomington: Indiana University Press, 1962), 28, 151; G.V. Stimson, Heroin and Behaviour: Diversity among Addicts Attending London Clinics (New York: John Wiley & Sons, 1973), 149, 178; G.M. Smith, C.W. Semke, and H.K. Beecher, “Objective Evidence of Mental Effects of Heroin, Morphine and Placebo in Normal Subjects,” Journal of Pharmacology and Experimental Therapeutics 136 (1962): 53, 58; A.S. Trebach, The Great Drug War and Radical Proposals That Could Make America Safe Again (New York: Macmillan Publishing Company, 1987), 345; U.S. Congress, House, Select Committee on Crime, Hearings, The Improvement and Reform of Law Enforcement and Criminal Justice in the United States (91 Cong., 1 sess., 1969) [SuDocs Y4.C86/3:L41], 287, 291 (Stephen Waldron statement); U.S. Congress, Senate, Committee on the Judi- ciary, Subcommittee on Improvements in the Federal Criminal Code, Hearings, Illicit Narcotics Traffic (84 Cong., 1 sess., 1955) [SuDocs Y4.J89/2:N16/1–10], 1326, 1339 (Hub- ert S. Howe testimony); A. Weil, The Natural Mind: An Investigation of Drugs and the Higher Consciousness, Rev. ed. (Boston: Houghton Mifflin Company, 1986), 55, 57–58; White House Conference on Narcotic and Drug Abuse, Proceedings (1962) [SuDocs Y3.W58/5:2P94/962], 305; N.E. Zinberg, Drug, Set, and Setting: The Basis for Controlled

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2. J.B. Bakalar and L. Grinspoon, Drug Control in a Free Society (Cambridge: Cam- bridge University Press, 1984), 47, 58, 135, 144; D.J. Bellis, Heroin and Politicians: The Failure of Public Policy to Control Addiction in America (Westport, CT: Greenwood Press, 1981), 25, 134, 210, 223; Biernacki, Pathways, 27, 43–44, 52, 95, 97, 99, 124–25, 161, 179, 226–28, 231; P.H. Blachly, Seduction: A Conceptual Model in the Drug Dependencies and Other Contagious Ills (Springfield, IL: Charles C. Thomas, 1970), 30, 37–38, 43, 80; J.S. Blackwell, “Drifting, Controlling and Overcoming: Opiate Users Who Avoid Becoming Chronically Dependent,” Journal of Drug Issues 13 (1983): 219–35; P.G. Bourne, “Issues in Addiction,” in P.G. Bourne, ed., Addiction (New York: Academic Press, 1974), 11; J.M. Boyle and A.F. Brunswick, “What Happened in Harlem? Analysis of a Decline in Heroin Use Among a Generation Unit of Urban Black Youth,” Journal of Drug Issues 10 (1980): 109; E.M. Brecher, and the Editors of Consumer Reports, Licit and Illicit Drugs: The Consumers Union Report on Narcotics, Stimulants, Depressants, Inhalants, Hallucino- gens, and Marijuana—Including Caffeine, Nicotine, and Alcohol (Boston: Little, Brown and Company, 1972), 39; Chein et al., Road, 6, 14, 22–23, 159, 364; I. Chein and E. Rosenfeld, “Juvenile Narcotics Use,” Law and Contemporary Problems 22 (1957): 54; Childress, “Ex- tinction of Conditioned Responses in Abstinent Cocaine or Opioid Users,” in L.S. Har- ris, ed., Problems of Drug Dependence, 1986: Proceedings of the 48th Annual Scientific Meeting, The Committee on Problems of Drug Dependence, Inc. (National Institute on Drug Abuse, Research Monograph Series, No. 76, 1987) [SuDocs HE20.8216/5:986], 189–95; Cuskey and Edington, “Drug Abuse as Self-Destructive Behavior,” in A.R. Roberts, ed. and comp., Self-Destructive Behavior (Springfield, IL: Charles C. Thomas, 1975), 138–39; Duster, Legislation, 209–11; Falk, “The Place of Adjunctive Behavior in Drug Abuse Research,” in T. Thompson and C.E. Johanson, eds., Behavioral Pharmacology of Human Drug Dependence (National Institute on Drug Abuse, Research Monograph no. 37, 1981) [SuDocs HE20.8216:37], 276; D.B. Graeven and K.A. Graeven, “Treated and Untreated Addicts: Factors Associated with Participation in Treatment and Cessation of Heroin Use,” Journal of Drug Issues 13 (1983): 207–18; R.E. Hinson and S. Siegel, “Nonphar- macological Bases of Drug Tolerance and Dependence,” Journal of Psychosomatic Re- search 26 (1982): 496–502; L.G. Hunt and C.D. Chambers, The Heroin Epidemics: A Study of Heroin Use in the United States 1965–75, Sociomedical Science Series (New York: Spec- trum Publications, 1976), 117; R. Jacobson and N.E. Zinberg, The Social Basis of Drug Abuse Prevention, Special Studies Series, no. 5 (Washington, DC: The Drug Abuse Coun- cil, 1975), 8, 14–15, 48, 50, 53, 60; B.D. Johnson, et al., Taking Care of Business: The Economics of Crime by Heroin Abusers (Lexington, MA: D.C. Heath and Company, 1985), 2; H.F. Judson, Heroin Addiction in Britain: What Americans Can Learn from the English Experience (New York: Harcourt Brace Jovanovich, 1973), 78, 80, 143–44; Kandel, “Con- vergences in Prospective Longitudinal Surveys of Drug Use in Normal Populations,” in Kandel, Longitudinal, 15–16; Kaplan, Hardest, 10, 33–34, 36–38, 43–46; King, Drug, 234, 261; Kolb, Drug, 83–84, 127; I.D. Leader-Elliott, “Heroin in Australia: The Costs and Consequences of Prohibition,” Journal of Drug Issues 16 (1986): 136; D.B. Louria, Overcoming Drugs: A Program for Action (New York: McGraw-Hill Book Company, 1971), 84; E.A. Nadelmann, “Drug Prohibition in the United States: Costs, Conse- quences, and Alternatives,” Science 245 (1989): 944; Peele, Love, 19, 59–60, 64–65, 67, 87; Platt and Labate, Heroin, 102, 107, 159–61, 193; D.H. Powell, “A Pilot Study of Occasional Heroin Users,” Archives of General Psychiatry 28 (1973): 586–94; V.H. Raveis and D.B. Kandel, “Changes in Drug Behavior from the Middle to the Late Twenties:

198 Heroin

Initiation, Persistence, and Cessation of Use,” American Journal of Public Health 77 (1987): 607–11; R.M. Restak, The Mind (New York: Bantam Books, 1988), 118; Robins, “The Interaction of Setting and Predisposition in Explaining Novel Behavior: Drug Initiations Before, In, and After Vietnam,” in Kandel, Longitudinal, 181; L.N. Robins, The Vietnam Drug Abuser Returns, Final Report (Special Action Office for Drug Abuse Prevention, 1974) [SuDocs PrEx20.9:A/2], 31–32; L.N. Robins, D.H. Davis, and D.N. Nurco, “How Permanent Was Vietnam Drug Addiction?” American Journal of Public Health 64 (Suppl. 1974): 38–43; L.N. Robins and J.E. Helzer, “Drug Use Among Vietnam Veterans: Three Years Later,” Medical World News 16 (October 27, 1975): 44–45, 49; L.N. Robins, J.E. Helzer, and D.H. Davis, “Narcotic Use in Southeast Asia and Afterward: An Interview Study of 898 Vietnam Returnees,” Archives of General Psychiatry 32 (1975): 959; Rublow- sky, Stoned, 128; C.R. Sanders, “Doper’s Wonderland: Functional Drug Use by Military Personnel in Vietnam,” Journal of Drug Issues 3 (Winter 1973): 71–72; Scher, “The Impact of the Drug Abuser on the Work Organization,” in J.M. Scher, ed., Drug Abuse in Industry: Growing Corporate Dilemma (Springfield, IL: Charles C. Thomas, 1973), 11; R.C. Schroeder, The Politics of Drugs: An American Dilemma, 2d ed. (Washington, DC: Con- gressional Quarterly Press, 1980), 72–73, 76, 82; H.B. Spear and M.M. Glatt, “The In- fluence of Canadian Addicts on Heroin Addiction in the United Kingdom,” British Journal of Addiction 66 (1971): 141–49; J. Stewart, H. de Wit, and R. Eikelboom, “Role of Unconditioned and Conditioned Drug Effects in the Self-Administration of Opiates and Stimulants,” Psychological Review 91 (1984): 251–68; T. Szasz, Ceremonial Chemistry: The Ritual Persecution of Drugs, Addicts, and Pushers, Rev. ed. (Holmes Beach, FL: Learn- ing Publications, 1985), 82–83; Trebach, Great, 110; A.S. Trebach, The Heroin Solution (New Haven: Yale University Press, 1982), 203; Trebach, “The Potential Impact of ‘Le- gal’ Heroin in America,” in A.S. Trebach, ed., Drugs, Crime, and Politics (New York: Praeger Publishers, 1978), 167–68; U.S. Congress, House, Select Committee on Crime, Improvement, 287, 290 (Stephen Waldron statement); Weil, Natural, 108; D.M. Wilner, et al., “Heroin Use and Street Gangs,” Journal of Criminal Law, Criminology, and Police Science 48 (1957): 401; C. Winick, “Epidemiology of Narcotics Use,” in D.M. Wilner and G.G. Kassebaum, eds., Narcotics, University of California Medical Extension Se- ries—Los Angeles (New York: McGraw-Hill Book Company, 1965), 8–9; N.E. Zinberg, “G.I.’s and O.J.’s in Vietnam,” New York Times Magazine, Dec. 5, 1971, pp. 122–23; Zin- berg, “Non-Addictive Opiate Use,” in J.C. Weissman and R.L. DuPont, eds., Criminal Justice and Drugs: The Unresolved Connection, Multi-Disciplinary Studies in the Law (Port Washington, NY: Kennikat Press, 1982), 5–11, 15; N.E. Zinberg, W.M. Harding, and R. Apsler, “What is Drug Abuse?” Journal of Drug Issues 8 (1978): 13, 28.


Pronunciation: high-droh-KOH-done
Chemical Abstracts Service Registry Number: 125-29-1. (Bitartrate form 34195-


Formal Names: Anexsia, Dicodid, Dihydrocodeinone, Duratuss HD Elixir, His- tussin D, Hycodan, Hycomine, Hycotuss, Hydrocet, Lorcet, Lortab, Norco, Tus- send, Tussionex, Tylox, Vicodin (tablets, ES tablets, HP tablets, and Tuss expectorant), Vicoprofen, Zydone

Informal Names: Tuss

Type: Depressant (opiate class). See page 22

Federal Schedule Listing: Schedule II if dispensed by itself (DEA no. 9193); Sched- ule III if dispensed as part of a combination product

USA Availability: Prescription Pregnancy Category: C

Uses. Physicians use this drug to suppress coughs and relieve pain. Com- mercial formulations of the substance routinely combine it with other drugs so a patient obtains multiple therapeutic effects. The combinations can also worsen effects from overdose. Hydrocodone is derived from thebaine, and body chemistry apparently converts some of a hydrocodone dose into hydro- morphone. Hydrocodone’s effects are likened to those of codeine, but de- pending on circumstances of dosage, hydrocodone is two to eight times stronger. Taking into account the differences in potency, hydrocodone pro- duces more sedation than codeine.

Drawbacks. Unwanted effects can include hiccups, muscle spasms, dizzi- ness, nausea, vomiting, constipation, and impairment of breathing. The drug can dull mental and physical alertness, so users should avoid operating dan- gerous machinery. Some pharmaceutical formats of hydrocodone combine that drug with the pain reliever acetaminophen, and excessive usage of that combination can cause deafness.

Abuse factors. Hydrocodone can produce euphoria, and the compound’s potential for abuse is rated similar to codeine’s. A medical experiment testing both those drugs found that 18 doses were not enough to produce tolerance. Urine from a person using codeine can test positive for hydrocodone. Drug abuse treatment programs seeking to switch heroin addicts to some other opiate have successfully used hydrocodone instead of methadone.

200 Hydrocodone

Drug interactions. Tricyclic antidepressants and monoamine oxidase inhib- itors (MAOIs, found in some antidepressants and other medication) may boost hydrocodone effects, and vice versa. When taken with other narcotics, hydro- codone may boost their actions. Taking the substance with anticholinergics, which are drugs affecting the parasympathetic nervous system that controls much of the abdomen, can cause intestinal blockage.

Cancer. Hydrocodone’s potential for causing cancer is unknown.

Pregnancy. Hydrocodone’s potential for causing birth defects is unknown, although malformations occurred when pregnant rabbits received hydroco- done bitartrate along with the pain reliever ibuprofen at doses strong enough to be poisonous. Malformations did not occur when the same combination was given at poisonous levels to rats. Hydrocodone by itself produced birth defects in hamsters at 700 times the normal human dose. A study of human pregnancy outcomes found no indication that hydrocodone causes birth de- fects or miscarriage, but nonetheless the drug should be avoided during preg- nancy unless the woman’s condition unquestionably requires treatment by the substance. Infants born to women who have been using hydrocodone can have dependence with the drug. Whether hydrocodone passes into a nursing mother’s milk is unknown.

Additional scientific information may be found in:

Friedman, R.A., et al. “Profound Hearing Loss Associated with Hydrocodone/Aceta- minophen Abuse.” American Journal of Otology 21 (2000): 188–91.

Hopkinson, J.H. “Hydrocodone—A Unique Challenge for an Established Drug: Com- parison of Repeated Oral Doses of Hydrocodone (10 Mg) and Codeine (60 Mg) in the Treatment of Postpartum Pain.” Current Therapeutic Research: Clinical and Experimental 24 (1978): 503–16.

Schick, B., et al. “Preliminary Analysis of First Trimester Exposure to Oxycodone and Hydrocodone.” Reproductive Toxicology 10 (1996): 162.

Vandam, L.D. “Drug Therapy: Analgetic Drugs—The Mild Analgetics.” New England Journal of Medicine 286 (1972): 20–23.

Vivian, D. “Three Deaths Due to Hydrocodone in a Resin-Complex Cough Medicine.” Drug Intelligence and Clinical Pharmacy 13 (1979): 445–46.


Pronunciation: high-droh-MOR-fohn
Chemical Abstracts Service Registry Number: 466-99-9. (Hydrochloride form 71-


Formal Names: Dilaudid, Hydrostat IR, Palladone

Informal Names: Big D, D, Delantz, Delats, Delaud, Delida, Dillies, Drugstore Heroin, Hospital Heroin, Little D, Lords, Pills

Type: Depressant (opiate class). See page 22
Federal Schedule Listing: Schedule II (DEA no. 9150) USA Availability: Prescription
Pregnancy Category: C

Uses. This pain reliever and cough suppressant was first produced in the 1920s. It is made from morphine. For pain relief hydromorphone is 2 to 10 times stronger than morphine (depending on why and how the drugs are administered), but hydromorphone effects do not last as long as morphine’s. Hydromorphone is recommended to reduce particularly severe pain, such as that encountered in cancer, kidney stone attack, heart attack, sickle-cell anemia crisis, burns, or surgery. One study of seriously ill persons and another study of surgery patients found hydromorphone to be as effective as morphine in pain relief. No difference emerged from surveys asking patients whether mor- phine or hydromorphone was the more effective pain reliever. In one study patients preferred hydromorphone to meperidine for reducing pain, although medical personnel observed no superiority of one over the other. In another study medical personnel judged hydromorphone as better than meperidine for pain control, and in still another study hydromorphone’s effects lasted longer than meperidine’s.

Drawbacks. Unwanted effects can include itching, nausea, vomiting, con- stipation, urination difficulty, sedation, sleepiness, dizziness, poor appetite, low blood pressure, muscle spasms, impairment of breathing, reduced mental clarity, and impaired male sexual function. Users should avoid running dan- gerous machinery such as an automobile until they know the drug is not impeding skills necessary for such tasks. One study involving abdominal sur- gery patients found that hydromorphone impaired thinking and reasoning more than morphine did, but the same study found that patients’ spirits rose more with hydromorphone.

202 Hydromorphone

Generally the drug should be avoided by persons suffering from asthma, urinary retention, enlarged prostate, deficient adrenal or thyroid glands, gall- bladder trouble, or epilepsy.

Abuse factors. Dependence can develop after hydromorphone has been taken regularly for several weeks. Although tolerance is unusual for medical effects of drugs, tolerance has been observed when hydromorphone is used for pain relief, with patients needing more of the drug for the same amount of relief.

Heroin addicts find hydromorphone to be a satisfactory substitute. Through cross-tolerance hydromorphone can reduce opiate withdrawal symptoms, and the drug has been used as an experimental medication in programs trying to switch opiate addicts to methadone or buprenorphine.

Drug interactions. Normally hydromorphone should not be taken along with antihistamines or various tranquilizers and antidepressants, including monoamine oxidase inhibitors (MAOIs, found in some antidepressants and in other medicine). Taking hydromorphone and cocaine together can increase each drug’s effects.

Cancer. Hydromorphone does not seem to cause cancer.

Pregnancy. In general the drug fails to produce birth defects, but some did appear when pregnant hamsters received 600 times the normal human dose. The potential for malformations is unknown among infants from pregnant women who use the drug in a medical context. Infants can be born with dependence if the mother has used hydromorphone during pregnancy. The drug is used to ease childbirth. Whether the substance passes into a nursing mother’s milk is unknown but is considered safe for the infant.

Additional information. The cough syrup form of Dilaudid may contain tartrazine (FD&C Yellow No. 5) to which some persons are allergic, particu- larly if they are allergic to aspirin.

Additional scientific information may be found in:

Hill, J.L., and J.P. Zacny. “Comparing the Subjective, Psychomotor, and Physiological Effects of Intravenous Hydromorphone and Morphine in Healthy Volunteers.” Psychopharmacology 152 (2000): 31–39.

“Hydromorphone HCl.” In Therapeutic Drugs, ed. C. Dollery. 2d ed. New York: Chur- chill Livingstone, 1999. H69–H71.

McBride, D.C., et al. “Dilaudid Use: Trends and Characteristics of Users.” Chemical Dependencies 4 (1980): 85–100.

Walker, D.J., and J.P. Zacny. “Subjective, Psychomotor, and Physiological Effects of Cumulative Doses of Opioid Mu Agonists in Healthy Volunteers.” Journal of Pharmacology and Experimental Therapeutics 289 (1999): 1454–64.


Pronunciation: i-BOH-gah-in
Chemical Abstracts Service Registry Number: 83-74-9 Formal Names: Endabuse, Tabernanthe iboga Informal Names: Bitter Grass, Iboga, Leaf of God Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7260) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This drug comes from roots of an equatorial African rainforest shrub called Tabernanthe iboga. Traditionally the natural product has been used in low doses as a mild stimulant, rather like coca or areca nut, to fight hunger, thirst, and weariness and also to improve confidence. The natural product’s active ingredient ibogaine was found in 1901. Its stimulant qualities gave it a potential role in Western medicine as a means of treating nervous exhaustion and generally helping sick persons recover from worn-down states. The drug was also viewed as a treatment for influenza and for illness caused by micro- scopic animals called Trypanosmatina protozoa. None of those applications received wide use. Ibogaine is, however, used as an aphrodisiac and has also seen illicit duty as a performance-enhancing substance in athletics.

In strong dosages ibogaine has been a component of African religious life. In that context the substance is used in its natural product format for medi- tation and to facilitate divine communication. Users may see rainbows around objects, lose barriers between senses (allowing sounds to be tasted, smells to be heard), and experience hallucinations. Fatal overdose is possible.

Drawbacks. Suspicion exists that ibogaine harms brain function in humans. Rat experiments show that high doses of ibogaine can injure some types of brain cells but that lower doses do not cause such damage. High dosage has caused body tremors and heartbeat trouble in rats. Rat experiments also show that the drug can impair emotions, reaction times, and ability to move.

Abuse factors. Some persons trying to break drug addiction claim that ibo- gaine drastically reduces craving for heroin, cocaine, and other opioids and stimulants. Switching an abuser from one drug to another one is routine in substance abuse treatment, but supposedly just one ingestion of ibogaine is enough to stop another drug’s withdrawal symptoms and to diminish craving

204 Ibogaine

for it, with no need to keep taking ibogaine. Scientific efforts to verify such claims were under way while this book was being written. Verification would make ibogaine unique in the history of substance abuse treatment and would also challenge much of what is known about why people abuse drugs.

Ibogaine was given to 33 heroin addicts who did not reside in a treatment center; 25 of them exhibited no effort to obtain heroin during the four days of subsequent observation. These 33 experiences were not, however, part of an experimental study but instead were individual instances noted from time to time over a 31-year period, an overall average of about one instance per year. A group of researchers reported that ibogaine not only suppressed desire for heroin and cocaine among residents being weaned off those drugs in a treatment facility but that ibogaine made the people less depressed as well— an improvement in mood that was still present 30 days after release from treatment. In another study 7 opiate addicts received a single dose of ibogaine. Although 1 addict shortly resumed opiate use, 3 avoided further opiate use for several weeks, and 3 avoided further drug abuse for at least 14 weeks. None of the 7 experienced an opiate withdrawal syndrome. Ibogaine reduces intake of alcohol, cocaine, heroin, morphine, nicotine, food, and water by rats. Lowered consumption of food and water raises question about whether ibo- gaine is affecting drug consumption per se or is exerting some broader action. An ibogaine derivative, however, reduces rats’ drug intake without reducing water intake.

Results are inconsistent on whether the drug improves or impedes learning in rats, an effect related to memory. One theory holds ibogaine allows humans to remember why they started using drugs, thereby helping abusers to stop. The instant results claimed for ibogaine, however, are inconsistent with the time necessary for memories to liberate persons from other psychiatric afflic- tions. And the memory theory also assumes that the reason an abuser started using drugs was either invalid in the past or is no longer valid in the present, an assumption inconsistent with much that is known about drug abuse. Nor does the memory theory explain why ibogaine reduces drug consumption in rats. The memory aspect is commonly mentioned by users, however, and some claim to achieve major positive realignment of their lives through ibogaine- induced insights into past experiences and allegorical interpretations of hallucinations. Nonetheless, some heroin addicts who initially announced themselves cured by ibogaine did not find the change permanent and resumed heroin use. One report says the ibogaine cure lasted less than a month for about 25% of heroin addicts who received it, longer for others who received supplemental therapy and who were dedicated to changing their lives.

A curiosity about the use of ibogaine in addiction treatment is that reported doses range from 500 mg to 1,800 mg. One authority says 1,000 mg is typical. An amount of 200 mg is considered sufficient to cause hallucinations. Addi- tional effects of 200 mg are described as nervousness (perhaps bordering on fear), unpleasant feelings in arms and legs, difficulty in muscular coordination, tremors with rapid and repeated contraction and relaxation of muscles, and inability to sleep. Nausea and vomiting are sometimes reported, along with so much uncomfortable sensitivity to light that people cover their eyes. Such unwanted actions might be publicized as substantial drawbacks in a street

Ibogaine 205

drug but receive little, if any, mention in reports where ibogaine is adminis- tered as an addiction treatment. Individual personality and the circumstance in which a drug is taken can, of course, make a big difference in effects. So perhaps massive doses of ibogaine do not affect addicts in the same way that people are affected outside a therapeutic context.

Drug interactions. In rat experiments alcohol raised ibogaine’s effects. Cancer. Not enough scientific information to report.
Pregnancy. Not enough scientific information to report.
Additional information. “Iboga” is a nickname for MDMA, but they are

not the same substance.
Additional scientific information may be found in:

Alper, K.R., D. Beal, and C.D. Kaplan. “A Contemporary History of Ibogaine in the United States and Europe.” The Alkaloids. Chemistry and Biology 56 (2001): 249–81.

Mash, D.C., et al. “Ibogaine: Complex Pharmacokinetics, Concerns for Safety, and Pre- liminary Efficacy Measures.” Annals of the New York Academy of Sciences 914 (2000): 394–401.

Mash, D.C., et al. “Medication Development of Ibogaine as a Pharmacotherapy for Drug Dependence.” Annals of the New York Academy of Sciences 844 (1998): 274–92.

Popik, P., and S.D. Glick. “Ibogaine.” Drugs of the Future 21 (1996): 1109–15.
Popik, P., R.T. Layer, and P. Skolnick. “100 Years of Ibogaine: Neurochemical and Pharmacological Actions of a Putative Anti-Addictive Drug.” Pharmacological Re-

views 47 (1995): 235–53.

Jimson Weed

Pronunciation: JIM-sn weed
Chemical Abstracts Service Registry Number: 8063-18-1 Formal Names: Datura, Datura stramonium

Informal Names: Angel Tulip, Devil’s Apple, Devil’s Trumpet, Green Dragon, Jamestown Weed, Locoweed, Mad Apple, Malpitte, Nightshade, Peru Apple, Sacred Datura, Stinkweed, Stinkwort, Thorn Apple

Type: Hallucinogen. See page 25
Federal Schedule Listing: Unlisted
USA Availability: Uncontrolled natural product Pregnancy Category: None

Uses. This bad-smelling plant grows around the world in temperate and subtropical climates and thrives without cultivation. Jimson weed can cause hallucinations and has been a component of witches’ potions and shaman experiences. Archaeological evidence exists for prehistoric spiritual use in North America, and accounts exist of such usage by native peoples into the twentieth century. Jimson weed is biologically related to several food plants including potato, pepper, eggplant, and tomato. Someone was able to graft a tomato plant onto jimson weed, with the resulting fruit so potent that con- sumers were hospitalized; one account described the incident as apparently “the first known instance of hallucinogenic tomatoes.”

Effects are similar to those of belladonna. Drugs found in jimson weed leaves, flowers, and seeds include atropine, hyoscyamine, and scopolamine, which are often called “belladonna alkaloids.” Folk medicine preparations from jimson weed flowers are put on bruises, wounds, or insect bites to di- minish discomfort; leaves and roots are used in a similar way and also to treat boils. A drink from the plant is given to help people endure the pain of setting broken bones. Inhaling jimson weed smoke is a traditional remedy for asthma, sore breathing, or coughing. Vapor from boiling the substance is used for the same purposes. Scientific measurement has confirmed that jimson weed smoke improves airway function of asthmatics. The natural product is also a treat- ment against cramps, eye inflammation, and feverish infection. The plant has been used as an aphrodisiac.

Drawbacks. Jimson weed has anticholinergic actions, meaning it can change heartbeat, affect eyesight (including extreme and prolonged dilation of pupils),

Jimson Weed 207

and halt progress of material through the intestines. Jimson weed should be avoided by persons with heart trouble, glaucoma, or slow bowels. Other body signs indicating that Jimson weed should be avoided include enlarged pros- tate, urination difficulty, fluid buildup in lung tissue, and obstruction that impedes movement of food from the stomach. The substance can raise blood pressure and body temperature while drying mucous membranes. Persons hospitalized following jimson weed ingestion have shown a flushed face, ex- aggerated reflexes, other reflexes consistent with a poison acting upon the brain, and changes involving prothrombin (a factor in blood clotting). Para- noia may be present. More than one report about jimson weed describes users with a saying such as this: “Blind as a bat, hot as a hare, dry as a bone, red as a beet, mad as a hatter, the bowel and bladder lose their tone, and the heart runs alone.”

Fever and breathing difficulty may occur after using jimson weed. People can become fidgety and even manic, talk continuously, go into delirium (which may be combative), and fall into an exhausted sleep. Reportedly such responses to the plant inspired medical use in past times against epilepsy and psychotic behavior. The atropine component of jimson weed is powerful enough to agitate an elephant.

Intoxicated persons can be unaware of what they are doing and unaware of what is going on around them, additional hazards on top of the drug’s sometimes dangerous physical effects. As with other substances accidental dosage can occur. Cases are documented of agricultural workers and garden- ers being affected by apparently rubbing their eyes after contact with jimson weed or other datura plants; a case report also exists of absorption through the skin. Contamination of food is known, and unsuspecting persons have used wine and honey made from the plants. Rats on a 90-day diet including jimson weed seed experienced lower cholesterol levels, less weight gain, and increased weight of livers. Investigators running the experiment described the consequences of chronic jimson weed seed diet as undesirable, but of course humans do not eat the seeds as a regular food. In this experiment female rats were more affected by jimson weed than males. Jimson seed meal has also been found to harm development of chickens. Horses, cattle, and pigs react badly to jimson weed, but rabbits and sheep are relatively unaffected.

Abuse factors. Europeans were using Datura plants such as jimson weed in the 1500s; one account from that era mentions long-lasting intoxication with emotions ranging from euphoria to weeping, with people having amnesia about what they did while under the influence. The same account mentions prostitutes using Datura to make clients more pliable, and old reports speak of sexual frenzy induced by the substance. During the 1600s soldiers sent to suppress Bacon’s Rebellion in colonial Virginia partook of jimson weed, and according to an account dating from 1722, some were incapacitated for days: “One would blow up a Feather in the Air; another would dart Straws at it with much Fury; and another stark naked was sitting up in a Corner, like a Monkey, grinning and making Mows [grimaces] at them; and a Fourth would fondly kiss, and paw his Companions, and snear [sic] in their Faces.”1 Such incidents still occurred in the twentieth century. In a three-week period during 1980 almost two dozen U.S. Marines at Camp Pendleton were treated for

208 Jimson Weed

hallucinations from recreational jimson weed usage. A few years earlier a sur- vey of drug users in the South African military found about 3% to be using jimson weed. U.S. military personnel have been known to “accidentally” inject themselves with the jimson weed component atropine, on hand as a nerve gas antidote but also able to create hallucinations.

Some jimson weed users describe sensations of flying, instant travel between one city and another, and communication with plants and inanimate objects. Although insects are a commonly reported visual hallucination from jimson weed, one uncommon sensation is a feeling of crawling insects, reminiscent of the “coke bugs” hallucination associated with cocaine. Jimson weed expe- riences have sometimes been likened to those from LSD, but reasons for that comparison are unapparent from accounts given by users of those substances. Both may be hallucinogens, but users relate very different observations. De- scriptions of jimson weed experiences often have an ominous tone and lack LSD qualities such as striking down barriers between senses (hearing colors, seeing sounds). In keeping with an old but largely abandoned tradition of medicine, an articulate medical journal author engaged in Datura self- experimentation and produced a graphic account of interactions with charms of nineteenth-century Paris and with horrors of twentieth-century monsters. A witness later “told me that I fought the restraining devices so violently that he thought every blood vessel in my face and neck would explode.”2 The researcher did not repeat the experiment.

Drug interactions. Not enough scientific information to report.

Cancer. The Ames test, a standard laboratory procedure that screens sub- stances for carcinogenicity, indicates jimson weed seeds have potential for causing cancer.

Pregnancy. Datura plants are suspected of causing birth defects in farm an- imals. Birth defects did not become more common in children of 450 pregnant women who received the atropine component of jimson weed. The same lack of effect on congenital abnormalities was observed in a similar number of pregnancies after the women used the scopolamine component of jimson weed, a finding consistent with a rodent study.

Additional information. Jimson weed is botanically classified as the stra- monium species of the Datura genus. Other Datura genus plants around the world are used for similar effects, but they are not jimson weed.

Additional scientific information may be found in:

DiGiacomo, J.N. “Toxic Effect of Stramonium Simulating LSD Trip.” Journal of the Amer- ican Medical Association 204 (1968): 265–66.

Gowdy, J.M. “Stramonium Intoxication: Review of Symptomatology in 212 Cases.” Jour- nal of the American Medical Association 221 (1972): 585–87.

Jacobs, K.W. “Asthmador: Legal Hallucinogen.” International Journal of the Addictions 9 (1974): 503–12.

Johnson, C.E. “Mystical Force of the Nightshade.” International Journal of Neuropsychi- atry 3 (1967): 268–75.

Keeler, M.H., and Kane, F.J., Jr. “The Use of Hyoscyamine as a Hallucinogen and Intoxicant.” American Journal of Psychiatry 124 (1967): 852–54.

Jimson Weed 209

Thabet, H., et al. “Datura Stramonium Poisonings in Humans.” Veterinary and Human Toxicology 41 (1999): 320–21.

Tiongson, J. “Mass Ingestion of Jimson Weed by Eleven Teenagers.” Delaware Medical Journal 70 (1998): 471–76.


1. [R. Beverley], The History of Virginia, in Four Parts, 2nd ed. (London: F. Fayram and J. Clarke and T. Bickerton, 1772), 121.

2. C.E. Johnson, “Mystical Force of the Nightshade,” International Journal of Neuro- psychiatry 3 (1967): 272.


Pronunciation: KEET-a-meen
Chemical Abstracts Service Registry Number: 6740-88-1. (Hydrochloride form


Formal Names: Ketaject, Ketalar, Ketanest, Ketavet

Informal Names: Bump, Cat Valium, Green, Honey Oil, Jet, K, Kay, Kay-Blast, Kay Jay, Keets, Keller, Kellys Day, Ket, Kit Kat, Mauve, Purple, Rockmesc, Spe- cial K, Special LA Coke, Super Acid, Super C, Super K, Vitamin K

Type: Depressant. See page 19
Federal Schedule Listing: Schedule III (DEA no. 7285) USA Availability: Prescription
Pregnancy Category: C

Uses. Ketamine is related to PCP and can produce a false-positive urine test for that substance. In contrast to the violent reputation of PCP, however, ke- tamine users are described as peaceful. Ketamine is likened to PCP, alcohol, and LSD—rather vague comparisons given the differences among those drugs. The substance was invented in the 1960s and was used as an anesthetic for Vietnam War combat casualties; it has been routinely used for war injuries ever since. Third World physicians report the drug is safe for surgical use outside high-tech environments. It is given as a pain reliever and, less com- monly, to reduce convulsions. Ketamine is also a veterinary anesthesia drug used with wild animals ranging from giraffes and gazelles to polar bears and arctic foxes.

Success has been reported with using ketamine to supplement alcoholism therapy. Two researchers reported that ketamine therapy with 42 alcoholics produced a two-year abstinence from drinking in 15 of them, an outstanding result. Other researchers report one-year abstinence in almost 66% of 111 al- coholics who received ketamine therapy (perhaps a single dose), as opposed to 24% in 100 who did not receive ketamine. Among the 111 in the original group, 81 were tracked for two years, and 40% of the 81 remained abstinent. Of 42 who were tracked for three years, 33% remained abstinent.1 Such results have prompted researchers to speculate that ketamine may also be useful in treating addiction to drugs other than alcohol. These reported beneficial effects of ketamine are surprising. Admittedly they are related to self-insights

Ketamine 211

prompted by the substance and guided by psychotherapists, but in principle a single dose of a drug is unlikely to stop addiction to some other drug.

Experiments indicate ketamine may have potential for treating migraine headache and depression, and researchers have seen evidence that ketamine may improve asthma and shrink breast cancer cells. Ketamine can reduce phantom limb pain, a strange affliction in which a person senses that an am- putated limb is still present and hurting. The drug has been used in psycho- therapy to help persons face and deal with unpleasant memories, a process accompanied by what researchers described as “mind expanding effects.” Ke- tamine has also been investigated as a potential defense against the chemical warfare agents soman and diisopropylphosphorofluoridate.

Healthy volunteers receiving ketamine in an experiment have experienced sensations reminiscent of LSD. Researchers have described such effects as “profound” among alcoholics, and illicit ketamine users have said such effects are “intense.” The substance can prompt people to feel like they are becoming transparent, blending into nearby individuals, or becoming an animal or ob- ject. Users may feel like their bodies are transforming into harder or softer substances. Persons may think they remember experiences from a past life. Some users take the drug to enter the “K-hole,” a semiparalytic state described as similar to near-death experiences in which people perceive their conscious- ness as floating above their bodies, sometimes accompanied by meaningful hallucinations and by insights about the user’s life and its proper place in the cosmos.

Examination of deaths among recreational ketamine users in New York City in a two-year period during the 1990s found none in which ketamine was the only substance in the person’s body. Children have accidentally been given 5 to 100 times the normal size dose and have survived with no apparent injury.

Drawbacks. A case report tells of recreational users experiencing temporary paralysis. Nausea and vomiting have been reported, and scientific literature contains several mentions of temporary breathing interruption caused by the drug. Increased pressure within the eye (a potential problem for glaucoma sufferers) has been measured following a ketamine dose, but not all research- ers looking for that effect have found it. The drug can interfere with a male’s physical ability to engage in sexual activity. Experiments show that ketamine can cause brain damage in rats and that simultaneous use of nitrous oxide worsens the damaging action. Ketamine can cause nervous agitation, extra salivation, blood pressure elevation, abnormal heartbeat, and muscle injury. Persons suffering from the body chemistry disorder porphyria should exercise caution about ketamine use.

The drug can change perceptions of one’s surroundings. Tests indicate ke- tamine can alter visual perception for at least 24 hours, causing people to misjudge size and speed of objects (implying that driving skills may be im- paired). Long-term use may cause persistent difficulties with attention, mem- ory, and learning ability. The substance can create amnesia about what happens while a person is under the drug’s influence.

Ketamine’s psychological actions have been characterized as similar to tem- porary schizophrenia. A study examining persons who received the drug dur- ing surgery found that upon awakening some felt they were floating; some

212 Ketamine

were euphoric; some screamed in apparent terror. A study found such effects to be twice as common in female patients as in males. Such effects are stronger among alcohol abusers. The floating sensation may occur as people regain consciousness before they regain sense of touch, a sequence that would tem- porarily eliminate awareness of gravity. One surgery patient experienced LSD- like effects that continued even after release from the hospital. Reports exist of patients experiencing psychological effects for a year after a dose. A re- viewer who examined many years of scientific reports about ketamine, how- ever, found a consensus that long-term psychological consequences from ketamine occur no more frequently than with other anesthetics—a conclusion about incidental effects from anesthetic use, not about deliberate effects in- duced as part of psychotherapy or illicit use.

One authority claims that the greatest physical hazard has a psychological base, as users sometimes become indifferent about death and take risks they would otherwise avoid. Persons intoxicated with ketamine may be woozy and have lower perception of pain, conditions that can cause or worsen accidents.

Female lemmings are more susceptible to the drug than males. While the male-female difference does not necessarily carry over to humans, use of ke- tamine’s anesthetic properties by sexual predators seeking to weaken victims was publicized in the 1990s. Researchers using the drug to treat alcoholism have found that ketamine makes a person more susceptible to suggestions, perhaps making a person more vulnerable to manipulation.

Abuse factors. Tolerance and dependence can develop when rats and mice receive ketamine. Those traditional signs of addictive potential seem uncon- firmed in human use, but people have been known to take the drug daily for no medical purpose and to feel they have a problem with that usage.

Drug interactions. In surgery patients administering diazepam simultane- ously with ketamine has diminished unwanted psychological effects such as delirium and nightmares. Midazolam may also help.

In experimentation with rats and mice the actions of ketamine and alcohol have similarities, and the two have cross-tolerance (meaning one can substi- tute for the other in various ways). Human alcoholics report that ketamine produces sensations like those of alcohol. A small study found that ketamine has stronger effects on perceptions and thinking skills in alcoholics than in other persons.

In rats morphine can boost some pain relief from ketamine, and ketamine can reduce pain relief from morphine. In contrast, a human experiment found that patients needed less morphine for pain relief if they also received keta- mine. In humans ketamine can boost opiate and barbiturate actions so much as to be fatal. Lorazepam can boost the sedative and amnesia qualities of ketamine in humans.

Cancer. Not enough scientific information to report.

Pregnancy. Experimentation on mice shows that birth defects can occur when ketamine and cocaine are used together, but the impact of just ketamine seems uncertain. Experiments on pregnant rats, rabbits, and dogs have pro- duced no harm. Ketamine has harmed hamster genes when they are experi- mented upon outside the body. Research published as the twenty-first century began indicated that the drug may harm fetal brain development in humans.

Ketamine 213

Citing possible danger to fetus survival, one authority recommends caution about using ketamine as an anesthetic in childbirth. While the drug may pass into breast milk, nursing is considered safe for infants.

Additional scientific information may be found in:

Corrigan, I.J. “Ketamine—A New Anesthetic.” Canadian Nurse 68 (April 1972): 43–44. Curran, H.V., and C. Morgan. “Cognitive, Dissociative and Psychotogenic Effects of Ketamine in Recreational Users on the Night of Drug Use and 3 Days

Later.”Addiction 95 (2000): 575–90.
Hetem, L.A., et al. “Effect of a Subanesthetic Dose of Ketamine on Memory and Con-

scious Awareness in Healthy Volunteers.” Psychopharmacology 152 (2000):

Jansen, K.L. “A Review of the Nonmedical Use of Ketamine: Use, Users and Conse-

quences.” Journal of Psychoactive Drugs 32 (2000): 419–33.
Krupitsky, E.M., and A.Y. Grinenko. “Ketamine Psychedelic Therapy (KPT): A Review

of the Results of Ten Years of Research.” Journal of Psychoactive Drugs 29 (1997):

Weiner, A.L., et al. “Ketamine Abusers Presenting to the Emergency Department: A

Case Series.” Journal of Emergency Medicine 18 (2000): 447–51. Note

1. E.M. Krupitsky and A.Y. Grinenko. “Ketamine Psychedelic Therapy (KPT): A Re- view of the Results of Ten Years of Research.” Journal of Psychoactive Drugs 29 (1997): 165–83; I.P. Sivolap and V.A. Savchenkov. “Opyt Primeneniia Preparatov Ketamina v Psikhoterapii Alkogolizma [Experience in Using Ketamine Preparations in the Psycho- therapy of Alcoholism].” Zhurnal Nevropatologii i Psikhiatrii Imeni S.S. Korsakova 94 (1994): 76–79. (Abstract in English.)


Pronunciation: KEET-ah-behm-ih-dohn
Chemical Abstracts Service Registry Number: 469-79-4 Formal Names: Cetobemidone, Ketogan
Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule I (DEA no. 9628) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This substance has no authorized medical use in the United States. Elsewhere, since the 1950s it has been used as a pain reliever for surgery, cancer, and other conditions. Figures for total legal usage of opioids/opiates in Denmark from 1981 to 1993 showed only morphine and methadone were used more than ketobemidone.

In an experiment ketobemidone caused less breathing difficulty than did buprenorphine (another opioid used for pain relief). Patients who receive morphine chronically may develop muscle twitches and experience more pain rather than less. After studying that problem one group of researchers rec- ommended that such patients be switched to ketobemidone, methadone, su- fentanil, or fentanyl. A case report indicates ketobemidone works in such a switch. Despite the drug’s usefulness for pain relief, test results conflict on whether it is better than a placebo for easing anxiety before surgery.

Drawbacks. Unwanted effects include shivering, coughing, nausea, and vomiting. Pain may cause vomiting, so paradoxically ketobemidone can also prevent vomiting through pain relief. A study noted that ketobemidone low- ers blood pressure, but not as much as morphine does.

Abuse factors. Although illicit use of this drug has received little attention in the United States, ketobemidone has been a prominent substance in the abuse scenes of Scandinavian countries. The drug is available in a pharma- ceutical intravenous format, but some illicit users crush oral tablets containing ketobemidone and inject the powder. That practice is suspected of harming eyesight. The same practice can cause skin to harden around injection sites and also break open into sores. In one report of several such cases medical personnel expressed puzzlement that the ketobemidone users acted like they felt no discomfort and were unconcerned about skin conditions that would prompt most persons to seek immediate medical aid. Such indifference about

Ketobemidone 215

physical well-being is typical among individuals engaged in self-destruction. A study of ketobemidone overdose deaths in Denmark was revealing in that respect as well; victims often had blood alcohol levels that would be fatal in themselves.

Drug interactions. A study comparing commercial intravenous pharmaceu- tical formats found morphine to be only half as strong as a combination prod- uct containing one part ketobemidone and five parts of a drug called A29. The latter drug is used to fight spasms. Experiments with rats and mice in- dicate that A29 boosts ketobemidone’s pain-relieving effect, so the human research comparing the combination to morphine does not mean that keto- bemidone alone is stronger than morphine. The same study did find, however, that when doses were adjusted for equivalent strength, the ketobemidone-A29 combination was still more effective at pain relief than morphine.

Cancer. Not enough scientific information to report.

Pregnancy. The drug passes into human milk. Based on a small number of cases involving 5,000 micrograms of ketobemidone given during childbirth, one study estimated that breast-fed infants would receive under 2 micrograms of ketobemidone from their first day’s milk.

Additional scientific information may be found in:

Kjaer, M., et al. “Bioavailability and Analgesic Effect of Sustained Release Cetobemi- done Capsules in Cancer Patients with Chronic Pain of Malignant Origin.” Acta Oncologica (Stockholm, Sweden) 31 (1992): 577–83.

Ohqvist, G., et al. “A Comparison between Morphine, Meperidine and Ketobemidone in Continuous Intravenous Infusion for Postoperative Relief.” Acta Anaesthesiol- ogica Scandinavica 35 (1991): 44–48.

Steentoft, A., and K. Worm. “Cases of Fatal Intoxication with Ketogan.” Journal—Fo- rensic Science Society 34 (July–September 1994): 181–85.

Wolff, T., et al. “Analgesic Treatment in Acute Myocardial Infarction. A Double-Blind Comparison of Ketobemidone the Spasmolytic A29 (Ketogan) and Morphine.” Acta Medica Scandinavica 223 (1988): 423–30.


Pronunciation: kaht
Chemical Abstracts Service Registry Number: 71031-15-7 (cathinone compo-

nent); 492-39-7 (cathine component)

Formal Names: Catha edulis
Informal Names: Abyssinian Tea, Arabian Tea, Goob, Jaad, Miraa, Qaad, Qat,

Shat, Somali Tea

Type: Stimulant (amphetamine class). See page 12

Federal Schedule Listing: Schedule I (cathinone DEA no. 1235); Schedule IV (ca- thine DEA no. 1230)

USA Availability: Illegal to possess Pregnancy Category: None

Uses. Although amphetamine is a laboratory creation and not a natural product, the khat plant is likened to a “natural amphetamine” due to the actions of the two scheduled substances found in it, cathinone and cathine. Because one of them is listed in Schedule I the plant is illegal to possess even though all other chemicals in it are legal. Cross-tolerance exists among am- phetamine, cathinone, and cathine. One thorough chemical analysis of khat found that the natural product also contains ephedrine.

Khat has the same psychological effects as those associated with ampheta- mine, both positive and negative. An additional effect can be vivid halluci- nations as people hover between wakefulness and sleep. In contrast to job performance benefits observed with true amphetamines, airplane crew mem- bers who use khat are found to have poorer visual memory and decision- reaction times when compared with nonusers. The substance is nonetheless used as a stimulant assisting physical labor, much as coca leaves are tradi- tionally used in South America.

The shrub is mainly found in countries along the Red Sea and Indian Ocean region of eastern and northeastern Africa. Leaves are traditionally harvested in the morning and wrapped to slow their drying. Potency declines as they dry out. The main active component cathinone transforms into the less-active component cathine over time, reducing the strength of a particular batch of khat. That factor formerly limited the product’s availability, but modern trans- portation and freezer technology allows khat to be exported around the world. The product has been a major cash crop in Ethiopia. Sometimes khat is used

Khat 217

as a tea or in a paste format, but just like coca, users generally chew the leaves while (in the delicate phrase of one scientist) “rejecting the residues.” Some people simultaneously drink sweet beverages to mask khat’s bitter flavor. The natural product’s potency is mild enough that dangerous overdose is unlikely. During the aftermath of the Persian Gulf War in the 1990s, concern was ex- pressed that American military personnel in that region might use khat in- stead of beverage alcohol.

Although khat has no approved medical use in the United States, elsewhere it is used against depression, stomach problems, headaches, coughs, as a mild stimulant, appetite suppressant, bronchodilator, aphrodisiac, and as a gonor- rhea remedy. An antiinflammatory compound has been found in the natural product. Khat raises body temperature, breathing rate, blood pressure, heart action, and muscle tension.

Drawbacks. Khat promotes constipation and may damage kidneys and liver. When fed to rabbits, khat lowers their vitamin C levels. The substance can raise diabetics’ blood sugar.

Despite theoretical possibilities for afflictions, investigation of khat use in North Yemen discovered little or no evidence of physical harm. Some re- searchers find better dental health among persons who regularly chew khat, but other researchers find the opposite (such results suggest that khat may be an “invalid variable” actually having no impact). Investigators in London at- tributed very few illnesses to khat in a group of 162 users. Tuberculosis may be the main physical peril from khat, not from the substance itself but from disregard of Western hygiene in social use of the drug (spitting around, shar- ing a water pipe). Khat psychosis is rare, probably because of the natural product’s relatively low strength. In two Israeli villages the mental illness rate for users was no worse than for nonusers; the same was found in Liverpool, England.

Abuse factors. Known as the “flower of paradise,” khat has wide recrea- tional use in countries of its traditional origin: A survey of over 10,000 Ethi- opian villagers found that half were currently using the substance; a survey of Ethiopian high school students found a still higher percentage of users. In cultures where khat usage originated, it is a social drug used to lubricate conversation. Users feel more alert and confident and even a little contentious, making for lively gatherings. Persons who have a troubled relationship with khat are generally persons who disregard social customs about it. For exam- ple, users will feel a letdown as the drug wears off. People who use khat in its traditional social context are likely to experience that letdown as simply part of a genial gathering breaking up as members go about their individual business and are unlikely to have interest in taking more khat right then. Someone alone in an apartment who feels let down may see more khat as the answer instead of more friends. Also, using a drug in a social context differing from its traditional one can cause trouble. People who use khat at all-night high-energy rave dance parties are unlikely to experience the same sensations as are found in an intimate circle of mutually trusting acquaintances who interact with each other in daily life.

Despite khat’s well-documented stimulant properties, the substance is con- sidered a threat to economic productivity in countries where it has long tra-

218 Khat

dition of use. The “threat” probably has less to do with chemistry and more to do with khat’s traditional societal role—helping people pass time genially while they sit around and visit.

Around a century ago famed novelist Theodore Dreiser wrote a short story “Khat” about using the substance. The story is an atmospheric portrayal of the drug’s cultural context, how khat aided the functioning of a society that had become archaic by the year 2000. The story is told from the perspective of a beggar, and ironically, the society that despised the beggar is now itself despised by Western modernists who condemn khat. A drug viewed as be- nevolent by a disappearing world is viewed as a threat in a new world pos- sessing different values. Yet nothing about khat’s chemistry has changed.

Tolerance appears to develop to some khat effects, such as elevations in pulse rate, blood pressure, body temperature, and respiration rate.

Drug interactions. The substance can interfere with amoxycillin and ampi- cillin antibiotics.

Cancer. A study searching for a link between khat chewing and precancer- ous conditions in the mouth found none, but some researchers feel the habit promotes oral cancer, and others suspect that khat causes cancer of the esoph- agus and stomach.

Pregnancy. Researchers have concluded that khat harms human sperm. Ex- periments on mice indicate that khat lowers male fertility and promotes fetal death from matings by those males. Rat experiments on females demonstrate that khat can cause fetal death and birth defects. Women who chew khat leaves tend to deliver lower-weight babies, but no birth defects were observed in infants from a sample of over 500 pregnant khat users. Nursing mothers can pass a psychoactive khat chemical into their milk, and the chemical can be measured in an infant’s urine.

Additional information. Khat’s main effects are attributed to the presence of the illegal drug cathinone (also called norephedrone), which is similar to dextroamphetamine and can be manufactured in a laboratory. Volunteers tak- ing cathinone show higher blood pressure and pulse rate, feel pepped up, and have a brightened mood. Scientists believe the substance has pain-relieving properties when given to rats. Animal experiments indicate the drug has 50% or more of amphetamine’s strength and that caffeine has a multiplier effect, boosting the impact of a cathinone dose. Animal experiments find no aphro- disiac qualities in cathinone but do find that it lowers testosterone levels and harms sperm and testes. Compared to the natural product khat, the pure lab- oratory drug has much more potential for harm. People can chew wads of khat for hours and get no more than mild effects, but a person using the pharmaceutical product can experience a much more powerful dose in an instant.

Khat also contains cathine. Cathine’s effects are similar to cathinone but so much weaker that khat users disdain old leaves that have lost cathinone but still retain cathine. Laboratories can make cathine. The compound has been known to produce cranial tics (uncontrollable jerking of the head) among per- sons using it for weight loss. The drug has been found in ma huang food supplements. A professional athlete was disqualified from competition after consuming such a supplement without knowing it was cathine laced.

Khat 219

“Khat” is a nickname for MDMA, but they are not the same substance. Additional scientific information may be found in:

Brenneisen, R., et al. “Amphetamine-Like Effects in Humans of the Khat Alkaloid Ca- thinone.” British Journal of Clinical Pharmacology 30 (1990): 825–28.

Kalix, P. “Cathinone, a Natural Amphetamine.” Pharmacology and Toxicology 70 (1992): 77–86.

Kalix, P. “Khat, an Amphetamine-Like Stimulant.” Journal of Psychoactive Drugs 26 (1994): 69–74.

Khattab, N.Y., and G. Amer. “Undetected Neuropsychophysiological Sequelae of Khat Chewing in Standard Aviation Medical Examination.” Aviation, Space, and En- vironmental Medicine 66 (1995): 739–44.

Krikorian, A.D. “Kat and Its Use: An Historical Perspective.” Journal of Ethnopharma- cology 12 (November 1984): 115–78.

Nencini, P., and A.M. Ahmed. “Khat Consumption: A Pharmacological Review.” Drug and Alcohol Dependence 23 (1989): 19–29.

Nencini, P., A.M. Ahmed, and A.S. Elmi. “Subjective Effects of Khat Chewing in Hu- mans.” Drug and Alcohol Dependence 18 (1986): 97–105.


Pronunciation: ehl-a ̄-a ̄-ehm
Chemical Abstracts Service Registry Number: 1477-40-3. (Hydrochloride form


Formal Names: Levo-Alpha-Acetylmethadol, Levo-alphacetylmethadol, Levome- thadyl acetate, Orlaam

Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II (DEA no. 9648) USA Availability: Prescription
Pregnancy Category: C

Uses. LAAM has pain-relieving qualities, but its main medical use is for treatment of opiate/opioid addiction, typically switching addicts from illegal heroin to the legal substance LAAM.

Drawbacks. LAAM can produce heartbeat irregularity, and although this unwanted action has not been known to harm users, it is a factor in deciding between LAAM or methadone for drug addiction treatment. When used for addiction therapy LAAM is generally considered to produce no significant reduction in alertness, but persons new to the drug or who take high doses are told to be careful about engaging in dangerous activity such as driving a car. One study involving over 600 users found weariness to be a frequent undesired LAAM effect, also constipation, abdominal discomfort, anxiety, per- spiration, and decreased male sexual ability. In one study scientists found that testosterone measurements in males declined to levels below normal when those persons used LAAM, but another study showed no change. In one study euphoria was an unusual effect, but another study typically found LAAM users to be “slightly euphoric” in comparison to methadone users. Researchers have noted aggressiveness in monkeys taking LAAM, but that effect is un- confirmed in humans. Rodent experiments measuring food intake have pro- duced conflicting results showing increased, unchanged, and decreased appetite. One human study reported no appetite change in LAAM users.

Because oral LAAM’s long-lasting effects are slow to start, some illicit users have taken more and more of the drug in order to feel expected effects and then died from a cumulative fatal overdose when LAAM’s full actions finally kicked in.

Abuse factors. In drug abuse treatment programs, some addicts prefer

LAAM 221

LAAM, and some prefer methadone. LAAM is related to methadone and is generally considered weaker, but some research has found LAAM stronger in certain ways. A dose of LAAM can last three times as long as one from meth- adone, making LAAM more convenient for addicts in a treatment program, as they can come less often to the clinic to receive LAAM than if they were receiving methadone. Convenience can influence an addict’s decision on whether to continue with a program. Another LAAM advantage is that the long-lasting nature of a dose means that effects may be steadier over a given amount of time than those from methadone, allowing more consistent job performance by addicted employees. A case report mentions addicts who pre- ferred LAAM over methadone because LAAM’s steadiness reduced mood swings that occurred with methadone. One experiment, however, discovered that LAAM users are far more physically active on days when they receive the drug than on days when they don’t—a finding that questions whether LAAM effects are as steady as commonly believed. Scientists know less about actions of LAAM than about those of methadone, so sometimes addicts with complicated medical conditions are given methadone instead of LAAM be- cause methadone’s influence on those conditions is better understood.

Experimentation with rhesus monkeys revealed that LAAM does not nec- essarily have uniform cross-tolerance with other opioids. Thus switching someone to LAAM from another opioid can be tricky; LAAM may closely match the other drug in some ways but not in others. For example, the same level of pain relief may be achieved by particular doses of LAAM or some other opioid, but those same doses will not necessarily affect breathing to the same extent.

LAAM is supposed to provide no drug high to persons on maintenance doses, but by definition a “maintenance” dose is only enough to hold off withdrawal symptoms and not enough to produce effects desired by drug misusers. So the lack of a high may be related to size of dose rather than to chemistry of the drug.

Dependence can develop.

Drug interactions. Because of oral LAAM’s slow onset of effects, judging safe amounts to take with other depressants can be perilous. Alcohol is con- sidered especially risky to use with LAAM. Phenobarbital is suspected of altering the effectiveness of an LAAM dose, and the same suspicion holds for the epilepsy drugs carbamazepine and phenytoin, the tuberculosis medicine rifampin, and the antacid-ulcer drug cimetidine.

Cancer. LAAM’s potential for causing cancer is unknown. Data from labo- ratory tests are inconclusive. One two-year test of the drug on rats and mice produced no evidence of cancer, but another two-year test yielded some evi- dence of liver cancer in rats. A human LAAM study looking for chromosome mutations, which can lead to cancer, found none. Another human study found no evidence of tumor development.

Pregnancy. LAAM’s impact on fetal development is unknown, but concern is high enough that women of childbearing age are supposed to have monthly pregnancy tests while on LAAM and to switch to methadone if pregnancy occurs. Upon examining results from chicken and rat experiments, however, some researchers suspect that more fetal damage may occur by stopping ex-

222 LAAM

posure to LAAM than by continuing it, and there has been speculation about whether the same applies to humans. Abnormal breathing is seen in puppies that had lengthy fetal exposure to LAAM. Rat experiments have attributed no physical birth defects to LAAM, but some researchers suspect that fetal ex- posure to the drug affects offspring behavior. Animal experiments also indi- cate that even if LAAM causes no birth defects, risk of miscarriage may increase. If pregnant rats routinely receive LAAM, their offspring quickly show withdrawal symptoms upon birth (an event that stops exposure to the drug) even though the drug is long-lasting in adults and would not produce withdrawal symptoms in adults for quite some time after the last dose.

Additional information. Scientific literature often refers to LAAM as meth- adyl acetate, short for levo-alpha-acetylmethadol. “Methadyl acetate,” how- ever, is also the name of a Schedule I substance occasionally called acetylmethadol, and some scientific literature uses acetylmethadol as a syno- nym for LAAM. Even the CAS Registry Numbers of these substances get mixed up, with articles sometimes assigning CAS RN 509-74-0 to LAAM. Add- ing even more confusion, LAAM and the Schedule I substances acetylmetha- dol, alphacetylmethadol, and betacetylmethadol all have the same molecular formula (and Orlaam is similar but with the addition of hydrochloride). Per- sons using this book as a starting point for more research about LAAM should look carefully at other information sources to be sure which drug is being discussed.

Additional scientific information may be found in:

Finn, P., and K. Wilcock. “Levo-Alpha Acetyl Methadol (LAAM). Its Advantages and Drawbacks.” Journal of Substance Abuse Treatment 14 (1997): 559–64.

Prendergast, M.L., et al. “Levo-Alpha-Acetylmethadol (LAAM): Clinical, Research, and Policy Issues of a New Pharmacotherapy for Opioid Addiction.” Journal of Psy- choactive Drugs 27 (1995): 239–47.

Rawson, R.A., et al. “A 3-Year Progress Report on the Implementation of LAAM in the United States.” Addiction 93 (1998): 533–40.

Sorensen, J.L., W.A. Hargreaves, and J.A. Weinberg. “Heroin Addict Responses to Six Weeks of Detoxification with LAAM.” Drug and Alcohol Dependence 9 (1982): 79–87.

Tennant, F.S., Jr., et al. “Clinical Experiences with 959 Opioid-Dependent Patients Treated with Levo-Alpha-Acetylmethadol (LAAM).” Journal of Substance Abuse Treatment 3 (1986): 195–202.


Pronunciation: lee-VOR-fa-nohl
Chemical Abstracts Service Registry Number: 77-07-6. (Tartrate anhydrous form

125-72-4; tartrate dihydrate form 5985-38-6) Formal Names: Levo-Dromoran
Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II (DEA no. 9220) USA Availability: Prescription

Pregnancy Category: C

Uses. Unlike many pain relievers, levorphanol’s oral formulation has an effectiveness almost as good as the intravenous version. An animal experiment demonstrated the drug can work when simply rubbed on an area of the skin that is hurting; that capability is an asset because it avoids the necessity of having the substance circulate through the entire body when only a particular spot needs treatment. Even severe pain can be successfully treated with the drug, which is used for conditions ranging from surgery to cancer. Studies have likened it to fentanyl, meperidine, and morphine. Levorphanol is con- sidered 4 to 15 times stronger than morphine. Pain control doses of levor- phanol take effect at about the same speed as morphine but last longer. Prolonged administration of morphine can reverse pain relief action and in- stead increase discomfort, while at the same time causing muscle spasms; morphine patients can be switched to levorphanol to avoid those outcomes.

Drawbacks. Levorphanol can cause dangerous and even fatal breathing dif- ficulty. For that reason medical personnel are supposed to carefully adjust dosage to a patient’s individual needs rather than depend upon customary amounts of the drug being safe. It is supposed to be used with special caution in patients with asthma, low thyroid function, urinary difficulty, or an en- larged prostate. Wariness is also prudent when using the substance to reduce heart pain, because the drug’s influence on cardiac function has not been con- firmed. The substance can lower blood pressure and may produce nausea, vomiting, and constipation. Levorphanol can make users woozy and harm skills needed for operating a car or other dangerous machinery. Although levorphanol is a depressant in humans, it increases leg activity in ponies—an effect that may not have escaped notice by persons seeking ways to improve the animals’ performance in races.

224 Levorphanol

Abuse factors. Tolerance and dependence can develop. When dependent rats were given a choice between water and a sweetened solution of levor- phanol, they preferred the drug solution, but when the choice was between the same drug solution and sweetened water they preferred the sweet water. When experimenters offered another set of dependent rats straight water and unsweetened levorphanol solution, those animals preferred straight water. Such results imply that the drug has a low addiction potential, but an impli- cation is not a fact. Also, animals do not always react to a substance in the same way humans do.

In humans the drug can improve spirits and even produce euphoria, and some users say they became addicted. A rat experiment demonstrated partial cross-tolerance with alcohol, suggesting that the two drugs appeal to the same kinds of people.

Some employer drug testing cannot distinguish between levorphanol and dextrorphan.

Drug interactions. Simultaneous use of levorphanol with alcohol or other depressants increases the possibility of cumulative overdose. In mice the an- esthetic lidocaine boosts levorphanol’s pain relief actions. Antihistamines and monoamine oxidase inhibitors (MAOIs, found in some antidepressants and other medicine) should be avoided when taking levorphanol. Levorphanol can also be dangerous when taken with alprazolam, diazepam, flurazepam, lor- azepam, phenobarbital, or temazepam.

Cancer. Levorphanol’s potential for causing cancer is unknown.

Pregnancy. Mice experiments with the drug have caused pregnancy failures and birth defects. Offspring from male mice exposed to the drug weighed less than normal, were slower to mature, and had abnormal motions in water. The potential for similar outcomes with humans is unknown. Rabbit experiments show the drug passing into the fetus of a pregnant animal, reducing fetal respiration. Milk from a nursing mother who uses levorphanol is assumed to contain enough of the drug to cause unwanted effects in a nursing infant, but that possibility may be minimized by waiting long enough after a dose before nursing (the delay can allow much of the drug to wash out of the woman’s body).

Additional scientific information may be found in:

Chernin, T. “Use of Opioids for Chronic Nonmalignant Pain.” Pharmacy Times 65 (1999): 18–20, 23–25.

Coniam, S.W. “Withdrawal of Levorphanol.” Anaesthesia 46 (1991): 518.
Friedler, G. “Effects of Limited Paternal Exposure to Xenobiotic Agents on the Devel-

opment of Progeny.” Neurobehavioral Toxicology and Teratology 7 (1985): 739–43. Fuchs, V., and H. Coper. “Development of Dependence on Levorphanol in Rats by Oral Intake of the Drug—The Influence of Taste on Drinking Behaviour in Rats Physically Dependent on Levorphanol.” Drug and Alcohol Dependence 6 (1980):

Knych, E.T. “Cross-Tolerance between Ethanol and Levorphanol with Respect to Stim-

ulation of Plasma Corticosterone.” Life Sciences 31 (1982): 527–32.


Pronunciation: lor-A-ze-pam
Chemical Abstracts Service Registry Number: 846-49-1 Formal Names: Ativan, Temesta
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2885) USA Availability: Prescription
Pregnancy Category: D

Uses. This antianxiety drug is also known for its sedative properties and is used to promote sleep and to fight convulsions. The substance is given to treat status epilepticus, a dangerous condition in which people have one epileptic seizure after another, back-to-back. It can reduce and sometimes even elimi- nate vomiting from cancer chemotherapy. Lorazepam has been used to treat LSD and methamphetamine overdose and has been a standard medicine to help alcoholics through the alcohol withdrawal syndrome. Recreational sed- ative users report euphoria from lorazepam. When given experimentally in combination with other drugs, it has helped reduce depression. In contrast, experimentation using motion picture excerpts to evoke particular emotions found that lorazepam may reduce happy feelings and increase unhappy ones. One study found that lorazepam worked as well as alprazolam for treating panic attacks, and a case report tells of success in treating mania. Lorazepam has been used to cure both catatonia (in which people are frozen in place) and akathisia (compulsive moving around). Patients being prepared for surgery receive the drug to calm them and to cloud their memory of the event.

Lorazepam is 5 times stronger than diazepam and 15 times stronger than oxazepam, and one experiment showed that lorazepam is 370 to 783 times stronger than meprobamate in producing some effects, ranging from de- graded performance in tests to amount of liking for one drug or the other.

Relatively little research seems to be done on whether members of different races respond differently to the same drug. This type of uncommon study has been done with lorazepam. The work found that although doses lasted about as long in young Americans as in young Japanese, a dose lasted about 20% longer in elderly Japanese than in elderly Americans—and a dose lasted about 20% longer in elderly Americans than in young Americans, so the difference became quite noticeable in Japanese subjects. (“American” and “Japanese” are

226 Lorazepam

nationalities, not races, but the research description stated that the issue of racial effect was being investigated; so those nationality labels were intended to have racial connotations.)

Drawbacks. Partial amnesia is a typical effect of the substance, and after using it for several days, people may have trouble gaining new memories. Investigators have also found that the drug interferes with detecting whether information is correct, while simultaneously reducing a person’s awareness of memory trouble. Occasionally lorazepam temporarily stops respiration, and people suffering from serious breathing trouble should avoid the substance. The same goes for persons with acute narrow-angle glaucoma. The drug can reduce body temperature and, depending on circumstances in experiments, either raise or lower heart rate and blood pressure.

Researchers find that the substance interferes with recognizing common items shown in distorted pictures; such trouble is considered evidence of the brain suffering from weakened ability to understand what the eyes see. A case report notes that lorazepam may impede movements of the mouth and face. The drug somewhat garbles speech. Because of adverse impact on mental clarity and physical performance, people are advised to avoid operating dan- gerous machinery (such as cars) for at least 48 hours after using lorazepam. Driving tests have shown the drug to reduce vehicle control skill while in- creasing risk-taking. Other tests demonstrate worsened attention, slower re- action time, and delay in reasoning out the solution to a problem. An experiment demonstrated that users may be unaware of how much the drug is interfering with their abilities. Dizziness and weakness may occur. Typically a dose has greater impact on the elderly, and all persons risk falling down until the drug wears off. A case report notes that lorazepam can eliminate a person’s interest in sexual activity. An unusual case report tells of someone who was hearing noises in an ear, and the noises became musical hallucina- tions of popular songs when the person began taking lorazepam. More typi- cally, however, the drug is able to stop auditory hallucinations. Other case reports tell of visual hallucinations after taking the compound, and that re- sponse was also observed in 3 children among 112 who were given the drug. Although lorazepam is used to reduce anxiety, case reports and formal ex- perimentation show that the substance can increase aggressiveness (perhaps because people are less afraid to do things). A schizophrenic who received the drug lost enough inhibitions to start acting out violent impulses, and similar reports exist. In formal experimentation volunteers receiving lorazepam be- came more aggressive but did not realize they were angrier than other persons in the experiment.

Abuse factors. Various psychological tests measure how much a drug ap- peals to someone. Among persons who already have a history of drug abuse (a population prone to like drugs much more than nonusers do), some results indicate lorazepam has about the same addictive potential as diazepam or meprobamate; some results simply show lorazepam to have an unspecified amount of appeal; and in one experiment abusers found the drug about as attractive as a placebo (indicating low addictive potential). Rats begin exhib- iting tolerance to lorazepam after several days of dosing. If a person takes lorazepam enough to develop dependence on it, suddenly quitting the drug

Lorazepam 227

can produce a withdrawal syndrome. If drug use has been heavy the with- drawal can include confusion, depression, perspiration, cramps, tremors, vom- iting, mania, and convulsions. Lighter use can produce lighter withdrawal such as insomnia and generally feeling out of sorts. Symptoms can be avoided altogether if a person gradually takes smaller and smaller doses rather than stopping abruptly.

Drug interactions. Lorazepam generally makes people more susceptible to effects of alcohol. If a person taking lorazepam simultaneously ingests other depressants (alcohol, barbiturates, opiates) the total depressant effects deepen. Although we might expect stimulants to counteract lorazepam’s actions, re- search has found that cocaine can boost some of them, with sleepiness becom- ing particularly greater. Thus cocaine users receiving lorazepam for medical treatment may require lower doses than normal.

Cancer. Mice and rat studies have not yielded evidence that lorazepam causes cancer.

Pregnancy. In mice lorazepam increases incidence of eyelid malformation and cleft palate. Mice having fetal exposure to lorazepam exhibit lasting neu- rochemistry abnormalities, and rats with fetal exposure demonstrate brain dif- ficulty. Extrapolating from rat test results, two researchers concluded that fetal exposure to the drug may result in male offspring having more anxiety than normal and females having less than normal. Pregnant rabbits receiving lor- azepam in an experiment produced more birth defects than usual. Persuasive evidence indicates that the drug passes from a pregnant woman into the fetus. The drug is not recommended for pregnant women unless the need is dire. Analysts examining thousands of medical records concluded that lorazepam does not necessarily cause birth defects but found that the drug may be in- volved with a deformity blocking an infant’s anal opening. Fetal exposure to lorazepam is suspected of slowing development of infants’ abilities to move and think. Case reports say that infants can have withdrawal symptoms if the mother used the drug during pregnancy, symptoms accompanied by abnor- mal muscle tone and trouble with eating. Nursing mothers are told to avoid lorazepam, as infants might be drugged from the amount of lorazepam that passes into milk.

Additional scientific information may be found in:

Bond, A., and M. Lader. “Differential Effects of Oxazepam and Lorazepam on Ag- gressive Responding.” Psychopharmacology 95 (1988): 369–73.

Funderburk, F.R., et al. “Relative Abuse Liability of Lorazepam and Diazepam: An Evaluation in ‘Recreational’ Drug Users.” Drug and Alcohol Dependence 22 (1988): 215–22.

“Lorazepam.” In Therapeutic Drugs, C. Dollery. 2d ed. New York: Churchill Living- stone, 1999. L98–L100.

O’Hanlon, J.F., et al. “Anxiolytics’ Effects on the Actual Driving Performance of Pa- tients and Healthy Volunteers in a Standardized Test. An Integration of Three Studies.” Neuropsychobiology 31 (1995): 81–88.

Schweizer, E., et al. “Lorazepam vs. Alprazolam in the Treatment of Panic Disorder.” Pharmacopsychiatry 23 (1990): 90–93.

Shader, R.I., et al. “Sedative Effects and Impaired Learning and Recall after Single Oral Doses of Lorazepam.” Clinical Pharmacology and Therapeutics 39 (1986): 526–29.


Pronunciation: ehl-ess-dee
Chemical Abstracts Service Registry Number: 50-37-3 Formal Names: Lysergic Acid Diethylamide

Informal Names: A, Acid, Acido, Angel Tears, Animal, Backbreaker (combined with strychnine), Barrel, Battery Acid, Beast, Beavis & Butthead, Big D, Bird- head, Black Acid, Black Star, Black Sunshine, Black Tab, Blotter, Blotter Acid, Blotter Cube, Blue Acid, Blue Barrel, Blue Chair, Blue Cheer, Blue Heaven, Blue Microdot, Blue Mist, Blue Moon, Blue Vial, Boomer, Brown Bombers, Brown Dots, California Sunshine, Cap, Chief, Chocolate Chips, Cid, Coffee, Conductor, Contact Lens, Crackers, Crystal Tea, Cubes, Cupcakes, D, Deeda, Delysid, Domes, Doses, Dots, Double Dome, Electric Kool Aid, Ellis Day, Elvis, Felix the Cat, Fields, Flash, Flat Blues, Ghost, God’s Flesh, Golden Dragon, Goofy, Grape Parfait, Green Double Domes, Green Single Dome, Green Wedge, Grey Shields, Hats, Hawaiian Sunshine, Hawk, Haze, Head Light, Heavenly Blue, Instant Zen, L, Lason Sa Daga, LBJ, Leary’s, Lens, Lime Acid, Little Smoke, Live Spit and Die, Logor, Loony Toons, Lucy in the Sky with Diamonds, Mellow Yellow, Mickey, Microdot, Mighty Quinn, Mind Detergent, One Way, Optical Illusion, Orange Barrel, Orange Cube, Orange Haze, Orange Micro, Orange Wedge, Owsley, Owsley’s Acid, Pane, Paper Acid, Peace, Peace Tablet, Pearly Gates, Pellet, Pink Blotter, Pink Panther, Pink Robot, Pink Wedge, Pink Witch, Potato, Pure Love, Purple Barrel, Purple Flat, Purple Haze, Purple Heart, Purple Ozoline, Rainbow, Recycle, Red Lips, Royal Blue, Russian Sickle, Sacrament, Sandoz, Smear, Snowman, Squirrel, Strawberry, Strawberry Fields, Sugar, Sugar Cubes, Sugar Lumps, Sunshine, Superman, Tab, Tail Light, Ticket, Trip, 25, Valley Dolls, Vodka Acid, Wedding Bells, Wedge, White Dust, White Lightning, White Owsley, Window Glass, Window Pane, Yellow, Yellow Dimples, Yellow Sun- shine, Ying Yang, Zen, Zig Zag Man

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7315) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. When LSD was invented in Switzerland during 1938 no one realized that this chemical was a hallucinogen even though it was known to be related to ergot. Its inventor Albert Hofmann wanted to make a stimulant to help

LSD 229

people push past weariness. Five years passed before he accidentally discov- ered the drug’s ability to alter physical and mental perceptions. One element of his discovery was the drug’s potency. A later estimate calculated that one ounce is enough for 300,000 doses. Authorities list the substance as 3,000 to 4,000 times stronger than mescaline. One authority lists LSD as 30 times stronger than DOM.

LSD strikes down barriers. Barriers between physical senses can disappear, allowing colors to be smelled and sounds to be seen. Psychological barriers can disappear, allowing insights that help people to cope with long-standing problems. Barriers between shared realities and personal fantasies can disap- pear, with people perceiving sights and sounds that no one around them is experiencing. Those perceptions can be so compelling that some people be- lieve the drug strikes down barriers separating us from realities that are oth- erwise inaccessible. Some users report a mystical experience; some simply gain pleasure. Other possibilities include terrifying hallucinations and psychoses impelling persons to do things that may harm themselves or other individuals (a 1968 report from a government official about LSD users staring at the sun until they were blinded turned out to be a hoax, but similar reports have appeared since then). An LSD user’s personality, expectations, and surround- ings all influence outcome of a dose. The drug’s effects are not invariable. Investigators have found that LSD is more rewarding for people who are spontaneous and inspired by impulses from within themselves than for people who are conforming and controlling.

Some results perceived by users turn out to be illusory. Artists who took the drug felt more creative for months afterward, but scientists who gave tests to detect elements of creativity found no change from predrug performance. On a test of sketching the human form the artists did worse than before, indicating that technical proficiency declined. An experiment involving word and image tests found LSD did not enhance creativity of normal persons.

Despite LSD’s power, volunteers have typically been able to push through their intoxication and produce almost normal results in psychological tests given during the drug experience. One investigator noted that the experimen- tal setting of such tests seemed to weaken the drug’s effects. Ability to perform “almost” normally in a laboratory does not necessarily transfer to tasks of everyday life, however. For example, a person intoxicated by LSD should not attempt to engage in dangerous activity such as driving a car. During 1943 in one of the first recorded LSD experiences the drug’s inventor was barely able to ride a bicycle, let alone drive a car, while under the influence. He had the illusion of being almost motionless, although he was actually traveling at nor- mal speed, an indication that so many events were happening to him at once that his perception of time contracted—and an indication that he was in no condition to judge the speed of vehicles on the road. His feeling of time con- traction in turn expanded his perception of space, a linkage that drug re- searchers can demonstrate, which probably made him feel he had a vaster distance to travel and was making little progress.

Before American government authorities certified LSD as having no medical value in 1970, the substance was used for a variety of therapeutic purposes. LSD has stimulant effects allowing it to be used as an antidote for barbiturate

230 LSD

poisoning. With varying degrees of success LSD has been used to treat neu- roses, sexual disorders, heroin addiction, alcoholism, and psychopathology. The drug has also been given to reduce cancer pain, to supplement drugs used for pain relief in surgery, and to treat phantom limb pain (a sensation that an amputated limb is still present and hurting). After legal LSD research was phased out in the 1970s, relatively little new information has emerged about the drug. In subsequent years even reports in scientific literature occa- sionally had a casualness not often associated with science. For example, in 1997 a medical journal published a report about “presumed LSD intoxica- tions,” but medical personnel did not confirm that their patients had taken the drug.

Drawbacks. Although LSD fatalities have been reported in animal experi- mentation, by the 1990s no human overdose deaths had been documented despite LSD’s tremendous potency. An overdose nonetheless can produce a physical collapse requiring hospitalization. In a population of psychiatric pa- tients who took the drug, only 2 in 1,000 had a resultant psychosis lasting more than 48 hours; such a result was even less frequent for psychologically normal persons. In the 1990s, however, one review of LSD research noted that lengthy psychoses can be instituted by the substance. Research found that the suicide rate for psychiatric patients who used the drug under medical super- vision was the same as for other psychiatric patients, indicating LSD might present no peril in that regard—although this aspect might be different in uncontrolled circumstances.

The drug’s physical effects can include headache, nausea, vomiting, hot or cold feelings, sweating, elevated body temperature, trembling, dizziness, blood pressure changes (up or down), increased heart rate, numb hands, sen- sitive hearing, and extra urine production. In dog experiments the substance reduced appetite.

Rat experimentation shows that administering LSD for a month can alter brain structure and chemistry. LSD has been reported to impair abstract think- ing, but one commentary on those reports noted that alcohol abuse among the studied persons might also explain their thinking problems. Brief visual afterimages (such as happens when someone looks at a bright object and then sees an image of it in opposite colors for a few seconds after looking away) are normal for everyone, but a formal experiment and a few case reports note lengthy visual afterimages in proper colors among LSD users. These are not flashbacks, incidentally.

Flashbacks are one of the most publicized effects of LSD. Flashback is a reappearance of LSD actions without taking a dose. This phenomenon is nor- mal in other contexts; something may remind a person of an event that had high emotional content, and the memory may flood one’s consciousness and temporarily sweep aside awareness of one’s surroundings. People are usually able to push out of an LSD flashback if they wish and are not taken over by it; a survey of 247 persons who experienced LSD flashbacks found only 1 who claimed to be unable to stop the experience at will. A case report indicates behavior therapy can stop LSD flashbacks, implying that their cause may have more to do with psychology than chemistry. Another case report notes ad- ditional evidence that personality affects likelihood of flashback. Still another

LSD 231

case report says that some types of antidepressants appear to promote flash- backs among LSD users, and a research study concluded that phenothiazine tranquilizers worsen flashbacks after they start. Investigations have revealed that many persons who claim to have LSD flashbacks do not really have them, that people often use the term casually and incorrectly to describe other types of experiences. Psychiatrists call the LSD type of flashback “hallucinogen per- sisting perception disorder.” Some persons, however, regard LSD flashbacks not as a disorder but as a sign they have learned to achieve altered states of consciousness without using a drug anymore.

Abuse factors. Tolerance has developed in rats and humans. Humans have shown LSD cross-tolerance with mescaline and psilocybin and slight cross- tolerance with DMT—meaning that the drugs can be substituted for one an- other, for some purposes at least.

Drug interactions. Two case reports indicate that LSD alone or in combi- nation with alcohol may cause muscles to stiffen, accompanied by fever and insensibility. Some antidepressants can increase LSD’s psychedelic effects; some others reduce them. Rat experiments show that various opioids in var- ious doses can either increase or decrease LSD actions and that the schizo- phrenia medicine clozapine can reduce LSD effects. Case reports say that chlorpromazine (Thorazine) can cause an LSD psychosis among persons who have used LSD in the past. Ambroxol, a substance used to help people clear congested respiratory tracts, can give a false-positive urine test for LSD.

Cancer. LSD stopped breast cancer growth in a rat experiment. Researchers believe this result came not because of hallucinogenic activity but probably because LSD reduced amounts of a hormone called prolactin. Animal and plant experiments show that LSD can be a mutagen, meaning it might have a potential for causing cancer. A mutagen effect has not been observed in humans who took LSD under controlled conditions.

Pregnancy. Researchers have demonstrated that LSD passes from a pregnant mouse into the fetus. In other experiments pregnant mice that received LSD produced offspring with eye defects. The same happened with rats, but in that experiment investigators noted no significant statistical difference between LSD and non-LSD rats in malformations of any type, so the LSD may not have been responsible for the eye problems. Researchers who gave LSD to dozens of rats, mice, and hamsters found no proof that the drug caused malformations in their fetuses (which numbered in the hundreds). In the 1970s claims arose that LSD causes human chromosome damage and birth defects even if the drug use stops before pregnancy begins, but subsequent research failed to verify those claims. Some of the original laboratory tests involved conditions that do not occur in the human body, and early investigators typically did not know what drug a woman had actually taken, nor what the dose was, nor did they consider whether a woman’s health problems promoted congen- ital malformations. The birth defect rate among children of LSD users is no higher than the general population’s. A case report notes a woman who took an LSD dose during early pregnancy with no apparent ill effect on her infant. A study of pregnant women who attempted to commit suicide with drugs found no infant malformation attributable to LSD, but the investigators said data were too scanty to allow a conclusion about LSD’s potential for causing

232 LSD

developmental abnormalities. The rate of birth defects was not elevated in 121 pregnancies of women who took LSD under medical supervision. Another study of 27 pregnancies reached no conclusion on whether LSD causes mis- carriage.

Additional scientific information may be found in:

Abraham, H.D., and A.M. Aldridge. “Adverse Consequences of Lysergic Acid Diethyl- amide.” Addiction 88 (1993): 1327–34.

Cohen, S. “LSD: The Varieties of Psychotic Experience.” Journal of Psychoactive Drugs 17 (1985): 291–96.

Hofmann, A. LSD, My Problem Child. Trans. J. Ott. New York: McGraw-Hill, 1980.
Li, J-H., and L-F. Lin. “Genetic Toxicology of Abused Drugs: A Brief Review.” Muta-

genesis 13 (1998): 557–65.
Mangini, M. “Treatment of Alcoholism Using Psychedelic Drugs: A Review of the

Program of Research.” Journal of Psychoactive Drugs 30 (1998): 381–418. Masters, R.E.L., and J. Houston. The Varieties of Psychedelic Experience. A Delta Book.

New York: Dell, 1966.
McGlothlin, W.H., and D.O. Arnold. “LSD Revisited.” Archives of General Psychiatry 24

(1971): 35–49.
Novak, S.J. “LSD before Leary. Sidney Cohen’s Critique of 1950s Psychedelic Drug

Research.” Isis 88 (March 1997): 87–110.

Ma Huang

See also Ephedrine

Pronunciation: mah-hwahng
Chemical Abstracts Service Registry Number: None

Formal Names: Ephedra sinica

Informal Names: Chinese Ephedra, Chinese Jointfir, Desert Tea, Herbal Ecstasy, Mexican Tea, Miner’s Tea, Mormon Tea, Popotillo, Sea Grape, Squaw Tea, Teamster’s Tea, Whorehouse Tea, Yellow Horse

Type: Stimulant (amphetamine class). See page 12 Federal Schedule Listing: Unlisted
USA Availability: Nonprescription natural product Pregnancy Category: None

Uses. Ephedra sinica is one of several Ephedra species classified as the Chinese medical herb ma huang (loosely translated as “yellow drug that constricts the tongue”). Each species is a plentiful source of ephedrine and pseudoephed- rine. A study found that the proportion of ephedrine to other mahuang com- ponents increased if the herb was boiled for two hours. A test comparing the natural herb to synthetic ephedrine (such as commonly found in medicines) revealed little difference in how the human body used ephedrine from those two different sources; investigators concluded that effects depend more on size of dose than source of drug.

The herb has been used in China for 5,000 years, principally to treat respi- ratory ailments. Ancient Greek utilization of Ephedra varieties is also noted. More recently ma huang has been used against narcolepsy. Though thought of as a Chinese herb, varieties of Ephedra plants also grow in Mexico and the American Southwest where they were once used to treat venereal disease. Mormon pioneers used the plants as alternatives to tea and coffee. Almost nothing is said of using the plants for food, although reports exist about bread made from the plants and about eating the berries, which are supposed to be a good source of vitamin C.

In Eastern medicine ma huang is administered as a tea to fight fever, asthma, and the common cold but has become popular in the Western world as a stimulant and for promotion of weight loss. One study found that people using a ma huang and cola nut combination lost over four times more weight than persons using a placebo. Ma huang is marketed as a muscle builder, as

234 Ma Huang

a means of improving sexual performance, and also as a legal substitute for MDMA. How well the product lives up to such advertising is debatable.

In the 1990s retail gross sales of ma huang products was estimated at over a half billion dollars a year. In the year 2000 surveys from 755 persons un- dergoing outpatient surgery were reported, saying that 18% were using ma huang.

Drawbacks. Purity of ma huang products is uncertain. Examination of 20 ma huang dietary supplements found them to vary widely in content of ephedrine and pseudoephedrine, and 4 even had inconsistency among various batches of the same product. One examined product lacked any ephedrine or pseudoephedrine at all. Many contained cathine, a Schedule IV prescription drug found in khat. Perhaps the most alarming finding was that actual con- tents of half the products did not match the label description. Another study of 9 ma huang products had similar results. In a separate instance, undeclared contents of a ma huang product was a factor causing an athlete to flunk when tested for drugs banned from competitive sports.

The herb is known to cause paranoia, delusions, combativeness, mania, and hallucinations similar to what amphetamine abuse can do. Someone with such behavior was diagnosed and medicated for mental illness because no one sus- pected ma huang use. Case studies offer vivid accounts of overdose causing users to direct violence against themselves and others. Psychiatric problems can persist for quite some time after drug use stops.

A study found that ephedrine did not account for all of ma huang’s adverse effects and that unwanted actions increased if the herb was ground up. Herb- alists commonly prescribe 5 or 6 grams of ma huang for steeping as one dose of tea, yielding (depending on potency) perhaps 38 to 75 mg of ephedrine. The U.S. Food and Drug Administration (FDA) has found many examples of hazard in an ephedrine dose exceeding 10 mg. Two studies found the sub- stance to be safe in that amount, although one of those studies and a third one noted heartbeat irregularity, reduced salivation, and difficulty with sleep. Headache, dizziness, nausea, vomiting, skin rash, urinary retention, kidney stones, and heart inflammation have been associated with using ma huang. Persons with glaucoma should avoid the substance. Ma huang is suspected of causing liver disease, but investigators are uncertain. Stroke, heart attack, and death have been attributed to the substance, but those claims are disputed. An experiment measuring heart rate and blood pressure yielded unclear re- sults about ma huang’s influence. The herb may cause adverse reaction with monoamine oxidase inhibitors (MAOIs, commonly found in antidepressants). Persons with diabetes or thyroid disease should consult with a physician be- fore using ma huang. Aircraft pilots have been advised to avoid the natural product.

Abuse factors. Stopping the usage of ma huang can cause a person to be tired, sleep a lot, be sad, and have trouble concentrating. Those are opposite of typical effects that the substance has, suggesting that a user’s body has developed a dependence on ma huang (because withdrawal from dependence often produces effects opposite to what a drug does). Dependence is a tradi- tional sign that a substance is addictive.

Drug interactions. The FDA considers combining ma huang with cola nut

Ma Huang 235

to be dangerous. The two prime drug components of those natural products are ephedrine and caffeine, and caffeine boosts ephedrine effects. Scientific study finds that ma huang with caffeine, but not ma huang alone, can improve functioning in physical exercise. The combination of ma huang with another medicinal herb called guarana may be particularly poisonous to dogs.

Cancer. Not enough scientific information to report.
Pregnancy. Ma huang is supposed to be avoided during pregnancy. Additional scientific information may be found in:

Chen, K.K., and C.F. Schmidt. “Ephedrine and Related Substances.” Medicine 9 (1930): 1–117.

Grauds, C. “Herbal Ephedra and the Pharmacist.” Pharmacy Times 64 (March 1998): 60, 62.

Jacobs, K.M., and K.A. Hirsch. “Psychiatric Complications of Ma-Huang.” Psychoso- matics 41 (2000): 58–62.

Mack, R.B. “ ‘All But Death, Can Be Adjusted.’ Ma Huang (Ephedrine) Adversities.” North Carolina Medical Journal 58 (1997): 68–70.

Powell, T., et al. “Ma-Huang Strikes Again: Ephedrine Nephrolithiasis.” American Jour- nal of Kidney Diseases 32 (1998): 153–59.

Sprague, J.E., A.D. Harrod, and A.L. Teconchuk. “Pharmacology and Abuse Potential of Ephedrine.” Pharmacy Times 64 (May 1998): 72–80.


Pronunciation: MAN-draik
Chemical Abstracts Service Registry Number: None Formal Names: Mandragora officinarum
Informal Names: Satan’s Apple
Type: Depressant. See page 19
Federal Schedule Listing: Unlisted
USA Availability: Nonprescription natural product Pregnancy Category: None

Uses. In some cultures European mandrake has traditional association with the devil, perhaps because a little imagination can envision the plant’s root as a small humanoid figure. The plant’s ominous connotation is illustrated in Romeo and Juliet as Juliet approaches death and shudders about hearing “shrieks like mandrakes’ torn out of the earth,” referring to a belief that the plant screams if harvested. Witches reputedly made preparations from the plant that enabled them to fly.

Medicinal usage of European mandrake may date back as far as ancient Egypt, but in twenty-first-century Western medicine, only practitioners of ho- meopathy use the substance for healing. (Homeopathy uses extremely weak preparations of medicines.) Folk practitioners have given European mandrake to fight depression, asthma, hay fever, whooping cough, colic, and stomach ulcers. The plant has also been administered as a folk treatment to promote fertility, perhaps inspired by the story in Genesis 30: 14–17. Such usage is referred to by the line “Get with child a mandrake root” from John Donne’s sonnet “Song: Go and Catch a Falling Star.” The plant is linked with romance (Song of Solomon 7:13) and is a traditional aphrodisiac, although such a char- acteristic has not received scientific confirmation. Sedative and pain relief ac- tions made the plant one of the first surgical anesthetics, and an image of it appears on the coat of arms of the British Association of Anaesthetists. Eu- ropean mandrake contains the so-called belladonna alkaloids atropine, hyo- scyamine, and scopolamine; therefore, European mandrake produces actions similar to those of belladonna.

Drawbacks. Unwanted effects can include rapid heartbeat, elevated body temperature, decrease in sweat and salivation, and difficulty with urination and bowel movements. The natural product initially acts as a sedative, but a

Mandrake 237

strong enough dose converts mandrake into a stimulant that can cause manic behavior, delirium, and hallucinations. An amount sufficient to bring on those latter effects may be an amount sufficient for dangerous poisoning. Expert guidance is recommended for anyone using the plant.

Abuse factors. Not enough scientific information to report about tolerance, dependence, withdrawal, or addiction.

Drug interactions. Not enough scientific information to report.
Cancer. Not enough scientific information to report.
Pregnancy. Not enough scientific information to report.
Additional information. Podophyllum peltatum (CAS RN 9000-55-9 for resin)

is the American mandrake, a different plant from the European one and one that persons sometimes use accidentally when they are seeking the European variety. The American version is also known as Devil’s Apple, Duck’s Foot, Ground Lemon, Hog Apple, Indian Apple, May Apple, Peca, Raccoon Berry, Umbrella Plant, Vegetable Calomel, Vegetable Mercury, Wild Jalap, Wild Lemon, Wild Mandrake, and Yellowberry. American mandrake is not a con- trolled substance.

Odor from the flowers may be unpleasant, yet the small fruit is not only edible but enjoyed by some persons. Leaves and stems are described as poi- sonous.

American mandrake is a traditional Native American medicine, and in for- mer times it was considered a substitute for mercury’s medical employment. Folk medicine uses the plant to treat fever, worms, constipation, warts, syph- ilis, jaundice, liver disease, and cancer. Etoposide, a substance derived from the plant, is scientifically known to work against cancer. American mandrake contains podophyllotoxin, a substance that acts against viruses causing mea- sles and herpes simplex type I. A study found podophyllotoxin and podo- phyllin (another American mandrake substance) to be effective against a type of wart. Application of American mandrake natural product preparations to the skin must be skillful because the plant can injure the skin and even be fatal if too much drug content is absorbed.

Animal experiments with the natural product have produced salivation, vomiting, pain, and straining to defecate. Those unwanted effects also appear in humans, with enough force to cause hemorrhoids and displacement of the rectum. One authority warns that if someone eats too much of the fruit, its laxative effect can become overpowering. Ulcers of the small intestine have developed in animals that ingest American mandrake. A case is known of damage to nerves providing sensation to limbs after a person drank an Amer- ican mandrake preparation. Persons working in an environment containing American mandrake dust have suffered irritated eyes and noses, along with coldness in their hands and feet.

The plant is suspected of causing birth defects, and usage is supposed to be avoided during pregnancy. A case report tells of fetal death after American mandrake was used to treat warts on a pregnant woman.

Additional scientific information may be found in:

Frasca, T., A.S. Brett, and S.D. Yoo. “Mandrake Toxicity: A Case of Mistaken Identity.” Archives of Internal Medicine 157 (1997): 2007–9.

238 Mandrake

Lust, J.B. The Herb Book. New York: Benedict Lust Publications, 1974. 259–60. Millspaugh, C.F. American Medicinal Plants. Philadelphia: John C. Yorston & Company,

1892. Reprint, New York: Dover Publications, Inc., 1974. 61–64.
Morton, J.F. Major Medicinal Plants: Botany, Culture and Uses. Springfield, IL: Charles C.

Thomas, 1977. 87–89.
Vlachos, P., and L. Poulos. “Case of Mandrake Poisoning.” Journal of Toxicology: Clinical

Toxicology 19 (1982): 521–22.
Weiner, M.A. Weiner’s Herbal. New York: Stein and Day, 1980. 124–25.


See also Dronabinol

Pronunciation: mair-i-WAHN-uh (also pronounced mah-ri-HWAH-nuh) Chemical Abstracts Service Registry Number: 8063-14-7
Formal Names: Cannabis, Cannabis sativa, Hashish, Marihuana, Sinsemilla

Informal Names: A-Bomb (with opium or heroin), Acapulco Gold, Acapulco Red, Ace, Afgani Indica, African Black, African Bush, Airplane, Alamout Black Hash (with belladonna), Alice B. Toklas (baked in brownie), AMP (with PCP, formal- dehyde, or other substance), Angola, Ashes, Assassin of Youth, Astro Turf, Atomic Bomb (with heroin), Atshitshi, Aunt Mary, Baby, Baby Bhang, Bad Seed, Bamba, Bambalacha, Bammy, Banano (mixed with cocaine), Bar, Bash, Ba- zooka (with coca paste), Belyando Spruce, B-40 (mixed with tobacco and al- cohol), Bhang, Black, Black Bart, Black Ganga, Black Gold, Black Gunion, Black Mo, Black Moat, Black Mote (with honey), Blanket, Blast, Block, Blonde, Blue de Hue, Blue Sage, Blue Sky Blond, Blunt, Bo, Bo-Bo, Bobo Bush, Bohd, Bomb, Bomber, Bone, Boo, Boo Boo Bama, Boom, Broccoli, Bud, Buda, Bud- dha (with opium), Burnie, Bush, Butter, Butter Flower, Cambodian Red, Cam Red, Cam Trip, Can, Canade (with heroin), Canadian Black, Canappa, Can- celled Stick, Candy Blunt (with codeine), Carmabis, Catnip, Caviar (with co- caine), Cavite All Star, Cest, Chamba, Champagne (with cocaine), Charas, Charge, Cheeba, Cheeo, Chiba Chiba, Chicago Black, Chicago Green, Chips (with PCP), Chira, Chocolate, Christmas Tree, Chronic, Chunky, Churus, Citrol, Clicker (with formaldehyde), Clickums (with PCP), Climb, Cochornis, Coli, Col- iflor Tostao, Colombian, Colorado Cocktail, Columbus Black, Cosa, Crack Back (with crack cocaine), Crazy Weed, Cripple, Crying Weed, Cryppie, Cryptonie, CS, Cube (tablet form), Culican, Dagga, Dawamesk, Dew, Diablito (with crack cocaine), Diambista, Dimba, Ding, Dinkie Dow, Dirt Grass, Dirty Joint (with crack), Ditch, Ditch Weed, Djamba, Domestic, Dona Juana, Dona Juanita, Don Jem, Don Juan, Donk (with PCP), Doob, Doobee, Doobie, Doradilla, Draf, Drag Weed, Dry High, Dubbe, Dube, Duby, Durong, Duros, Dust (combined with other substances), Earth, El Diablito (with cocaine, heroin, and PCP), El Diablo (with cocaine and heroin), Elephant, Endo, Esra, Fallbrook Redhair, Fatty, Feel- ing, Fine Stuff, Finger, Finger Lid, Fir, Flower, Flower Tops, Fraho, Frajo, Frios (with PCP), Fry (with PCP or other substances), Fry Daddy (with crack cocaine), Fry Sticks (with PCP), Fu, Fuel (with insect poison), Gage, Gange, Gangster, Ganja, Garbage, Gash, Gasper, Gauge, Geek (with crack cocaine), Ghana, Gig- gle Smoke, Giggle Weed, Gimmie (with crack cocaine), Goblet of Jam, Gold,

240 Marijuana

Golden, Golden Leaf, Gold Star, Gong, Gonj, Good Butt, Good Giggles, Goody- Goody, Goofy Butt, Grass, Grasshopper, Grata, Green, Green Buds, Green God- dess, Greeter, Gremmies (with cocaine), Greta, Griefo, Griefs, Grifa, Griff, Griffa, Griffo, Gunga, Gungeon, Gungun, Gunja, Gyve, Haircut, Hanhich, Happy Cigarette, Harsh, Has, Hash, Hawaiian, Hawaiian Black, Hawaiian Homegrown Hay, Hay, Hemp, Herb, Herba, Hit, Hocus, Homegrown, Hooch, Hooter, Hot Stick, Hydro, Illies (with PCP), Illing (with PCP), Indian Boy, Indian Hay, Indian Hemp, Indo, Indonesian Bud, Instaga, Instagu, J, Jamaican Gold, Jane, Jay, Jim Jones (with cocaine and PCP), Jive, Joint, Jolly Green, Joy Smoke, Joy Stick, Juanita, Juan Valdez, Juice Joint (with crack cocaine), Juja, Ju-Ju, Jumbo (with crack), Kalakit, Kali, Kansas Grass, Kate Bush, Kaya, Kee, Kentucky Blue, Key, KGB (Killer Green Bud), Ki, Kick Stick, Kief, Kiff, Killer Weed (with PCP), Kilter, Kind, King Bud, Kumba, Lace (with cocaine), Lakbay Diva, Laughing Grass, Laughing Weed, Leaf, Leak (with PCP), Leno, Lid (quantity), Light Stuff, Lima, Liprimo (with crack), Little Smoke, LL, Llesca, Loaf, Lobo, Loco, Loco- weed, Log, Love Boat (with formaldehyde or heroin), Love Leaf (with PCP), Lovelies (with PCP), Love Weed, Lubage, M, Machinery, Macon, Maconha, Mafu, Magic Smoke, Manhattan Silver, Mari, Marimba, Mary, Mary and Johnny, Mary Ann, Mary Jane, Mary Jonas, Mary Warner, Mary Weaver, Matchbox (quantity), Maui Wauie, Maui-Wowie, Meg, Megg, Meggie, Messorole, Mexican Brown, Mexican Green, Mexican Locoweed, Mexican Red, Mighty Mezz, M.J., M.O., Mo, Modams, Mohasky, Mohasty, Monte, Mooca, Moocah, Mooster, Moota, Mooter, Mootie, Mootos, Mor A Grifa, Mota, Mother, Moto, M.U., Mu, Muggie, Muggle, Muta, Mutah, Mutha, Nail, Nigra, Number, O.J., Oolies (with crack), Ozone (marijuana alone or with PCP and crack), Pack, Pakalolo, Paki- stani Black, Panama Cut, Panama Gold, Panama Red, Panatella, Parsley, Pasto, Pat, P-Dogs (with crack), Pin, Pocket Rocket, Pod, Poke, Pot, Potlikker, Potten Bush, Prescription, Pretendica, Pretendo, Primo (with crack), Queen Ann’s Lace, Ragweed, Railroad Weed, Rainy Day Woman, Rangood, Rasta Weed, Red Bud, Red Cross, Red Dirt, Reefer, Righteous Bush, Rip, Roach, Roacha, Rockets, Rom- pums (with horse tranquilizer), Root, Rope, Rose Marie, Rough Stuff, Rubia, Salt & Pepper, Sandwich Bag (quantity), Santa Marta, Sasfras, Scissors, Seeds, Sen, Sess, Sezz, Shake, Siddi, Sinse, Skunk, Smoke, Smoke Canada, Snop, Speedboat (mixed with crack cocaine and PCP), Spliff, Splim, Square Mackerel, Squirrel (with crack and PCP), Stack, Stems, Stick, Stinkweed, Stoney Weed, Straw, Sugar Weed, Super Grass (marijuana alone or with PCP), Super Pot, Sweet Lucy, Swishers, T, Taima, Takkouri, Tea, Texas Pot, Texas Tea, Tex-Mex, Thai Sticks, 13, 38 (combination with crack cocaine), 3750 (with crack), Thumb, Toke, Torch, Torpedo (with crack), Tray (quantity), Turbo (with crack), Tustin, Twist, Twistum, Unotque, Vega, Viper’s Weed, Wac (with PCP), Wacky Weed, Wake & Bake, Water (with other substances), Water-Water (with embalming fluid or PCP), Weed, Weed Tea, Wet (with PCP), Whack (with insect poison), Whack- atabacky, Wheat, White-Haired Lady, Wicky Stick (with crack and PCP), Wollie (with crack), Woolah (with crack), Wooly (with crack or PCP), X, Yeh, Yellow Submarine, Yen Pop, Yeola (with crack), Yerba, Yerba Mala (with PCP), Yerhia, Yesca, Yesco, Zacatecas Purple, Zambi, Zay (with other substances), Zig Zag Man, Zol, Zoom (with PCP)

Marijuana 241

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7360) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. As the twenty-first century began, the recreational use of marijuana was mainly for relaxation. The drug is often used in a social setting of mellow geniality. The drug can produce euphoria; in that context recreational usage can leak over into self-medication easing depression. One authority has said that psychological effects are facilitated by the substance, not caused by it. In other words, marijuana may help people achieve states of consciousness that they can learn to achieve in other ways.

When the federal government’s drug scheduling system was adopted in the 1970s, marijuana was classified as Schedule I, certifying it as having no med- ical value. Like many other substances, over the years marijuana had been used for medical purposes that became obsolete as better treatments were discovered. Then, by accident, a glaucoma sufferer discovered that his con- dition improved when he smoked marijuana, and subsequent scientific tests confirmed that the natural product had a hitherto unknown ability to relieve that devastating eye disease that can cause blindness. Marijuana’s long-known antinausea and appetite enhancement qualities also became publicized as a help to patients undergoing the rigors of AIDS (acquired immunodeficiency syndrome) and cancer treatments. As researchers began discovering other po- tential therapeutic actions of marijuana (including treatment of pain, multiple sclerosis, muscle spasticity, ulcerative colitis, and hiccups), medical use be- came a controversial issue in the 1990s. Among the debated points was whether the natural product had advantages over pharmaceutical dronabinol (containing delta-9-tetrahydrocannabinol, also called THC, which is mari- juana’s main active ingredient). Instead of swallowing dronabinol capsules, some patients prefer to smoke marijuana because they can fine-tune the THC dosage more easily, puffing just enough instead of taking a capsule that might have more THC than they need. Marijuana smoke may also reduce some of the unwanted actions of THC. Although belladonna and jimson weed ciga- rettes were used for many years to treat asthma, given what is known about the hazards of both tobacco and polluted air, few medical caregivers today are likely to favor inhaling any kind of smoke. Ancient Greeks reportedly put marijuana seeds on hot stones to release vapor, and modern efforts are de- vising other ways to produce vapor without igniting the substance, providing aerosol delivery without smoke.

Scientific debate aside, controversy about medical marijuana also had po- litical components. Many powerful individuals and institutions had a vested interest in maintaining marijuana’s Schedule I status. Also, many persons saw legalization for medical purposes as the first step toward lifting the ban on recreational use. Passionate claims and counterclaims about marijuana’s med- ical value swirled as this book was written, and doctors could not prescribe marijuana.

242 Marijuana

Drawbacks. Although calling marijuana a hallucinogen stretches the defi- nition of that type of drug, this book follows the governmental custom of classifying marijuana in that category. Despite that official classification, re- ports of hallucinations from marijuana are uncommon.

Physical effects can include reddened eyes, accelerated heartbeat, higher body temperature, lower testosterone level, and arousal of senses. In the 1970s reports began appearing from laboratory and animal experiments indicating that marijuana’s active ingredient THC harms immune system functions, meaning infections may become more likely. Those experiments frequently involved conditions that are not duplicated in the human body, however, and by the 1990s fears about damage to the human immune system had quieted.

Marijuana is sometimes described as making people less interested in ac- complishing tasks in life. Someone jokingly suggested that the substance in- stead creates insatiable ambition to hold elective office. In reality, marijuana does not make people unambitious. Such persons may be attracted to heavy marijuana use, but probably they were unambitious before using the sub- stance. One research study found that marijuana users who lack ambition tend to be depressed and concluded that depression (not marijuana) was the un- derlying cause for these persons’ diminished motivation. Case studies indicate that marijuana can worsen psychoses, neuroses, and phobias.

In one study a battery of thinking tests given to groups of marijuana users and nonusers found no difference in performance; in another study daily users did worse than occasional users. Long-term memory (the ability to recall many long-known things, such as remembering the year Columbus sailed to Amer- ica) has been unaffected in experiments. Short-term memory performance (brief ability to recall a few newly known things, such as a list of random words) can decline during intoxication but afterward returns to normal. Some researchers have found marijuana to have no influence on muscular coordi- nation, sensory perception, mental ability, or learning; other researchers have found that marijuana impedes muscular coordination and mental abilities. Driving skill tests have shown similar variation; some studies find that mar- ijuana harms such skill, and some do not. Some research shows marijuana having no effect on users’ performance the next day; some research shows impairment 24 hours after use. Such differing results may relate to intoxication levels, to volunteers’ experience with handling the substance, and to how long persons have been using it (some researchers believe that long-term use pro- duces long-term effects extending beyond the time of acute intoxication).

The most obvious unwanted physical effects of marijuana are caused or promoted by inhaling smoke, afflictions caused by the manner of dosing rather than by the substance itself. In an animal experiment primates that inhaled marijuana smoke were compared to those in a smoke-free group; the marijuana group developed lung damage that could have led to bronchitis or emphysema, had the smoking continued long enough. Among humans fre- quent marijuana smoking is known to produce coughing, wheezing, and spu- tum. Marijuana smoking reduces lung function in ways suggesting that chronic obstructive pulmonary disease (COPD) might develop if a person smokes four or five marijuana cigarettes daily for 30 years (with a lesser amount needed if a person also smokes tobacco). Certain kinds of lung dam-

Marijuana 243

age have been seen in marijuana smokers but not in tobacco smokers. Mari- juana smokers typically use big puffs and deep inhalations, held for a long period of time. Such a technique deposits larger quantities of damaging ma- terials in lungs than the ordinary tobacco-smoking technique. Efforts to doc- ument lesser-known health risks have been flawed or outright unsuccessful. Reports of physical disease in marijuana users often fail to account for other possible (and perhaps more likely) causes.

Despite conceivable health hazards from marijuana, it seems safe in mod- eration, no more dangerous than many foods (such as items high in sugar, salt, fat, and cholesterol). The natural product is extraordinarily safe from a dosage standpoint.1 No human fatality has been confirmed, although cattle deaths have been reported after consuming bales of dried marijuana.

Abuse factors. Tolerance and dependence have been reported. A marijuana abstinence syndrome is described as including physical and mental tenseness, peevishness, less happiness, and diminished appetite. Such symptoms, how- ever, sound much like the reasons many persons use marijuana. If a chronic headache sufferer reported discomfort when pain relievers were unavailable, that would not be considered evidence of dependence on and withdrawal from pain relievers. Self-administration of a drug by laboratory animals is a traditional sign of addictive potential, but researchers have mixed success in getting animals to self-administer THC.

Drug interactions. Not enough scientific information to report, although it is reasonable to assume interactions could be similar to those occurring with dronabinol.

Cancer. Laboratory tests indicate that marijuana smoke can cause cancer. Oral and lung cancer is reported among marijuana users, although we must remember that typical users also smoke tobacco. One study did find that mar- ijuana, even when tobacco use is accounted for, increases chances of getting head and neck cancer. One of the more impressive studies of marijuana’s cancer-causing potential involved medical records of 64,888 persons and dis- covered that people who used marijuana, whether frequently or infrequently, were in general no more likely to get cancer than anyone else. That study did find evidence, however, that marijuana promotes prostate and cervical cancer. Researchers have found that children are more likely to develop acute non- lymphocytic leukemia if their mothers used marijuana during pregnancy. This is a rare disease; in a population of 1 million children, about 5 will have the affliction. The disease is also associated with pesticide exposure, and investi- gators are uncertain whether pesticide contamination of marijuana is a more important factor than marijuana itself.

Chromosome damage can indicate a potential for development of cancer. Some laboratory and animal experiments indicate marijuana causes chromo- some damage, but a study found human chromosome abnormalities to be about the same in moderate users of marijuana and nonusers. Researchers conducting one human study sent the same samples to two laboratories, but neither lab was able to find chromosome damage attributable to marijuana.

Pregnancy. Normally we think of marijuana as a recreational substance, but some women use it to ease discomforts of pregnancy and childbirth. Mari- juana chemicals pass from a pregnant woman into the fetus. Almost all re-

244 Marijuana

search finds no evidence that marijuana causes human birth defects. A study examining infants of adolescent mothers who used marijuana during preg- nancy noted some “minor” birth defects, but even these researchers did not conclude that marijuana was necessarily the cause. Studies of newborns’ birth- weights have been inconclusive about an impact from prenatal marijuana ex- posure. No major effect on muscular coordination and balance turned up in an examination of preschool children having prenatal marijuana exposure, but investigators cautioned that the tests lacked measures of subtle skills. Behavior problems have been reported among children who had prenatal marijuana exposure, but we do not know whether those problems were caused by mar- ijuana or by years of exposure to a particular type of parent. Investigators watching development of children up to age 5 found no difference attributable to maternal marijuana use during pregnancy; differences existed but were ascribed to home environment and schooling. Examination of reading and language abilities in children aged 9 to 12 years found no significant impact from prenatal marijuana exposure. Some researchers believe they have found problems caused by prenatal marijuana, but most research is consistent with marijuana being benign.

Marijuana’s THC passes into human milk, and researchers report deficient development of muscle and limb coordination among infants nursed on such milk. One case report noted the THC level in milk was eight times higher than the mother’s blood level.

Additional information. Marijuana and hemp come from different portions of the same plant, Cannabis sativa. Leaves, flowers, and resin are the illegal drug marijuana; the resin is also called hashish. Stalks and seed (if processed so it will not germinate) are the legal commercial product hemp. The terms hemp and marijuana are sometimes used interchangeably, but such use is in- correct. After marijuana was outlawed in the 1930s, hemp raising continued to thrive because law enforcement authorities of the era were familiar with the industry and understood that crops were not entering the illegal drug market even though the plants had leaves and flowers and resin. During World War II the federal government subsidized hemp farming to replace natural fiber supplies cut off by the war. In the 1950s subsidies finally stopped, and the American hemp industry also stopped because it could no longer make money at the unsubsidized world market price.

Some food products contain hemp components and can cause false positives for marijuana in urine drug screen tests. Hemp lotions and creams rubbed on the skin produce marijuana chemicals in urine, but not enough to cause false positives in a drug screen.

“Locoweed” and “stinkweed” are nicknames for both jimson weed and mar- ijuana, but the substances are different.

Additional scientific information may be found in:

Carlson, B.R., and W.H. Edwards. “Human Values and Marijuana Use.” International Journal of the Addictions 25 (1990): 1393–401.

Fried, P., et al. “Current and Former Marijuana Use: Preliminary Findings of a Lon- gitudinal Study of Effects on IQ in Young Adults.” CMAJ: Canadian Medical Association Journal 166 (2002): 887–91.

Marijuana 245

Gruber, A.J., H.G. Pope, and P. Oliva. “Very Long-Term Users of Marijuana in the United States: A Pilot Study.” Substance Use and Misuse 32 (1997): 249–64. Hendin, H., et al. “The Functions of Marijuana Abuse for Adolescents.” American Jour-

nal of Drug and Alcohol Abuse 8, no. 4 (1981–1982): 441–56.
Iversen, L. “Marijuana: The Myths Are Hazardous to Your Health.” Cerebrum 1, no. 2

(1999): 37–49.
Labouvie, E.W. “Alcohol and Marijuana Use in Relation to Adolescent Stress.” Inter-

national Journal of the Addictions 21 (1986): 333–45.
Reilly, D. “Long-Term Cannabis Use: Characteristics of Users in an Australian Rural

Area.” Addiction 93 (1998): 837–46.
Sidney, S., et al. “Marijuana Use and Mortality.” American Journal of Public Health 87

(1997): 585–90.
Solomon, D., ed. The Marihuana Papers. Indianapolis, IN: Bobbs-Merrill, 1966.
Taylor, D.R., et al. “A Longitudinal Study of the Effects of Tobacco and Cannabis

Exposure on Lung Function in Young Adults.” Addiction 97 (2002): 1055–61. Thompson, K.M. “Marijuana Use among Adolescents: Trends, Patterns, and Influ-

ences.” Minerva Pediatrica 53 (2001): 313–23.
U.S. Commission on Marihuana and Drug Abuse. Marihuana, a Signal of Misunderstand-

ing. Washington, DC: Government Printing Office, 1972.
Von Sydow, K., et al. “The Natural Course of Cannabis Use, Abuse and Dependence

over Four Years: A Longitudinal Community Study of Adolescents and Young Adults.” Drug and Alcohol Dependence 64 (2001): 347–61.


1. Decades of studies indicating marijuana’s relative safety when used in moderation include Advisory Committee on Drug Dependence, Cannabis (Wooten Report) (Lon- don: HMSO, 1968); J. Brandt and L.F. Doyle, “Concept Attainment, Tracking, and Shift- ing in Adolescent Polydrug Abusers,” Journal of Nervous and Mental Disease 171 (1938): 559; E.M. Brecher and the Editors of Consumer Reports, Licit and Illicit Drugs: The Consumers Union Report on Narcotics, Stimulants, Depressants, Inhalants, Hallucinogens, and Marijuana—Including Caffeine, Nicotine, and Alcohol (Boston: Little, Brown and Com- pany, 1972), 395; N.Q. Brill and R.L. Christie, “Marihuana Use and Psychosocial Ad- aptation: Follow-up Study of a Collegiate Population,” Archives of General Psychiatry 31 (1974): 713; Commission of Inquiry into the Non-Medical Use of Drugs (Le Dain Com- mission), Interim Report (Toronto, Canada: Addiction Research Foundation of Ontario, 1970); C.M. Culver and F.W. King, “Neuropsychological Assessment of Undergraduate Marihuana and LSD Users,” Archives of General Psychiatry 32 (1974): 707; E. Goode, Drugs in American Society (New York: Alfred A. Knopf, 1972), 56, 59 n. 1; Jaffe, “Drug Addiction and Abuse,” in L.S. Goodman and A. Gilman, The Pharmacological Basis of Therapeutics, 7th ed. (New York: The Macmillan Company, 1955), 560; The Indian Hemp Drugs Commission Report (Silver Spring, MD: Jefferson Press, 1969) (reprint of summary volume); T.H. Mikuriya, “Historical Aspects of Cannabis Sativa in Western Medicine,” New Physician 18 (1969): 905; J.B. Murray, “Marijuana’s Effects on Human Cognitive Functions, Psychomotor Functions, and Personality,” Journal of General Psychology 113 (1986): 29, 40–41; National Commission on Marihuana and Drug Abuse, Marihuana: A Signal of Misunderstanding (Washington, DC: GPO, 1972) (SuDocs Y3.M33/2:2MM33, plus appendix volumes); H.G. Pope, Jr., A.J. Gruber, and D. Yurgelun-Todd, “Residual Neuropsychologic Effects of Cannabis,” Current Psychiatry Reports 3 (2001): 507–12; H.G. Pope, Jr., et al., “Neuropsychological Performance in Long-Term Cannabis Users,” Archives of General Psychiatry 58 (2001): 909–15; J.F. Siler, et al., “Mariajuana Smoking in Panama,” Military Surgeon 73 (1933): 269–80; C. Stark-Adamec, R.E. Adamec, and R.O. Phil, “Experimenter Effects in Marihuana Research: A Note of Caution,” Psycho-

246 Marijuana

logical Reports 51 (1982): 203; D. Solomon, ed., The Marihuana Papers (Indianapolis: Bobbs-Merrill, 1966) (including the classic LaGuardia Committee Report); Swiss Federal Commission for Drug Issues (EKDF), Cannabis Report (1999); G. Teichner, et al., “The Relationship of Neuropsychological Functioning to Measures of Substance Use in an Adolescent Drug Abusing Sample,” International Journal of Neuroscience 104 (2000):113– 24; A.S. Trebach, The Great Drug War and Radical Proposals That Could Make America Safe Again (New York: Macmillan Publishing Company, 1987), 81; J.T. Ungerleider and T. Andrysiak, “Bias and the Cannabis Researcher,” Journal of Clinical Pharmacology 21 (1981): 153 S-85 S; United Kingdom House of Commons, Cannabis, Library Research Paper 00/74 (2000); A. Weil, The Natural Mind: An Investigation of Drugs and the Higher Consciousness, Rev. ed. (Boston: Houghton Mifflin Company, 1986), 47; A. Weil, N.E. Zinberg, and J.M. Nelsen, “Clinical and Psychological Effects of Marihuana in Man,” Science 162 (1968): 1234–42; R.C. Wert and M.L. Raulin, “The Chronic Cerebral Effects of Cannabis Use. I. Methodological Issues and Neurological Findings,” International Journal of the Addictions 21 (1986): 602–28; R.C. Wert and M.L. Raulin, “The Chronic Cerebral Effects of Cannabis Use. II. Psychological Findings and Conclusions,” Inter- national Journal of the Addictions 21 (1986): 629–42.


Pronunciation: MA-zin-doll (also pronounced MAYZ-in-dohl) Chemical Abstracts Service Registry Number: 22232-71-9 Formal Names: Mazanor, Sanorex, Teronac
Type: Stimulant (anorectic class). See page 15

Federal Schedule Listing: Schedule IV (DEA no. 1605) USA Availability: Prescription
Pregnancy Category: C

Uses. Mazindol reduces appetite, and the drug’s main medical usage is short-term promotion of weight loss. For that purpose one study showed ma- zindol having about 10% to 20% of dextroamphetamine’s strength; another study noted that regardless of relative strength per milligram, patients on mazindol shed about twice as many pounds as those on dextroamphetamine. In studies examining diet drugs, persons using mazindol lost as many or even more pounds compared to persons using phenmetrazine. One 12-week ex- periment found mazindol considerably more effective than diethylpropion for human weight loss, although a rat study found those two drugs’ effectiveness comparable. Some human studies put mazindol as about equal to fenflura- mine for weight loss. Still other studies call mazindol’s performance the same as a placebo. Perhaps these various findings are less a commentary on mazin- dol than on the unclear effectiveness of diet drugs in general.

Although mazindol appears to produce depression among some users, in others the drug works as an antidepressant. This antidepressant characteristic is considered helpful in promoting weight loss, as some overweight persons use food to compensate for sadness. As one condition improves, generally the other one does also. Mazindol’s dual action as an anorectic and antidepressant can make it especially appropriate for persons struggling to lose both mel- ancholy and weight.

Some mazindol effects are like those of amphetamine, but the two sub- stances are described as chemically unrelated. Mazindol seems to pep up rats. In rat experiments the drug increases tendency to move around, more in fe- males than in males. In humans the compound is used to combat narcolepsy and the decline of muscle tone sometimes associated with that affliction. Ma- zindol acts as a pain reliever in mice. One study found the drug made humans more sensitive to pain, but other experimental usage reduced pain in terminal

248 Mazindol

cancer patients. Researchers believe mazindol can aid sufferers from Parkin- son’s disease. A case is reported of the drug acting as an aphrodisiac in a human female. The compound can reduce cholesterol levels.

Drawbacks. Mazindol increases pulse rate, may cause hallucinations, and disrupts sleep. In one study users complained of headache, skin rash, dry mouth, perspiration, tremor in heart and other muscles, nausea, and difficult urination and bowel movements. Users also report being wired, edgy, and dizzy. In human males mazindol can make the testes painful, interfere with erection and ejaculation, and cause urine retention. The latter effect has been exploited to treat incontinence. Mazindol may interfere with production of human growth hormone, a consideration when juveniles take the drug. When tested as a treatment for schizophrenia the drug at best had no effect and even worsened some symptoms. A medical journal article published in 2000 linked mazindol to pulmonary hypertension, the first time such an association was reported. Earlier reports noted development of heart disorder after taking ma- zindol in combination with fenfluramine or dexfenfluramine, but such afflic- tion has been attributed to those latter two drugs by themselves, so mazindol’s role is uncertain.

Abuse factors. In rhesus monkey experiments the animals show a liking for mazindol, but a review of clinical studies found no instances of patients be- coming addicted. Although reports exist of mazindol inducing euphoria, hu- man users show no particular liking for the drug. Volunteers comparing several diet drugs found mazindol to have the least appeal by far. Scientists evaluating another experimental study of the drug described it as a “punisher” that persons wanted to avoid.

Drug interactions. Researchers say mazindol and alcohol have a multiplier effect when used together, boosting each other’s potency and producing an extra buzz for recreational users. Mazindol interferes with some cocaine ef- fects, but studies examining mazindol’s potential for treating cocaine addiction find a placebo to be about as good. One study even found the two drugs to have a hazardous multiplier effect raising blood pressure and pulse rate, and rat experiments find that mazindol reduces the size of a cocaine dose needed to cause death. Mazindol can react adversely with antimania drug lithium and can counteract drugs intended to lower blood pressure.

Cancer. Laboratory experiments show mazindol promoting cell mutations and chromosome breaks (traditional signs of cancer-causing potential), but that finding’s real-life meaning is unclear.

Pregnancy. The drug’s influence on fetal development is unestablished. Whether the drug passes into milk of nursing mothers is unknown. Doses that kill female rats while pregnant or after giving birth can leave males and non- pregnant females unscathed. Whether such findings mean that pregnancy in- creases human sensitivity to the drug is unknown.

Additional scientific information may be found in:

Alvarez, B., et al. “Mazindol in Long-Term Treatment of Narcolepsy.” Lancet 337 (1991): 1293–94.

Bierger, P., F. Gawin, and T.R. Kosten. “Treatment of Cocaine Abuse with Mazindol.” Lancet 1 (1989): 283.

Mazindol 249

Chait, L.D., E.H. Uhlenhuth, and C.E. Johanson. “Reinforcing and Subjective Effects of Several Anorectics in Normal Human Volunteers.” Journal of Pharmacology and Experimental Therapeutics 242 (1987): 777–83.

Hagiwara, M., et al. “Delayed Onset of Pulmonary Hypertension Associated with an Appetite Suppressant, Mazindol: A Case Report.” Japanese Circulation Journal 64 (2000): 218–21.

Preston, K.L., et al. “Effects of Cocaine Alone and in Combination with Mazindol in Human Cocaine Abusers.” Journal of Pharmacology and Experimental Therapeutics 267 (1993): 296–307.


Pronunciation: em-dee-a ̄

Chemical Abstracts Service Registry Number: 4764-17-4

Formal Names: Amphedoxamine, 3,4-Methylenedioxyamphetamine

Informal Names: Chocolate Mescaline, Hug Drug, Love, Love Pill, Mellow Drug of America

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7402) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This drug is a derivative of amphetamine and an analog to MDMA, with effects similar to the latter and to MDEA. MDA is stronger than those two hallucinogens. Researchers also report it to be three to five times stronger than mescaline, to which it is chemically related. MDA is legally defined as a hallucinogen, but its stimulant qualities put it in the entactogen pharmaco- logical class—a type of drug with both stimulant and hallucinogenic qualities. MDA is an illicit drug designer’s delight; by the 1970s thousands of offshoots had been made.

First produced in a laboratory in 1910, MDA was intended to help people lose weight. One authority believes the drug has potential for stopping allergic reactions to a variety of allergens. As the 1960s arrived the drug had been patented as a cough suppressant and as a tranquilizer, but MDA never went into legal commercial manufacture.

Reports of MDA’s psychological effects date back to the 1930s, but not until three decades later did the substance become a recreational drug. It has the capability to change how a person views time and space. While under the influence a user’s hearing and sense of touch can become more sensitive, and a person’s sense of identity can alter. Emotions and caring about other persons can intensify, as can ability to communicate feelings. Such aspects allowed MDA to find a niche in psychotherapy as well as on the street. Strong doses can bring on hallucinations, with experiences so similar to LSD and mescaline that users cannot tell whether they were dosed with the latter drugs or with MDA.

Drawbacks. MDA raises heart rate, blood pressure, body temperature, and salivation. The substance can cause nausea, along with high acid levels in

MDA 251

blood. Although one authority notes that the drug can relax muscles, none- theless tremors and seizures are also possible; MDA is known to worsen Par- kinson’s disease. MDA can tense up jaw muscles and cause grinding of teeth. As drug effects go away, users may experience weariness and muscle aches accompanied by depression. Users coming off the drug may also be short- tempered, suspicious of others, and nervous. Typically the effects desired by a user decline with repeated use of the drug, while undesired postintoxication effects increase. MDA can cause organic brain damage in rats, in some aspects worse than what MDMA does.

Overdose symptoms resemble those of amphetamine and MDMA, including massive perspiration and strange conduct prone to combativeness. The per- centage of fatalities among abusers is small, but the size difference between a recreational dose and a serious overdose can vary tremendously between in- dividuals. What one person can tolerate without apparent ill effect can send another person to a hospital. Blood and urine tests in one fatal overdose case showed only MDA, demonstrating that this drug can be lethal even when it is not part of a polydrug abuse mix.

Men may suffer fewer ill effects from MDA than women do. In one animal study documenting a gender difference in effects, male rats showed a higher body temperature increase than female rats did, but blood levels of MDA stayed higher in the female.

Abuse factors. Not enough scientific information to report about tolerance, dependence, or withdrawal. In animal experiments self-administration is a traditional sign of addictive potential; rats show mild interest in self- administration of MDA.

Drug interactions. Animal experiments suggest that taking certain drugs along with MDA can reduce its toxicity.

Cancer. MDA causes cancer in mice and rats, with males being more sus- ceptible than females.

Pregnancy. Not enough scientific information to report.

Additional information. At one time MDA was nicknamed Ecstasy, but that street name was later transferred to MDMA. An industrial chemical called MDA (methylene dianiline) is not the drug of abuse.

Additional scientific information may be found in:

Climko, R.P., et al. “Ecstacy: A Review of MDMA and MDA.” International Journal of Psychiatry in Medicine 16 (1986–1987): 359–72.

Hegadoren, K.M., G.B. Baker, and M. Bourin. “3,4-Methylenedioxy Analogues of Am- phetamine: Defining the Risks to Humans.” Neuroscience and Biobehavioral Re- views 23 (1999): 539–53.

Poklis, A., M.A. Mackell, and W.K. Drake. “Fatal Intoxication from 3,4-Methylenediox- yamphetamine.” Journal of Forensic Sciences 24 (1979): 70–75.

Richards, R.N. “Experience with MDA.” Canadian Medical Association Journal 106 (1972): 256–59.

Richards, K.C., and H.H. Borgstedt. “Near Fatal Reaction to Ingestion of the Hallu- cinogenic Drug MDA.” Journal of the American Medical Association 218 (1971): 1826–27.


Pronunciation: em-dee-ee-a ̄
Chemical Abstracts Service Registry Number: 82801-81-8 Formal Names: 3,4-Methylenedioxyethylamphetamine, MDE Informal Names: Eve, Intellect
Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7404)
USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This substance is related to MDA, MDMA, amphetamine, and meth- amphetamine. Drug laws call MDEA a hallucinogen, but it has stimulant ef- fects also. Those dual properties put it in the entactogen pharmacological group, a type of drug with both stimulant and hallucinogenic qualities. Effects are similar to those from MDA and MDMA.

MDEA can create contentedness and feelings of intimacy with other per- sons. It may promote self-insight, gesturing, and articulate talking. Halluci- nations can occur, described as less intense than those brought on by psilocybin. Volunteers had normal results in tests of numerical ability while using MDEA, indicating that people can force themselves to overcome at least some of the drug’s effects if necessary. Even though users feel more relaxed after taking the substance, it has general stimulant effects—raising the pulse rate, blood pressure, and body temperature. It also elevates the level of cor- tisol, a hormone that increases blood sugar.

Drawbacks. Apparently MDEA inhibits secretion of human growth hor- mone. The drug disrupts sleep and dreaming. Psychosis is possible. In exper- iments with normal volunteers a minority had mental aftereffects including nervousness and discontent.

Some researchers describe MDEA as less toxic than MDMA, but damage is still possible to kidneys, liver, brain, and heart. Persons with heart disease may be in particular danger from MDEA. Overdose symptoms include hal- lucinations, excessive body temperature, massive perspiration, violent con- duct, muscle spasms, difficulty moving arms and legs, convulsions, distress in breathing, and passing out. Fatalities have shown blood clots throughout the body and damage to skeletal muscle. Although deaths from “normal”

MDEA 253

doses are unlikely among healthy users, the same dose can have stronger effects on some users than on others.

In rat experiments comparing the strength of MDMA to MDEA, about twice as much MDEA is needed to induce excessive body temperature and about four times as much to cause one kind of organic brain damage. The experi- menters note, however, that these findings do not extrapolate well to humans because people might take greater doses of MDEA than MDMA to get the desired psychological effects, so any net difference in harm to abusers may be nil despite difference in drug potency.

Abuse factors. Not enough scientific information to report about tolerance, dependence, withdrawal, or addiction.

Drug interactions. Medical investigators suspect that heroin and MDEA counteract each other’s effects in humans.

Cancer. Not enough scientific information to report. Pregnancy. Not enough scientific information to report. Additional scientific information may be found in:

Gouzoulis, E., et al. “Neuroendocrine and Cardiovascular Effects of MDE in Healthy Volunteers.” Neuropsychopharmacology 8 (1993): 187–93.

Gouzoulis-Mayfrank, E., et al. “Psychopathological, Neuroendocrine and Autonomic Effects of 3,4-Methylenedioxyethylamphetamine (MDE), Psilocybin and D- Methamphetamine in Healthy Volunteers. Results of an Experimental Double- Blind Placebo-Controlled Study.” Psychopharmacology 142 (1999): 41–50.

Hegadoren, K.M., G.B. Baker, and M. Bourin. “3,4-Methylenedioxy Analogues of Am- phetamine: Defining the Risks to Humans.” Neuroscience and Biobehavioral Re- views 23 (1999): 539–53.

Hermle, L., et al. “Psychological Effects of MDE in Normal Subjects. Are Entacto- gens a New Class of Psychoactive Agents?” Neuropsychopharmacology 8 (1993): 171–76.


Pronunciation: em-dee-em-a ̄

Chemical Abstracts Service Registry Number: 42542-10-9

Formal Names: Methylenedioxymethamphetamine, 3,4-Methylenedioxymetham- phetamine

Informal Names: A, Adam, Baby Slits, B-Bomb, Bens, Benzedrine, Biphetamine, Blue Kisses, Blue Lips, California Sunrise, Chrystal Methadrine, Clarity, Cristal, Debs, Decadence, Dex, Dexedrine, Diamonds, Disco Biscuit, Doctor, Dolls, Domex, Draf, Drivers, E, E-Ball, E-Bomb, Ecstasy, Ekies, Elaine, Essence, Eu- phoria (combined with mescaline and methamphetamine), Everclear, Fastin, Gaggler, Go, Greenies, Hamburger, H-Bomb (with heroin), Honey Flip (with 2C-B), Hug Drug, Hydro, Iboga, Ice, Khat, Kleenex, Love Doctor, Love Drug, Love Potion Number 9, Lovers’ Speed, Love Doves, Love Trip (with mescaline), Lucky Charmz, M&M, MAO, MDM, Methedrine, Mini Beans, Mitsubishi, Molly, Monoamine Oxidase, Morning Shot, M25, New Yorkers, 19, Number 9, Orbit, Pikachu (mixed with PCP), Pink Studs, Pollutants, Rave, Road Runner, Rolling, Running, Scooby Snacks, Shabu, Slamming, Spivias, Strawberry Shortcake, Sweeties, 10, USP, Venus, Vitamin E, West Coast Turnarounds, Wheels, Whif- fledust, White Dove, Whiz Bombs, Wigits, X, XTC, Yuppie Drug, Zen

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7405) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. MDMA was discovered and patented in Europe as World War I be- gan, intended to make soldiers feel less hungry. In civilian usage the drug was supposed to help people lose weight, but other effects portended the product’s commercial failure, and it never went on the market. Those other effects attracted attention in the 1960s and 1970s among therapists and rec- reational drug users alike.

MDMA intensifies sensory sensations (taste, touch, etc.), alters old under- standings of what people observe, and allows people to feel distant from themselves. Some users experience self-insights and closer emotional attach- ment to other persons. Generally the drug does not appear to act as an aph- rodisiac, but users report enhanced sexual experiences while under the influence. In therapeutic doses, which may be lighter than those taken by

MDMA 255

recreational abusers, effects occur without hallucinations and without causing apparent mental cloudiness while intoxicated. Before being banned by the U.S. Drug Enforcement Administration (DEA), doses were given to encourage pa- tients to participate more freely in psychotherapy discussions—a usefulness that still found advocates in the 1990s—and to facilitate understandings among patients, understandings that helped reduce their problems. Under- ground knowledge of psychiatric usage persists despite an absolute legal pro- hibition against using the compound: Medical literature reports someone illegally taking the drug for self-medication of posttraumatic stress disorder.

In the history of abused drugs, psychological benefits claimed by propo- nents have often been deflated by scientific investigation. MDMA is no excep- tion. Psychological tests have compared polydrug users who have or have not taken MDMA and also persons who have abstained from any illicit drug. These tests find no difference among these groups in anger, anxiety, or mood. Whatever feelings of peacefulness that recreational MDMA users experience while intoxicated, those results do not seem to persist afterward. Indeed, ex- perimenters who gave these tests found the MDMA group to have more psy- chological trouble than the nondrug group. In such findings a key question is whether the drug caused psychic problems or whether problems caused the drug use. Staff members at a Spanish hospital’s psychiatric service reviewed a substantial amount of medical literature about MDMA users and observed that the case reports did not sustain a conclusion that MDMA was the primary cause of users’ psychiatric problems.

One significant exception exists in findings about MDMA’s limited value in promoting personal insight and healthy integration with the world. That ex- ception comes with persons using the drug for spiritual purposes rather than recreationally. Here the all-important influence of set and setting are dem- onstrated. Spiritual users tune in to certain kinds of psychic effect promoted by the drug and apparently are able to focus their attention so intensely that they can disregard and be unaffected by psychological effects that trouble recreational abusers. This situation appears to demonstrate a principle familiar to historians of drug use, who find that a substance can be beneficial in a particular cultural context and yet have catastrophic consequences when used by someone who disregards that context. Any spiritual purpose for which MDMA may be used will, of course, have no impact on the drug’s physical actions, although persons who seldom use it may be spared various hazards documented by scientists.

MDMA is legally classified as a hallucinogen, but it is pharmacologically classified as an entactogen—a type of drug with both stimulant and hallucin- ogenic qualities. MDMA is recreationally used more for its hallucinogenic ac- tions than for stimulant actions. It is an analog to MDA and related to MDEA, amphetamine, methamphetamine, and mescaline. MDMA is described as mellower than MDA, and some users experience MDMA as less potent than mescaline. MDMA can alter perceptions of time and space and induce feelings of peacefulness. Users typically understand that MDMA hallucinations (such as floating in midair or seeing geometrical designs) are unreal; users normally do not undergo a temporary psychosis in which the sensations are misper- ceived as objective reality.

256 MDMA

After recreational use became publicized, MDMA was made a Schedule I controlled substance. Despite that ban, during the 1990s MDMA was popular at high-energy all-night rave dance parties, not only for psychic actions but for enabling people to go without sleep, food, and drink while physically exerting themselves. A person using MDMA in that way will likely feel com- plete exhaustion when the drug experience ends. The compound reduces pain and promotes talkativeness, factors that might be appealing at raves.

The Drug Abuse Warning Network (DAWN) tracks “mentions” of illicit drugs in hospital emergency room cases. A “mention” means that examination of a patient showed traces of a drug, not that the drug caused injury. DAWN thereby helps track a drug’s popularity. In 1993 MDMA had 196 DAWN men- tions; in 1998 the total was 143,600. As the twenty-first century began, the DEA reported 750,000 doses being consumed each week in just the New Jersey and New York City areas.

Drawbacks. Scientific literature portrays MDMA as a drug of extremes, pro- ducing pleasures and afflictions that either enrapture or kill users. Compared to many other drugs, much more is known about MDMA’s hazards simply because so many persons have used it and received medical aid when things went badly. The volume of medical emergencies, however, is more than just a statistical phenomenon caused by sheer numbers of users. Some drugs used even more widely do not generate nearly as many medical complaints. MDMA really is more dangerous than many other substances.

One problem in evaluating MDMA dangers, a problem openly acknowl- edged by some scientists, is the challenge of confirming that a sick person indeed ingested MDMA a month ago rather than a fake substitute. All sorts of substances can produce effects similar to those of MDMA, which is why illicit dealers can so easily sell fake merchandise. Nonetheless, researchers in- vestigating drug actions can often enough verify that MDMA is the actual substance. The following information reflects the scientific consensus about MDMA.

It has the physical and mental actions typical of amphetamine. A group of persons who at one time or another used amphetamine, LSD, and MDMA said they felt most pepped-up with amphetamine, least so with LSD, but had the greatest euphoria and contentedness with MDMA. Another group com- paring amphetamine and MDMA reported MDMA to have fewer drawbacks. The DEA considers the drug less addictive than cocaine or heroin.

The substance degrades thinking processes. In tests of alertness, memory, learning, and intelligence a group of marijuana users performed as well as nonusers of marijuana, while a group that had used both marijuana and MDMA did worse. MDMA causes persistent and even permanent organic changes in the brain. Grand mal brain seizures have been attributed to the substance. Brain damage observed in MDMA users is consistent and is related to how much drug has been used (size of dose and frequency with which the drug is taken). Psychological tests verify that persons with such damage have trouble remembering things that are seen and heard, although the brain dam- age has not been proven to cause the memory difficulty. Whatever the precise cause, in memory tests polydrug users who have taken MDMA do worse than those who have never taken the compound. Evidence exists that MDMA re-

MDMA 257

duces attention span and interferes with reasoning. The drug produces brain injury suspected of increasing someone’s impulsiveness. In tests comparing polydrug users who have used MDMA with those who have not, MDMA users show increased impulsiveness correlating with how much they have used the drug. Interviews comparing polydrug users find the MDMA group more prone to paranoia, to physical complaints lacking any apparent bodily cause, to nervousness and unfriendliness, to phobias, and to obsessing on various things. Panic disorder with agoraphobia (fear of open spaces) can occur.

MDMA has various influences on blood. The drug is suspected of causing anemia. Under the influence of MDMA, blood components may block vessels, having the effect of tiny clots that can cause internal bleeding, evidenced by purple spots on the skin. Blood clots in the brain and death of cerebral tissue have been credited to MDMA. Autopsies have shown massive blood clotting throughout organs, accompanied by skeletal muscle deterioration.

Many other hazards exist. MDMA increases body temperature, sometimes enough to mimic heat stroke, and animal experiments indicate that tempera- tures in surroundings or inside the body can affect the amount of brain dam- age caused by MDMA. The drug boosts pulse rate. Initially a dose increases blood pressure (sometimes enough to burst vessels in the brain), but later, as the effects of a dose proceed, blood pressure falls below the user’s original reading (a decline that can promote fainting). MDMA can create heart mal- function, kidney failure, and liver disease. Liver cirrhosis and failure can re- sult—sometimes treatable, sometimes fatal. Cramps and muscle tics have been observed, even including one case where Parkinson’s disease developed. Cases are reported of MDMA causing pneumomediastinum, an ailment in- volving severe breathing difficulty. The drug promotes nausea. Hazy eyesight and a case of temporary double vision caused by MDMA have been reported. Jaw clenching and grinding after taking the drug result in excessive tooth wear; one study of teeth in MDMA users found enamel completely worn away from some areas, an affliction seen far less often in people who did not use the drug. MDMA can cause skin rash and pimples.

Gender difference in drug effect is possible. One survey of case reports noted that men tended to use more MDMA than women did, and an exper- iment found that at any given dose the drug seemed to harm verbal memory more in men than in women. Another experiment showed male users having more change in two measures of brain chemistry function than females did. An experiment with rats showed males maintaining higher blood levels of the drug than females did, while females experienced more increase in body tem- perature than male rats did.

Abuse factors. In a survey of 100 American university students, two thirds said that desirable actions declined and undesirable ones increased as MDMA use continued; similar results came from a survey of 100 users in Australia, and scientists studying the drug concur with those survey findings. As with other potent stimulants, abusers are known to use MDMA in binges, taking one dose after another before the previous ones wear off. Heavy MDMA users have scored low in measures of harm avoidance, and MDMA use correlates with unprotected male homosexual conduct. Such findings raise the question

258 MDMA

of cause and effect: Does MDMA promote reckless behavior, or are self- destructive users simply indifferent about all sorts of life hazards, of which MDMA is only one?

Flashbacks are reported, with case reports mentioning time lengths ranging from less than one minute to two hours.

Drug interactions. Taking MDMA together with the drug saquinavir (used against human immunodeficiency virus [HIV] in AIDS [acquired immuno- deficiency syndrome]) may be dangerous; usage with the HIV/AIDS drug ritonavir can be fatal. Untoward reaction with the antidepressant fluoxetine (Prozac) is suspected, and reaction with the antidepressant phenelzine sulfate (a monoamine oxidase inhibitor—MAOI) can produce excessive blood pres- sure, heavy sweating, muscle tics, and rigidity. Such perils are quite possible with any other MAOI. Keeping in mind the need to be cautious about extrap- olating animal experiments to humans, we can note that taking MDMA with LSD (candyflipping) produces a multiplier effect intensifying MDMA actions in rats. Chloral hydrate permits some MDMA action in rats while reducing subsequent organic brain change. Also in rats MDMA boosts pain relief pro- vided by morphine. In male rats the malaria and heart drug quinidine can increase MDMA’s tendency to raise body temperature. Alcohol allegedly re- duces some effects sought by MDMA users, but that belief has not received general scientific sanction. Scientists have confirmed that alcohol increases MDMA’s reduction of immune system function, which may increase risk of infections. Physicians treating MDMA overdose find that water can worsen dangerous effects, and these doctors have concluded that people should not drink much liquid of any sort while using the drug (hard advice for sweaty and overheated dancers).

Cancer. Not enough scientific information to report.

Pregnancy. Scientists who studied what happened with 49 women who used MDMA while pregnant were unable to reach any conclusions about in- fluence on fetal development. The researchers did conclude that the women’s lifestyles routinely included assorted factors perilous to achieving healthy off- spring—tobacco smoking, consuming alcohol to excess, unwanted pregnancy. A study of 136 women who used MDMA while pregnant noted an incidence of birth defects much higher than normal (15.4% versus normal 2% or 3%), but the usual confounding factors, such as polydrug abuse and unwanted pregnancy, hindered conclusions about effect on fetal development. Rat ex- periments confirm maternal brain damage but have not found brain damage in offspring even though their behavior differs in some respects from rats whose mothers receive no MDMA during pregnancy. An experiment with chickens found no MDMA effect on measured aspects of embryo develop- ment.

Additional information. “Benzedrine,” “biphetamine,” “dexedrine,” “iboga” (ibogaine), and “khat” are nicknames for MDMA, but none of those substances is MDMA.

Additional scientific information may be found in:

Downing, Joseph. “The Psychological and Physiological Effects of MDMA on Normal Volunteers.” Journal of Psychoactive Drugs 18 (1986): 335–39.

MDMA 259

Gouzoulis-Mayfrank, E., et al. “Impaired Cognitive Performance in Drug Free Users of Recreational Ecstasy (MDMA).” Journal of Neurology, Neurosurgery, and Psy- chiatry 68 (2000): 719–25.

Greer, G., and R. Tolbert. “Subjective Reports of the Effects of MDMA in a Clinical Setting.” Journal of Psychoactive Drugs 18 (1986): 319–27.

McGuire, P. “Long Term Psychiatric and Cognitive Effects of MDMA Use.” Toxicology Letters 112–13 (2000): 153–56.

Rochester, J.A., and J.T. Kirchner. “Ecstasy (3,4-Methylenedioxymethamphetamine): History, Neurochemistry, and Toxicology.” Journal of the American Board of Family Practice 12 (1999): 137–42.

Shulgin, A.T. “The Background and Chemistry of MDMA.” Journal of Psychoactive Drugs 18 (1986): 291–304.

Vollenweider, F.X., et al. “Psychological and Cardiovascular Effects and Short-term Sequelae of MDMA (“Ecstasy”) in MDMA-Naive Healthy Volunteers.” Neuro- psychopharmacology 19 (1998): 241–51.


Pronunciation: me-PER-i-deen
Chemical Abstracts Service Registry Number: 57-42-1. (Hydrochloride form 50-


Formal Names: Centralgin, Demer-Idine, Demerol, Dolantin, Dolosal, Mepergan, Pethidine, Pethoid

Informal Names: Demmies
Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II (DEA no. 9230) USA Availability: Prescription
Pregnancy Category: B

Uses. This drug has been used since the 1930s for easing pain in many conditions, including migraine headaches, surgery, gallbladder attack, sickle cell anemia crisis, childbirth, and emergency treatment of injury on moun- taineering expeditions. The drug is also used to manage porphyria, a body chemistry disorder that can make a person extremely sensitive to light and that can include violent outbursts. The substance is used to bring persons out of a PCP psychosis. Experimental usage of meperidine and dextroampheta- mine together has reduced symptoms of mental depression, but the test was too brief to measure how long benefits might continue. Oral meperidine dos- age can partly numb a person’s mucous membranes, and the drug is used as one element of general and local anesthesia. The substance has a calming action but is not considered to be a sleep inducer at medical dosage levels. Upon prolonged usage the calming action can be replaced by depression and uneasiness. Depending on specifics of use, morphine is 6 to 10 times stronger than meperidine.

Drawbacks. Meperidine can reduce blood pressure and can make a person feel faint upon suddenly standing up. Itching, perspiration, muscle tremors, nausea, and vomiting are other unwanted effects. Although constipation is a classic unwanted action of opiates/opioids, meperidine may produce less than morphine does. Meperidine can cause cardiac and breathing difficulty and has been known to cause seizures, delirium, and hallucinations. The drug may promote convulsions in persons who are already susceptible to such affliction. Some tests show the drug to have slight influence on eye-hand coordination and no effect on other voluntary physical movement. Tests oriented specifi-

Meperidine 261

cally toward driving skills, however, led researchers to conclude that people should not operate a motor vehicle for 24 hours after an intramuscular injec- tion of meperidine. Anyone with enlarged prostate, urinary difficulty, Addi- son’s disease, or underactive thyroid should be wary about using the drug. An unusual case report tells of a patient developing Parkinson’s disease symp- toms from meperidine; more commonly such reports arise from contaminated illicit substances related to meperidine. Another illicit peril occurs when per- sons grind up and inject oral meperidine tablets; the talc in those tablets can block tiny blood vessels throughout the body and also cause those vessels to bleed—serious business in the eyes or brain. Illicit intramuscular injection of the drug over a period of years can cause muscle damage. Injecting into an artery can lead to gangrene.

Abuse factors. Meperidine tolerance occurs. Dependence may develop faster than with morphine, but meperidine’s withdrawal syndrome may be briefer; symptoms also tend to be more limited than with morphine, perhaps just muscle spasms and unrest. When medical personnel are withdrawing addicts from heroin, meperidine has enough cross-tolerance to control withdrawal symptoms.

Drug interactions. Meperidine should be avoided by persons taking mon- oamine oxidase inhibitors (MAOIs, found in some antidepressants). That com- bination can be dangerous or even fatal. Alcohol and other depressants should be used carefully with meperidine in order to avoid cumulative overdose. Amphetamines boost pain relief provided by meperidine. The HIV/AIDS (hu- man immunodeficiency virus/acquired immunodeficiency syndrome) drug ri- tonavir is believed to lengthen a meperidine dose, meaning that too much of the opioid could build up in a person who is on a normal meperidine medi- cation schedule. Experiments with the ritonavir-meperidine combination, however, have shown the risk to be less than expected. Air pressure affects a meperidine dose; the higher the altitude, the longer a dose lasts. Phenobar- bital, the antipsychotic drug chlorpromazine (Thorazine), and the heartburn- ulcer medicine cimetidine interfere with meperidine. Brewer’s yeast is said to produce a bad reaction with meperidine, such as raising blood pressure so high that a medical emergency occurs.

Cancer. One analysis of medical records in Great Britain found a statistical association between receiving meperidine at birth and subsequent develop- ment of childhood cancer. A statistical association, however, simply provides guidance for future research and does not demonstrate cause and effect. Anal- ysis of a different and smaller set of records found no association.

Pregnancy. An experiment on pregnant mice produced no birth defects def- initely attributable to the drug, but meperidine has caused congenital malfor- mations in hamsters. Medical records from a few dozen women who used meperidine during pregnancy revealed no congenital malformations attrib- utable to the substance. If a pregnant woman takes the drug, it will pass into the fetus, where the substance tends to build up. Difficulties have not been seen in infants from such women unless the drug has been administered dur- ing childbirth. In those latter cases a respiratory emergency can occur in in- fants who acquired the drug during birth, and less serious newborn behavioral abnormalities are common. Rhesus monkeys who received fetal exposure at

262 Meperidine

time of birth were tested for perception and thinking ability. On one test they did worse than monkeys who had no meperidine exposure, and on another test they did better. In humans, meperidine enters the milk of nursing moth- ers, but the level is low enough to be considered safe for the infant.

Additional information. An injectable format of the drug called Mepergan is intended for deep intramuscular administration. Intravenous injection can diminish breathing and stop the heart. Subcutaneous administration can cause sores at the injection site and even kill patches of skin. The product ingredients include sodium metabisulfite, to which some persons have a dangerous al- lergy. Mepergan is to be used cautiously by asthmatics.

Additional scientific information may be found in:

Clark, R.F., E.M. Wei, and P.O. Anderson. “Meperidine: Therapeutic Use and Toxicity.” The Journal of Emergency Medicine 13 (1995): 797–802.

Henderson, M.E. “Central Nervous System Effects of Meperidine.” Hospital Pharmacy 20 (1985): 934.

Korttila, K., and M. Linnoila. “Psychomotor Skills Related to Driving after Intramus- cular Administration of Diazepam and Meperidine.” Anesthesiology 42 (1975): 685–91.

Miller, R.R., and H. Jick. “Clinical Effects of Meperidine in Hospitalized Medical Pa- tients.” Journal of Clinical Pharmacology 18 (1978): 180–89.

Zacny, J.P., et al. “Subjective, Behavioral and Physiological Responses to Intravenous Meperidine in Healthy Volunteers.” Psychopharmacology 111 (1993): 306–14.


Pronunciation: mef-oh-BAR-bi-tal
Chemical Abstracts Service Registry Number: 115-38-8
Formal Names: Mebaral, Methylphenobarbital, Methylphenobarbitone Type: Depressant (barbiturate class). See page 20
Federal Schedule Listing: Schedule IV (DEA no. 2250)
USA Availability: Prescription
Pregnancy Category: D

Uses. Mephobarbital has both sedative and anticonvulsant effects. Anticon- vulsant properties make the drug a standard treatment for epilepsy. When used for that condition, stoppage of the drug must be handled carefully lest a person start having a streak of seizures one after another (a potentially fatal condition called status epilepticus). Sedative qualities make mephobarbital an effective tranquilizer, with users feeling lighthearted and mellow without get- ting very sleepy. Men metabolize the drug faster than women do, meaning a dose will last longer in women. After ingestion the drug metabolizes into phenobarbital, which seems to be a more potent sedative. Health care prac- titioners sometimes administer those two drugs together.

Drawbacks. In an experiment comparing mephobarbital to phenobarbital in epileptic children, parents reported fewer unwanted behavioral effects with mephobarbital, and some pediatricians agree with that observation. The most typical behavior problem in such children is hyperactivity. A formal test com- paring the two drugs, however, found no difference in either unwanted con- duct or therapeutic power.

Mephobarbital is to be avoided if a person has porphyria, a disease reflect- ing a body chemistry disorder and in which a person may be harmed by exposure to light. The drug should also be avoided if a person has a muscle- weakening disease called myasthenia gravis, or a thyroid deficiency causing an affliction called myxedema.

Persons using this drug may need extra vitamin D, due to possible defi- ciency that might be caused by faster metabolism of the vitamin.

Abuse factors. Not enough scientific information to report on tolerance, de- pendence, withdrawal, and addiction.

Drug interactions. Taking mephobarbital with acetaminophen (Tylenol and similar products) may promote liver injury. Mephobarbital can interfere with

264 Mephobarbital

effectiveness of birth control pills and with actions of medicines used to con- trol epilepsy and blood clotting. Drugs used to treat asthma, blood pressure, and heart ailment may not work as well if a person also takes mephobarbital.

Cancer. Not enough scientific information to report.

Pregnancy. Additional vitamin K is recommended for pregnant women us- ing mephobarbital as childbirth approaches, in order to reduce bleeding in the women and offspring. Mephobarbital can help reduce fetal pulse rate ir- regularity but has been found to cause birth defects, with the risk malforma- tions increasing if other antiepileptic drugs are also used. The drug is found in breast milk of nursing mothers who use the substance.

Additional scientific information may be found in:

De Haan, J., and L. Stolte. “Drugs and the Fetal Heart Rate.” British Medical Journal 4 (October 16, 1971): 171.

Willis, J., et al. “Barbiturate Anticonvulsants: A Neuropsychological and Quantitative Electroencephalographic Study.” Journal of Child Neurology 12 (1997): 169–71.

Young, R.S., et al. “A Randomized, Double-Blind, Crossover Study of Phenobarbital and Mephobarbital.” Journal of Child Neurology 1 (1986): 361–63.


Pronunciation: meh-proh-BA-mait

Chemical Abstracts Service Registry Number: 57-53-4

Formal Names: Deprol, Equagesic, Equanil, Micrainin, Miltown, Stopayne, Ten- avoid

Informal Names: Mother’s Little Helper
Type: Depressant. See page 19
Federal Schedule Listing: Schedule IV (DEA no. 2820) USA Availability: Prescription
Pregnancy Category: D

Uses. This drug became available in the 1950s as an alternative to barbitu- rates. It works as a sleep aid and muscle relaxant, the latter property perhaps a result of the drug’s antianxiety property rather than a direct effect. Mepro- bamate’s muscle relaxant action improved breathing in experimental treat- ment of tetanus. A person’s appetite may get better with the drug, but again as a result of anxiety reduction rather than direct appetite stimulation—an agricultural experiment using meprobamate to encourage weight gain in chickens was unsuccessful. The drug may lessen petit mal epilepsy seizures but worsen grand mal seizures. Meprobamate has also been used against neu- roses and attention deficit hyperactivity disorder (ADHD), against a type of muscular discomfort called myofascial pain, and as part of therapy treating skin lesions brought on by worry. Meprobamate has helped improve stubborn cases of gastrointestinal afflictions, which may have a component of stress. An experiment showed that persons using the drug can fool a lie detector test.

Meprobamate became perhaps the most highly regarded tranquilizer in the United States. In some research during that era of meprobamate’s popularity the question was no longer whether the drug worked but how much better it worked for some groups of people (married, widowed, overweight) than for others. Nonetheless, meprobamate’s medical uses declined after benzodiaze- pine class depressants became available. In retrospect skepticism arose about whether meprobamate had ever been as beneficial as its reputation indicated. Some experts decided that its muscle relaxant and antianxiety actions were no stronger than those inherent to any sedative. One team of scientific inves- tigators concluded that in some circumstances patients’ therapeutic reactions to meprobamate were “no worse than to placebo”—faint praise indeed. Trans-

266 Meprobamate

formation of the medical establishment’s attitude toward meprobamate is, however, a social history study beyond the scope of this book.

Drawbacks. Meprobamate can cause euphoria and, even though it is a de- pressant, can have stimulant actions in some circumstances—indeed, mania has been known to occur after a dose. Unwanted actions include headache, vision trouble, nausea, diarrhea, dizziness, slurred speech, burning or prick- ling sensations, rashes or other skin outbreaks, severely reduced body tem- perature, low blood pressure, accelerated heartbeat, fainting, and difficulty in moving around. Users should avoid operating dangerous devices such as au- tomobiles. Tests have measured worsened learning ability, physical coordi- nation, and reaction time while a person is under meprobamate’s influence— although such problems are not found with all tests designed to detect them.

During meprobamate’s medical popularity in the 1960s military tests ex- plored the drug’s influence on performance under stress. One test series sim- ulated aircraft pilot situations involving simultaneous tracking of locations in two dimensions, monitoring changes in audio signals, and decoding mes- sages—while exposed to reduced oxygen levels simulating altitudes up to 17,000 feet. In another test series civilian experimenters adapted techniques used by the Swedish air force in a task where persons had to push buttons, pull levers, and press pedals in response to lights and sounds. Investigators basically found that the drug acted as a distraction; people could perform adequately when low levels of skill were required, but as more and more tasks had to be accomplished at higher speeds, the drug interfered with perfor- mance. Such a result was hardly surprising, although details may have been relevant to military decision makers.

In mice the drug promotes amnesia. Experimenters gave the drug to rats for 12 weeks and found it reduced the amount of DNA in brain cells. Mepro- bamate may aggravate porphyria, a blood chemistry disorder that can make people violent and sensitive to light. Although some persons use the drug for years without untoward effect, case reports note uncommon instances where the drug may have caused serious and sometimes fatal blood diseases such as agranulocytosis and aplastic anemia.

One disquieting effect of meprobamate is its ability to produce flat brain- wave readings, which could cause medical personnel to cease vital treatment in a mistaken belief that the patient has died.

Abuse factors. Meprobamate’s abuse potential has been described as similar to benzodiazepine depressants. Dependence on meprobamate can develop if excessive amounts are routinely used. Abuse of this drug is considered a par- ticular risk with addicts to alcohol or other drugs. Symptoms of withdrawal from meprobamate have been likened to delirium tremens of alcohol with- drawal and can include tremors and twitches, trouble in controlling move- ment, insomnia, headache, vomiting, anxiety, confusion, and hallucinations. Convulsions are possible but uncommon. On rare occasion death has been attributed to withdrawal, but not all authorities agree that meprobamate is the sole cause. For sure, however, dogs that are dependent on the substance can go into convulsions and die if their supply is suddenly cut off.

Drug interactions. In mice nicotine reduces the time they are physically uncoordinated after a meprobamate dose, just as we might expect when a

Meprobamate 267

stimulant (nicotine) is taken after a depressant. In contrast, injection of mari- juana’s main active component THC increases the power of a meprobamate dose in animals. Meprobamate has been used in combination with dex- troamphetamine for human weight loss, a combination that had uncertain effectiveness but that produced fewer unwanted actions than dextroamphet- amine alone. Alcohol and meprobamate each have similar unwanted effects, and in that regard using both together can be the equivalent of taking extra doses of one or the other. Among steady drinkers, however, blood levels of meprobamate decline faster than in nondrinkers, meaning a meprobamate dose lasts a shorter time in the drinkers. A mice study indicated that poison- ous effects of meprobamate worsen if either alcohol or phenobarbital is also used. Phenobarbital and other barbiturates have cross-tolerance with mepro- bamate, meaning that the barbiturates can substitute for meprobamate in at least some respects.

Cancer. Not enough scientific information to report.

Pregnancy. Meprobamate administered into chicken eggs results in embryo malformations, and skeletal deformity has been observed with fetal develop- ment in rats exposed to the compound. The drug passes into a human fetus. A study of over 50,000 pregnancies, including many women who used mepro- bamate, found no evidence of birth defects linked to the drug, findings du- plicated by another analysis of outcomes in more than 6,000 pregnancies. Nonetheless, meprobamate is suspected of causing birth defects. Indeed, in a study of almost 20,000 pregnancies, birth defects were over twice as common among women using meprobamate during early pregnancy than among women who used other antianxiety drugs and more than four times as com- mon compared to women who took no drug at all in early pregnancy. One study found that congenital heart lesions occurred more often if meprobamate was used during pregnancy. Rats with fetal exposure to meprobamate show learning difficulties, and tests of five-year-old children who had prenatal ex- posure to the substance reveal impaired reasoning ability. The meprobamate level in milk of nursing mothers has been measured as up to four times higher than the level in their blood.

Additional scientific information may be found in:

Carson, J. “Meprobamate Revisited.” New York State Journal of Pharmacy 2 (1989): 45–46.

Gomolin, I. “Meprobamate.” Clinical Toxicology 18 (1981): 757–60.
Greenblatt, D.J., and R.I. Shader. “Meprobamate: A Study of Irrational Drug Use.”

American Journal of Psychiatry 127 (1971): 1297–1303.
Logan, B.K., G.A. Case, and A.M. Gordon. “Carisoprodol, Meprobamate, and Driving

Impairment.” Journal of Forensic Sciences 45 (2000): 619–23.
McNair, D.M. “Antianxiety Drugs and Human Performance.” Archives of General Psy-

chiatry 29 (1973): 611–17.
“Meprobamate.” Medical Letter on Drugs and Therapeutics 7 (1965): 36.


Pronunciation: MES-kuh-lin (also pronounced MES-kuh-leen) Chemical Abstracts Service Registry Number: 54-04-6 Formal Names: 3, 4, 5-Trimethoxyphenethylamine

Informal Names: Beans, Big Chief, Blue Caps, Button, Cactus, Cactus Buttons, Cactus Head, Chief, Love Trip (combination with MDMA), Mesc, Mescal, Mes- calito, Mescap, Mese, Mezc, Moon, Musk, Peyote, Topi

Type: Hallucinogen. See page 25
Federal Schedule Listing: Schedule I (DEA no. 7381) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. This is the main active drug in the peyote cactus. In addition to being found in that natural product, mescaline can also be manufactured in a lab- oratory. Researchers have noted that mescaline, LSD, and psilocybin have similar actions even though the substances have significant chemical dissim- ilarities. Effects are so alike that volunteers who took the drugs in experiments could not tell which of the three they received. Studies indicate cross-tolerance exists among the three. Mescaline is related to amphetamine.

Mescaline has been used to study mechanisms of schizophrenia, and at one time the substance was used in experimental psychotherapy. The drug en- couraged self-examination in patients and helped them to see significance in ordinary things they had barely noticed before. Such effects have also been described by persons who took the drug simply to find out what it is like. When mescaline was used as an experimental drug in psychotherapy, thera- pists reported that the substance helped people recall repressed memories. Debate existed, however, about whether the apparent memories were real and whether the recollection experience turned out to have therapeutic benefit. One experiment found that mescaline could help persons achieve creative an- swers to work-related problems that had resisted resolution for months. Re- search designed to measure whether the drug promotes creativity has found that volunteers’ feelings of increased creativity were supported in general and as a group by higher test scores on elements of creativity. “In general” and “as a group” may be important qualifiers about the results, however.

Users have reported expansion of color perception, but a test designed to detect such a phenomenon produced mixed results. A rabbit study found that

Mescaline 269

mescaline could relieve pain. In a human experiment mescaline promoted growth hormone levels. In rats appetite may increase.

Drawbacks. Individuals with a personal or family history of serious mental illness may be particularly vulnerable to lengthy psychosis from mescaline, although a study of former and current users of mescaline, LSD, or psilocybin found that they scored normally on psychological tests—with the exception that persons who engaged in current hallucinogen use were more depressed and nervous and prone to risk-taking.

Visual hallucinations during a mescaline dose are common; auditory ones less so. Aside from visual hallucinations, users not only may have trouble recognizing faces but may see startling transformations of their own faces in a mirror, viewing the image as not only something apart from themselves but as something ominous. People may feel like their bodies are changing in shape and be unable to detect portions of their bodies. Perceptions of time and space may also change. The drug intoxication typically begins with euphoria, but in a laboratory setting, the euphoria often converts to nervousness and suspicion, possibly ending in depression. Subjects have been known to say and do things they did not want to but were unable to stop themselves. Persons under the drug’s influence may be very open to suggestions, a state that could be ex- ploited by unscrupulous persons.

Research shows that the drug can cause headache, perspiration, hot or cold sensations, feelings of prickling or burning, dizziness, cramps, nausea, and vomiting accompanied by small increases in pulse rate and blood pressure. In a sufficient dose mescaline can impair breathing, increase body temperature, and lower pulse rate and blood pressure. Hearing may become so sensitive that ordinary noises are painful. Other senses may have abnormal reactions also.

Tests of reasoning and mental focus produce low scores while people use the drug. Mescaline-related deaths are usually not caused by the chemical itself but by things people did while their judgment was impaired. After rats receive mescaline they appear to forget how to navigate a maze and also take longer to solve problems (figuring out how to get past obstacles). The drug promotes fighting among rats; one group of researchers described the aggres- sion as “robust.” Debate exists about whether the drug makes rats fiercer or simply reduces inhibitions in stressful situations. Aggression and wild behav- ior are not seen as consequences of the drug among human users, and in some circumstances mescaline makes rats lethargic.

Dogs assume odd body stances after receiving the drug and act so lethargic as to be almost insensible. Monkeys seem fascinated as they look at ordinary objects, a reaction that may indicate visual hallucinations. Monkeys first act excitable after dosage, then lethargic. Rats, dogs, and monkeys all exhibit re- petitive convulsivelike movements at high doses. In monkeys a fatal dose may not kill them until three or four days have passed.

Abuse factors. A rat experiment found evidence of tolerance, but investi- gators surmised that the rats might simply have been learning how to com- pensate for drug effects on performance as the experiment continued. Rather than dosage effectiveness declining, the effects may have been unchanging as rats pushed through them by strength of will. Investigators running a rabbit

270 Mescaline

experiment reported tolerance. Evidence exists for tolerance in animals and humans who receive the drug daily, but such tolerance dissipates quickly once the drug is stopped; two or three days later a dose can produce the same level of effects as before. Dependence does not seem to occur.

Drug interactions. Not enough scientific information to report.
Cancer. Not enough scientific information to report.
Pregnancy. The drug will pass into the fetus of a pregnant monkey. In ham-

sters mescaline has caused birth defects and delayed development of bone structures, along with reducing the number of offspring in litters. Human birth defects are suspected.

Additional information. “Mescal” is both a nickname for mescaline and the name of an alcoholic beverage; they are different substances.

Additional scientific information may be found in:

Adlaf, E.M., et al. “Nonmedical Drug Use among Adolescent Students: Highlights from the 1999 Ontario Student Drug Use Survey.” CMAJ: Canadian Medical Association Journal 162 (2000): 1677–80.

Hermle, L., et al. “Mescaline-Induced Psychopathological, Neuropsychological, and Neurometabolic Effects in Normal Subjects: Experimental Psychosis as a Tool for Psychiatric Research.” Biological Psychiatry 32 (1992): 976–91.

Hoch, P.H., J.P. Cattel, and H.H. Pennes. “Effects of Mescaline and Lysergic Acid (D- LSD-25).” American Journal of Psychiatry 108 (1952): 579–84.

Hollister, L.E., and A.M. Hartman. “Mescaline, Lysergic Acid Diethylamide and Psi- locybin: Comparison of Clinical Syndromes, Effects on Color Perception and Biochemical Measures.” Comprehensive Psychiatry 3 (1962): 235–42.

Huxley, A. The Doors of Perception, and Heaven and Hell. New York: Harper and Row, 1963.

Kapadia, G.J., and M.B.E. Fayez. “Peyote Constituents: Chemistry, Biogenesis, and Bio- logical Effects.” Journal of Pharmaceutical Sciences 59 (1970): 1699–1727.

Unger, S.M. “Mescaline, LSD, Psilocybin and Personality Change.” Psychiatry: Journal for the Study of Interpersonal Processes 26 (May 1963): 111–25.


Pronunciation: METH-a-dohn (also pronounced METH-a-don)
Chemical Abstracts Service Registry Number: 76-99-3. (Hydrochloride form


Formal Names: Amidone, Dolophine, Eptadone, Heptanal, Ketalgin, Mephanon, Methadose, Physeptone, Symoron, Tussol

Informal Names: Balloons, Breeze, Burdock, Buzz Bomb, Cartridges, Dollies, Dolls, Done, Fixer, Fizzies, Juice, Juicer, Jungle Juice, Medecina, Meth-A-Done, Mud, Phyamps, Pixie, Red Rock, Tootsie Roll, Wafers

Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II (DEA no. 9250) USA Availability: Prescription
Pregnancy Category: B

Uses. This drug was invented by Germany’s Nazi regime in 1941 as a sub- stitute for inadequate morphine supplies. Today methadone is best known as a legal substitute for heroin. In addition to that use in addiction treatment programs, methadone is given to adults and children as a pain reliever for surgery, cancer, burns, and other conditions. The substance is used as a cough suppressant and also has calming qualities. In racehorses the drug can pro- mote running ability and is banned from the sport. A human dose can last for 24 hours, rather long for a drug of this type and class. For pain relief a dose of methadone may be roughly 2.5 to 14.3 times stronger than morphine, depending on how and why the drug is administered.

Drawbacks. Some persons experience euphoria from methadone. Unwanted effects can include vitamin deficiency, constipation, sleepiness, breathing dif- ficulty, and low blood pressure. People may feel faint if they suddenly stand up from a sitting or prone position. Nausea, vomiting, constipation, urinary difficulty, sweating, lowered sex drive, and impaired sexual performance are other well-known problems. Liver disease may allow dangerous buildup of methadone levels from normal doses.

Abilities to operate dangerous machinery such as automobiles may be re- duced. Tests of persons undergoing methadone maintenance therapy indicate they may be able to drive satisfactorily if they use no other drugs, but most methadone maintenance patients also use other drugs that worsen driving

272 Methadone

performance and exhibit assorted types of personality problems that leak over into driving habits.

In the 1970s methadone was suspected of causing memory trouble, but a group of researchers who investigated the question found no such difficulties. In 2000 a study reported significant memory problems in a group of metha- done maintenance recipients, but the same group also had confounding con- ditions such as head injury and alcoholism that may have affected memory test performance. Another 2000 study comparing methadone users to nonusers concluded that life factors other than methadone were the best explanation for differences in scores on thinking tests.

Abuse factors. Although methadone is sometimes described as blocking her- oin’s effects, the two drugs simply have cross-tolerance, meaning one of them can substitute for the other in some ways. In addition, persons who find one of the drugs pleasant will probably find the other one just as appealing. For those reasons, heroin addicts can often be switched to methadone in order to maintain their drug habit legally, but the switch does not cure their drug addiction. Some heroin users even like methadone better; some methadone recipients continue using heroin on the side. On the basis of death statistics, some authorities feel methadone is more dangerous than heroin.

Addicts in methadone maintenance programs have chaotic lives. One study of program participants found 7% were likely to be pathological gamblers; another study of methadone program participants found 16% to be patholog- ical gamblers and an additional 15% to have a gambling problem. Researchers have noted that violent traumas are more frequent among methadone pro- gram participants than among the average population. In one survey 34% of patients said they received treatment for mental disorder, 64% of the women said they used psychoactive drugs during pregnancy, 80% of parents said they were arrested while their children were growing up, and parents reported that 30% of their children were suspended from school and 41% failed at least one grade in school and had to take that year of education again. For meth- adone maintenance patients and their families, drug abuse is simply one el- ement in multiproblem lifestyles.

A rhesus monkey experiment showed the animals having no preference between water and a methadone solution. Such lack of interest is consistent with human experience. Some persons find opiates or opioids attractive, but most do not. Personality and life circumstances have much to do with such choices.

Methadone’s calming qualities dissipate if tolerance occurs, so some other antianxiety medicine must then be used. Methadone’s abstinence syndrome is reminiscent of morphine’s but is generally described as more gradual in de- velopment and disappearance, longer lasting but with symptoms of lesser severity. Some research, however, has found no difference in morphine and methadone withdrawal, and some addicts say withdrawal from methadone is more difficult than withdrawal from heroin. Evidence suggests that metha- done withdrawal symptoms are harsher in nonblack infants than in blacks.

Drug interactions. Using other depressants (including alcohol) or tricyclic antidepressants with methadone can increase the risk of a cumulative over- dose—each individual dose may be safe, but all together may be dangerous.

Methadone 273

Methadone should be used cautiously if a person is also taking monoamine oxidase inhibitors (MAOIs, found in some antidepressants and other medi- cine). Blood levels of methadone can be drastically altered by phenobarbital, by the epilepsy medicines phenytoin and carbamazepine, and by the tuber- culosis medication rifampin. A case report notes that the HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syndrome) drug rito- navir reduces methadone blood levels, and methadone interacts with other HIV/AIDS drugs as well. Taking doses of methadone along with the psychiatric medicine fluvoxamine (Luvox) can be fatal. Depending on how a person uses alcohol, that drug can raise or lower blood levels of methadone. Data from one study showed that methadone did not decrease likelihood for alcohol abuse and that persons already abusing alcohol drank even more while on methadone. Other drug combinations common among illicit users can be hazardous with methadone, and methadone alone can be dangerous if a person who once had tolerance resumes usage at the old high-dose level. Experiments have found that consumption and enjoyment of tobacco ciga- rettes increase after volunteers use methadone, and another experiment found that methadone consumption increases after volunteers use nicotine (in gum or cigarettes).

Cancer. Chromosome damage is one measure of a drug’s potential for caus- ing cancer. A study of persons receiving methadone for 40 weeks found no more chromosome damage than a nondrug population would have.

Pregnancy. Safety for use during pregnancy is unknown. Researchers who gave various opioids to pregnant hamsters described methadone as one of the most powerful inducers of birth defects. Mice research shows that offspring are smaller than normal but have ordinary brain development. Compared to morphine, much more of a maternal methadone dose reaches a fetus. One group of investigators developed findings implying that methadone may harm human fetal central nervous system development. Those discoveries are consistent with research demonstrating abnormal development of neurons in rats that had prenatal methadone exposure; researchers speculate that such abnormalities may explain various behaviors in human infants who had pre- natal methadone exposure. Use of methadone for easing pain of childbirth is not recommended because newborns can suffer breathing difficulty after pick- ing up the drug from the maternal blood supply. Infants from women who use methadone chronically can be born with dependence to the drug.

A study compared pregnant women on methadone maintenance to a preg- nant group on morphine maintenance and discovered that the morphine group used fewer benzodiazepine class drugs and fewer opiates than the methadone program participants. Another study noted that pregnant addicts in a methadone program received better prenatal care than addicts who were not in such programs, but program participants typically continued illicit drug use, their infants weighed no more than infants from pregnant addicts not in a methadone program, and infants from both those drug groups (program and nonprogram) weighed less than those of women who were not drug abus- ers. Such results have led more than one group of researchers to ask whether methadone maintenance helps pregnancy outcomes, but those researchers do

274 Methadone

not offer an answer. Nonetheless, some authorities report that pregnancy out- comes are substantially better for addicts in methadone programs.

A group of clinical observations found that infants from mothers addicted to heroin had better sucking ability than infants from methadone addicts (in- cluding those in methadone maintenance programs). Research finds that breast-feeding by methadone-using mothers does no harm to infants, and one investigator concluded that methadone in the milk helps ease a dependent child’s withdrawal symptoms. Investigators have found that infants with fetal exposure to methadone eat more than normal but do not gain more weight than normal, a finding that suggests defective ability to use nutrition from food. A study of two-year-old children found that fetal exposure to methadone had no influence on ability to focus attention. Examination of school-age chil- dren who had fetal exposure to methadone found them to have normal scores in thinking tests and somewhat lower IQs than normal and to be more nervous and aggressive than typical children. How much of this is related to the drug and how much is related to tumultuous family life is uncertain. Another follow-up study found that girls had normal gender behavior, but boys had more female characteristics in their conduct.

A study found pregnancy outcomes to be much the same among methadone and cocaine users.

Additional scientific information may be found in:

Darke, S., et al. “Cognitive Impairment among Methadone Maintenance Patients.” Ad- diction 95 (2000): 687–95.

De Cubas, M.M., and T. Field. “Children of Methadone-Dependent Women: Devel- opmental Outcomes.” American Journal of Orthopsychiatry 63 (1993): 266–76.

Fainsinger, R., T. Schoeller, and E. Bruera. “Methadone in the Management of Cancer Pain: A Review.” Pain 52 (1993): 137–47.

Jarvis, M.A., and S.H. Schnoll. “Methadone Treatment during Pregnancy.” Journal of Psychoactive Drugs 26 (1994): 155–61.

Martin, W.R., et al. “Methadone—A Reevaluation.” Archives of General Psychiatry 28 (1973): 286–95.

Rossler, H., et al. “Methadone-Substitution and Driving Ability.” Forensic Science Inter- national 62 (1993): 63–66.

Schneider, J.W., and S.L. Hans. “Effects of Prenatal Exposure to Opioids on Focused Attention in Toddlers during Free Play.” Journal of Developmental and Behavioral Pediatrics 17 (1996): 240–47.

Specka, M., et al. “Cognitive-Motor Performance of Methadone-Maintained Patients.” European Addiction Research 6 (2000): 8–19.


Pronunciation: meth-am-FET-uh-meen
Chemical Abstracts Service Registry Number: 537-46-2
Formal Names: Anadrex, Desoxyn, Norodin, Pervertin, Stimulex

Informal Names: Bambita, Bathtub Crank, Batu, Blue Meth, Boo, Bump, Chalk, Chicken Feed, Crank, Crink, Cris, Cristina, Cristy, Croak, Crossles, Crypto, Crys- tal, Crystal Meth, Desocsins, Desogtion, Geep, Glass, Go-Fast, Granulated Or- ange, Hanyak, Hironpon, Hiropon, Hot Ice, Ice, Jet Fuel, Kaksonjae, L.A. Glass, L.A. Ice, Lemon Drop, Load of Laundry, Maui-Wowie, Meth, Methlies Quik, Mexican Crack, Motorcycle Crack, Nazi Vitamins, Peanut Butter, Quartz Smok- able, Quill Cocaine, Red Devils, Redneck Cocaine, Schmiz, Scootie, Shabu Ice, Sketch, Smoke, Soap Dope, Sparkle, Speed, Spoosh, Stove Top, Super Ice, Tick Tick, Trash, Twisters, Water, Wet, White Cross, Working Man’s Cocaine, Yellow Bam, Yellow Powder

Type: Stimulant (amphetamine class). See page 12 Federal Schedule Listing: Schedule II (DEA no. 1105) USA Availability: Prescription
Pregnancy Category: C

Uses. Methamphetamine was first manufactured in 1919. This stimulant of the central and sympathetic nervous systems is comparable to dextroamphet- amine. Psychic effects are the same as for any amphetamine class drug.

Methamphetamine is used to treat narcolepsy, attention deficit hyperactivity disorder (ADHD), and adult obesity. Typically the drug is not recommended for juvenile obesity. Although patients lose more weight than if they use a placebo, the difference is only a few ounces per week. Researchers do not know how the drug promotes weight loss. Scientists are even unsure if the drug is responsible or if diet, coaching, attitude, and other factors explain the difference. In general, the longer patients take the drug, the lower their rate of weight loss. Standard practice is to stop the drug when weight benefits decline, rather than increase dosage.

To achieve top performance during World War II, pilots of the German Luftwaffe and the British Royal Air Force used methamphetamine. In 1953 Hermann Buhl was the first person to climb the mountain Nanga Parbat in the Himalayas, and during that feat he used methamphetamine tablets. Some observers wonder if that pharmaceutical aid was crucial. A person who

276 Methamphetamine

climbed Mt. Everest without using supplementary oxygen noted, “Because mountaineering is, thank God, not an organized Olympic sport, there are no regulations about the use of drugs, so the choice is up to the individual.” When methamphetamine was tested on champion cyclist athletes, they could not achieve a higher level of performance than normal, but they could extend top performance far longer than normal, a feat made possible in part by the drug’s apparent ability to mask the body’s normal signals of exhaustion. Re- searchers speculate that the drug could cause athletes to overextend them- selves, collapse, and die. Another experiment found that the drug could improve work performance, but performing a few tasks under controlled con- ditions cannot be extrapolated to the whole world of real-life work.

The human body metabolizes assorted medical drugs into dextroampheta- mine and methamphetamine, so if a body fluid test is used to accuse someone of unauthorized use, a blameless person should check whether any over-the- counter or prescribed drugs might be the explanation.

Drawbacks. Measurements have found damage to brain neurons correlated with amount of methamphetamine abuse, damage that does not seem to re- cover upon cessation of drug dosage. Some of that damage may promote Parkinson’s disease. Tests show normal scores for methamphetamine abusers on some psychological perception tests, below normal scores on others. Ani- mal experiments confirm that methamphetamine can alter DNA molecules, and some researchers ask whether these changes may invalidate DNA iden- tifications made by law enforcement authorities.

Methamphetamine raises blood pressure; the most catastrophic consequence can be rupture of the aorta. The compound raises body temperature. Euphoria and overdose symptoms are similar to those of cocaine but last longer. Meth- amphetamine overdose can cause convulsions, heart attack, kidney failure, and stroke. Stroke can occur days after overdosage. Temporary blindness has developed. The drug can severely and permanently impair vision, apparently by temporarily cutting blood flow to the optic nerve. Serious ulcers may de- velop in the cornea. Although methamphetamine can slightly stimulate breathing and help open lung airways, the substance can also produce tem- porary emphysema. Animal experiments and human experience indicate that concealed heart damage caused by the drug can repair itself if methamphet- amine administration ceases.

Methamphetamine’s smokable format is considered twice as strong as dex- troamphetamine, can produce pulmonary edema, and has been identified as causing skin affliction. Smoking methamphetamine can narrow blood vessels, which will increase blood pressure. Another suspected consequence of the narrowing is acidosis found among methamphetamine users, a condition in which levels of acid in blood rise high enough to make a person sick. Studies of patients suffering from harm to bones and to skeletal muscles have found possible association with methamphetamine. Ischemic colitis, a bowel problem normally associated with old age, has been seen among young methamphet- amine users. The substance is also associated with duodenal ulcers and malignant giant gastric ulcers. Inhaling the drug (as opposed to smoking, in- jecting, or swallowing) promotes excessive wear on teeth.

Methamphetamine affects insulin needs of diabetics. Persons with the same

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physical afflictions that make dextroamphetamine inadvisable should also avoid methamphetamine.

Abuse factors. Experiments with intravenous injection of pure pharmaceu- tical methamphetamine found that recipients did not experience the almost instantaneous rush of effect that would normally be expected from such a path of administration. Recipients instead began experiencing significant ef- fects hours later. A study of Japanese abusers receiving treatment for their drug habit compared injectors to smokers. Injectors had less schooling and more criminality and were more likely to have alcoholic parents. Such back- ground is typical in persons having a bad relationship with drugs. Contented people rarely fall victim to drug abuse.

Methamphetamine flashbacks are possible. Someone who experienced a threatening situation while undergoing frightening psychosis brought on by methamphetamine can have a flashback when later confronted with a mildly stressful situation. In one study of abusers methamphetamine was blamed for long-term psychosis, in one case lasting 38 years after abuse stopped, but most of those patients also had other troubles (broken homes, criminality) promot- ing maladjustment.

Persons who abuse methamphetamine are typically disappointed with their lives. The drug is sometimes blamed for causing “amotivational syndrome” in which abusers lack much interest in life, but abusers typically have much to be discouraged about regardless of drug use. One study of Japanese alco- holics compared those who had also abused methamphetamine to those who had not. The abusers were more afflicted with alcohol hallucinations, were much less likely to live together with someone, and were twice as likely to collect welfare and three times as likely to live in slums. (And about one fourth of the abusers had tattoos versus none of the nonabusers—the researchers called the variation “significant,” but that term was surely meant in its statis- tical sense.) Another study of Japanese abusers found that only 5% came from an upper income background, in contrast to 71% of marijuana users. Still an- other study of Japanese abusers found that they ended their schooling early, hung out with gangs or other groups, and experienced effects typical of am- phetamine class drugs (restlessness, irritability, low appetite, suspicion of other persons). Some negative aspects seemed to depend on how much the drug users perceived themselves as victims of society. Pepped-up feelings and drug-induced happiness declined as methamphetamine abuse continued over the years. One authority has noted that persons who get drunk on alcohol every day are five times more prone to smoke methamphetamine than persons who consume alcohol either moderately or not at all. This does not mean that alcohol itself promotes methamphetamine use, but a person who is so mis- erable as to get drunk daily will also be likely to seek additional ways to obliterate perception of problems. One of those choices may be methamphet- amine.

Compared to persons who don’t abuse methamphetamine, abusers are known for more frequently engaging in risky sexual practices (no condoms, partners with sexually transmitted diseases, multiple casual partners). Less is known about whether such conduct is promoted by the drug or whether the drug is simply one component of a life filled with risk-taking.

278 Methamphetamine

Methamphetamine abusers tend to get injured more often in accidents than nonusers. That correlation, however, does not tell us whether the cause is the drug or a reckless lifestyle that happens to include drug abuse—one study of methamphetamine user deaths found that over 25% were murders. Types of accidents experienced by methamphetamine users are similar to those suffered by alcohol abusers, with road mishaps being most common. A study of violent emergency room patients requiring “chemical restraint” (that is, involuntary administration of a sedating drug) found that 72% were intoxicated with methamphetamine, and many were also drunk on alcohol. Violent patients requiring restraint are, of course, a small minority; those figures do not mean that 72% of all patients were using methamphetamine. The figures do, how- ever, indicate that persons who lose control of themselves cannot handle meth- amphetamine well, or alcohol either.

As for the drug’s popularity, a 1999 analysis found that deaths related to methamphetamine in San Francisco had not particularly risen over a 13-year period. In contrast, toxicology tests at a California hospital (not involving all patients) showed 3% positive for either dextroamphetamine or methamphet- amine or both in 1978, 10% in 1986 and 1987. Another California hospital found that 7.4% of trauma patients had been using the drug in 1989, 13.4% in 1994. As the drug promotes medical problems, we can expect evidence of methamphetamine abuse to be higher in a hospital patient population (com- posed of people seeking medical help) than in the general population. When the twenty-first century began, about 2% of the general American population was estimated to have used methamphetamine one or more times in their lives, and the percentage of regular users would be lower than that. Patients in medical cases examined in California, Taiwan, and Japan tend to be male, perhaps indicating a gender preference in use of this drug. Evidence exists for a gender difference in psychic reaction to the drug, with males feeling pepped up and happy while under the influence and postmenopausal women feeling tired and sad. The substance causes more brain changes in male mice than in female.

Drug interactions. Methamphetamine can have serious interactions with an- esthesia and opioid drugs given in dentistry. Animal research indicates that smoking tobacco cigarettes can create a multiplier effect in which the nicotine and methamphetamine interact, boosting each other’s potency. Opiate addicts receiving oral methadone report that injecting themselves with methamphet- amine produces a heroin-type high lasting a full 24 hours.

A hospital emergency room study found that persons admitted for the same cause of injury had lower alcohol level in their blood if they had also been taking methamphetamine. Combining the two drugs allows mice to tolerate a higher methamphetamine dose than normal, but research on humans finds just the opposite, that alcohol can transform a normal dose of methampheta- mine into a fatal one. Laboratory research on humans shows that using the two drugs together adds strain on the heart, while reducing pleasure gained from the alcohol and maintaining mental satisfaction from the methamphet- amine. An unusual report tells of that drug combination rupturing a bladder, the alcohol helping to fill it up as the methamphetamine narrowed the bladder

Methamphetamine 279

neck while taking away the normal sensation of pain that would warn a per- son to seek medical help.

Cancer. Not enough scientific information to report.

Pregnancy. Pregnant methamphetamine abusers tend to produce full-term babies having characteristics of premature infants. While such a problem mer- its attention, a California study of 563,573 women who gave birth in 1992 helped put a perspective on the situation: Only 774 used methamphetamine during their pregnancies. Pooling results from seven California hospitals pro- vided still another perspective. Among one group of mothers in 1996 and 1997, 0.5% had positive drug tests for methamphetamine during pregnancy, and those women typically used other drugs as well. And that percentage is not from the total population of pregnant women but only from those whose infants required assistance in breathing, a group where drug abuse was more prevalent.

Animal studies involving many times the normal human medical dose have produced birth defects. Confirming fetal harm from methamphetamine in hu- mans is difficult because of other drugs the women use (particularly alcohol), nutrition, amount of prenatal care, and other factors that simultaneously affect fetal development. Methamphetamine accumulates in the fetus where blood level can be two and even six times higher than elsewhere in the woman’s body. One study measuring pregnancy outcome where umbilical blood showed misuse only of methamphetamine found the infants to be normal.

Additional scientific information may be found in:

Anglin, M.D., et al. “History of the Methamphetamine Problem.” Journal of Psychoactive Drugs 32 (2000): 137–41.

Beebe, D.K., and E. Walley. “Smokable Methamphetamine (‘Ice’): An Old Drug in a Different Form.” American Family Physician 51 (1995): 449–53.

Boe, N.M., et al. “Methamphetamine Use during Pregnancy Increases the Risk of Ad- verse Maternal and Neonatal Outcomes.” American Journal of Obstetrics and Gy- necology 180 (January 1999, pt. 2): S71.

Lan, K.C., et al. “Clinical Manifestations and Prognostic Features of Acute Metham- phetamine Intoxication.” Journal of the Formosan Medical Association 97 (1998): 528–33.

Logan, B.K. “Methamphetamine and Driving Impairment.” Journal of Forensic Sciences 41 (1996): 457–64.

Mayfield, D.G. “Effects of Intravenous Methamphetamine.” International Journal of the Addictions 8 (1973): 565–68.

Mendelson, J., et al. “Methamphetamine and Ethanol Interactions in Humans.” Clinical Pharmacology and Therapeutics 57 (1995): 559–68.

Simon, S.L., et al. “Cognitive Impairment in Individuals Currently Using Metham- phetamine.” American Journal on Addictions 9 (2000): 222–31.


Pronunciation: meth-AN-dree-ol

Chemical Abstracts Service Registry Number: 521-10-8

Formal Names: Andris, Arbolic, Crestabolic, Drive, Durandrol, Filibol Forte, Geld- abol, Hybolin, Methylandrostendiol, Methylandrostenediol, Novandrol, Spec- triol

Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000) USA Availability: Prescription

Uses. Although the substance is banned from sports, some bodybuilders and other athletes use it. A rat study found augmented muscle protein among animals receiving the drug. Researchers have noted that chickens gain more weight when getting methandriol. Other researchers, however, found no weight alteration after giving the drug to mares daily for 18 months. The compound has been tested as a treatment for excessive menstrual bleeding, but results left investigators rather unimpressed.

Drawbacks. Methandriol can masculinize women’s body signs and behav- ior, though to a lesser degree than many drugs of this type. Indeed, when tested on horses, no change was seen in mares’ conduct. Nonetheless, women’s voices can deepen, and facial hair can appear—effects that may be permanent. Among bodybuilders there is a claim that the drug feminizes men’s body signs and behavior. Boys and girls receiving the drug may un- dergo premature sexual maturity and stop growing in height. Reduced fertility may occur in men. Unwanted effects can include acne, hair loss, and tissue swelling due to fluid retention. Researchers noted development of high blood pressure in rats that steadily dosed on methandriol for several weeks. The drug is not recommended for persons with high blood pressure, heart trouble, or prostate disorder. Methandriol is suspected of causing liver damage.

Abuse factors. Not enough scientific information to report on tolerance, de- pendence, withdrawal, or addiction.

Drug interactions. Not enough scientific information to report.
Cancer. Not enough scientific information to report.
Pregnancy. Pregnant women are supposed to avoid methandriol. Bisexual

fetal development in rats has been attributed to the drug. Other research has

Methandriol 281

noted that genetic females can have outward male appearance after fetal ex- posure. The drug may interfere with milk production.

Additional scientific information may be found in:

Rendina, G.M., and D. Patrono. “The Use of a Biological Preparation in the Treatment of Some Gynaecological Diseases.” Current Medical Research and Opinion 4 (1976): 151–57.

Rogozkin, V. “Metabolic Effects of Anabolic Steroid on Skeletal Muscle.” Medicine and Science in Sports 11 (1979): 160–63.

Turner, J.E., and C.H. Irvine. “Effect of Prolonged Administration of Anabolic and Androgenic Steroids on Reproductive Function in the Mare.” Journal of Repro- duction and Fertility, no. 1 (1982, Suppl.): 213–18.


Pronunciation: meth-an-droh-STEN-oh-lohn
Chemical Abstracts Service Registry Number: 72-63-9 Formal Names: Anabolin, Dianabol, Methandienone, Nerobol Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000)
USA Availability: Prescription

Uses. Medical uses of methandrostenolone include promoting growth in small boys, although with the risk of accelerating increase in height for awhile and then stopping further increase permanently. The drug has also been used to bring on male puberty when that development is delayed. A research study found that the substance increases sexual desire in men while simultaneously reducing their fertility. The drug has been given to control hereditary angio- edema, a disease producing giant hives on the skin. A lung disease called silicosis has been treated with the drug, and so have burns, cancer, and a type of anemia. Using the substance against a brittle bone condition called osteo- porosis has been tried, with mixed results. Protection against lead poisoning was noted in a rat experiment. Levels of triglycerides, which are associated with heart attack and stroke, declined in diabetic humans who received the drug.

The substance is forbidden in sports competitions, but some athletes con- tinue to use it, either because they will not be tested for it or because they hope to evade tests. Experiments have compared athletes using methandro- stenolone to others not receiving the drug (either two different groups of ath- letes were compared, or the same volunteers were tested under both drug and nondrug conditions). In one study the drug group showed higher increase in weight and strength. In another experiment the drug group gained more weight than the drug-free group, but the scientists noted that water retention could have been the reason. Blood pressure also increased in the drug group. In still another comparison experiment the methandrostenolone users gained more weight and achieved more muscle development, but despite additional muscle mass their strength and performance did not differ from the drug-free group—scientists running those tests were unsure that anabolic steroid actions explained physical development in the drug group; as with an experiment mentioned above, a plausible alternative explanation was that methandrosten-

Methandrostenolone 283

olone simply caused fluid swelling in tissues. Yet one more experiment mea- sured increase in muscle mass among athletes using the substance but detected no increase in strength.

Stock raisers administer methandrostenolone to promote sheep and cattle growth.

Drawbacks. A case report warns that using the substance on girls can pro- duce male qualities in voice while reducing female sexual characteristics; these changes can be long-lasting and perhaps permanent. Although a skin cream containing nandrolone is used to combat eczema, the same use of a cream containing methandrostenolone has had serious consequences when applied to girls, causing some female physical characteristics to diminish while mas- culine ones appeared.

A case report attributed a 28-year-old bodybuilder’s heart disease and hard- ening of the arteries to a dozen years of using methandrostenolone and other steroids. Another case report blamed methandrostenolone alone for blockage of blood vessels between heart and lungs in a 26-year-old bodybuilder. At- tempts to treat the condition with the anti–blood clot drug warfarin became complicated when the steroid boosted that drug’s actions.

When taking methandrostenolone daily, a person experienced delusions and paranoia. Excessive self-confidence created by the drug inspired one user to buy a $17,000 automobile on credit despite his inability to make payments. After going off methandrostenolone the person sold the car, but upon resum- ing the drug, he purchased a $20,000 vehicle. Medical literature also records that a 22-year-old athlete using methandrostenolone and stanozolol devel- oped feelings of powerfulness and aggression, accompanied by impatience.

Methandrostenolone apparently causes acne and is suspected of worsening tics in Tourette’s syndrome. Men may experience urinary difficulty and low- ered testosterone levels. The substance can bring on an attack of porphyria in persons who suffer from that body chemistry disease, an affliction that some- times involves violence and sensitivity to light.

Abuse factors. An opiatelike dependence was reported in a 23-year-old bodybuilder who had been on a steady regimen including methandrosteno- lone, oxymetholone, and oxandrolone. When given a drug that counteracts opiate actions he quickly exhibited nausea, chills, dizziness, and headache— classic flulike opiate withdrawal symptoms. When his supply of steroids ceased he craved them and felt weary and depressed. Another case report notes a bodybuilder who dosed extensively on methandrostenolone and other steroids and experienced severe depression when he stopped.

Drug interactions. Not enough scientific information to report.

Cancer. Researchers examining reported deaths from a type of liver cancer called hepatic angiosarcoma found a total of 168 throughout the United States from 1964 to 1974, of which the investigators associated 1 with methandrosten- olone (this individual was also a former alcohol abuser, conduct that is no- toriously hard on the liver). Methandrostenolone and other steroids are suspected of causing kidney cancer in a 38-year-old bodybuilder.

Pregnancy. Mice studies indicate that the drug can produce lethal mutations in sperm, causing pregnancy failure.

Additional scientific information may be found in:

284 Methandrostenolone

Freed, D.L.J., et al. “Anabolic Steriods in Athletics: Crossover Double-Blind Trial on Weightlifters.” British Medical Journal 2 (1975): 47–73.

Hervey, G.R., et al. “Anabolic Effects of Methandienone in Men Undergoing Athletic Training.” Lancet 2 (1976): 699–702.

Holma, P.K. “Effects of an Anabolic Steroid (Metandienone) on Spermatogenesis.” Con- traception 15 (1977): 151–62.

Johnson, L.C., and J.P. O’Shea. “Anabolic Steroid: Effects on Strength Development.” Science 164 (1969): 957–59.

Kilshaw, B.H., et al. “Effects of Large Doses of the Anabolic Steroid, Methandrosten- olone, on an Athlete.” Clinical Endocrinology 4 (1975): 537–41.

Madea, B., and W. Grellner. “Long Term Cardiovascular Effects of Anabolic Steroids.” Lancet 352 (1998): 33.

Robinson, R.J., and S. White. “Misuse of Anabolic Drugs.” British Medical Journal 306 (1993): 61.


Pronunciation: meth-a-KWAY-lohn

Chemical Abstracts Service Registry Number: 72-44-6

Formal Names: Dormutil, Hyminal, Mandrax, Melsed, Melsedin, Mequelone, Me- quin, Methadorm, Mozambin, Optimil, Parest, Quaalude, Revonal, Somnafac, Sopor, Toquilone Compositum, Triador, Tuazole

Informal Names: Bandits, Beiruts, Blou Bulle, Blue Bulls, Drunken Monkey, Ew- ings, Flamingos, Flowers, Four Strokes, Genuines, Germans, Golfsticks, Hum- bles, Knoppies, Lizards, Loss of Memory, Love Drug, Ludes, Luds, Lula, Magwheels, Mandies, Mind Benders (with heroin), Pressouts, Pupumala, Q, Randy Mandies, 714, Shiny Tops, Sopes, Sporos, Strawberries, Wagon Wheels, White Pipe (Mandrax and marijuana)

Type: Depressant. See page 19
Federal Schedule Listing: Schedule I (DEA no. 2565) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. Methaqualone was invented in India during the 1950s as part of a program seeking substances for treating malaria. Experiments suggest meth- aqualone has anticonvulsant properties. Although the substance does little to relieve pain, experimentation indicates it might boost pain relief provided by codeine. Methaqualone may have cough suppression qualities but has not received general medical usage for that purpose. When introduced into Amer- ican medicine in the 1960s, the compound was used to calm people and help them sleep and was welcomed as an alternative to barbiturates. The drug’s actions have been likened to those of pentobarbital.

A clinical experiment found that a bedtime dose of the drug did not affect users’ ability to move around after awakening the next morning, which is not always the case with insomnia medicine. Those results were supported by another experiment where volunteers did so well on tests the next day and the following day that the researchers optimistically speculated that job per- formance might improve among people using the drug against insomnia. Brit- ain’s Royal Air Force even thought the drug had potential to help pilots get proper rest on long missions.

Drawbacks. Unwanted actions of methaqualone may include tingling sen- sations in hands and feet, weariness, sweating, rashes, dry mouth, nausea,

286 Methaqualone

vomiting, and diarrhea. Instances are known of methaqualone causing people to act as if injury has occurred to nerves affecting the arms and legs. Poisoning by methaqualone is associated with bleeding, and a case report revealed that an overdose can even cause bleeding inside the eye. Research with rats showed the drug impeded learning ability.

Although fatal overdose with methaqualone or any other drug is possible, a 1983 study found that methaqualone users in that era were primarily dying from accidents involving poor decisions while under the drug’s influence rather than from the poisonous effects of the drug itself. Also, if someone is intoxicated with the compound, driving skills are known to be impaired, an effect that does not involve poisoning but can have serious consequences. A study of emergency room admissions found that methaqualone poisoning cases typically involved some other substance as well, a finding indicating a certain recklessness among abusers. The same polydrug habit was observed among methaqualone abusers in the U.S. Army during the 1970s. That finding is unsurprising; most drug abusers use more than one substance.

The drug is fast acting, and persons unprepared for the speed with which methaqualone takes effect have been injured while engaged in ordinary activ- ity that becomes dangerous if a person passes out, such as taking a bath or being near a fire. Methaqualone has the disturbing capability of causing flat brainwave readings, a standard sign that medical caregivers rely upon to ver- ify a person’s death and that could therefore cause them to stop efforts that are keeping the methaqualone patient alive.

Abuse factors. In Europe methaqualone was initially a nonprescription item. In the United States the drug was first put in Schedule V, but as methaqualone became popular among illicit users seeking euphoria and relaxation, more restrictions were placed on its legal accessibility. The drug became a Schedule II substance in 1973. When President Jimmy Carter’s drug policy adviser Dr. Peter Bourne wrote a methaqualone prescription that violated regulations, that incident started a series of events that hounded Bourne out of office. Even- tually concern about the drug grew so high that it was reclassified in 1984 as a Schedule I substance having no recognized medical function.

One study found that patients using methaqualone against insomnia readily changed to some other drug on advice from a medical practitioner; apparently they did not find methaqualone particularly attractive. Tolerance and depen- dence can develop, although one study was able to confirm tolerance only among heavy abusers. Withdrawal symptoms are similar to those with bar- biturates and can include weakness, nausea, vomiting, heartbeat abnormality, tremors, seizures, and delirium tremens.

In the 1970s researchers surveyed college students who were using metha- qualone, a broader population group than persons who have so much trouble with the drug that they seek medical treatment. Survey answers showed drug use to be the main difference between students who used methaqualone and those who did not; as a whole the methaqualone users were ordinary people. Investigators found that a cross section of Midwestern users had positive at- titudes about themselves.

An exception to such a self-portrait emerged when someone interviewed users who claimed to be using methaqualone as an aphrodisiac. They turned

Methaqualone 287

out to be loners with a cold family background: Fully 10% said their closest family relationship was with the dog; 30% said they weren’t close to any family member at all. Almost all the persons using methaqualone as an “aph- rodisiac” had previously been using other drugs for the same purpose. None of the persons seemed capable of intimacy while sober, and all used metha- qualone and other substances simply to get intoxicated enough to permit some form of temporary superficial imitation of intimacy. Such drug use has an air of desperation and sadness inconsistent with the normal understanding of what an aphrodisiac does.

One study found that emergency psychiatric hospital patients who abused methaqualone (definitely not a population of ordinary individuals) tended to menace other persons.

Drug interactions. Animal research shows that injection of THC, the main active component of marijuana, reduces the amount of methaqualone that is normally needed to get the drug’s effects, which can make an overdose more likely. Animal and human studies using alcohol have had the same effect on a methaqualone dose—such findings are supported by examination of hospital emergency room cases, where analysis showed that methaqualone emergen- cies typically involved simultaneous ingestion of alcohol. Using alcohol and methaqualone simultaneously is a practice called “luding out.” Indulgers in that technique say it makes them feel relaxed, interferes with their ability to move, makes them more tolerant of pain, and produces tingling in their fin- gers, lips, and tongue.

Tests can detect methaqualone in the body days after a dose, and alcohol lengthens the time that a methaqualone dose lasts. That combination can in- fluence performance on various behavior and performance tests even three days after methaqualone is taken.

A woman’s menstrual cycle can affect her body’s ability to metabolize meth- aqualone; a dose can last a much shorter time when she is ovulating, but oral contraceptives can eliminate that effect.

Cancer. Not enough scientific information to report.

Pregnancy. The drug has produced birth defects in rats, and offspring had a death rate four times higher than that of a matched group receiving no drug. Researchers doing that work cautioned that the results do not necessarily carry over to humans. In rabbit studies the rate of birth defects from pregnant fe- males receiving methaqualone did not significantly differ from drug-free fe- males, but there was a big difference in death rates of offspring. Rabbits with fetal exposure to methaqualone died three times as often as those without exposure, a 6% death rate for those with exposure and 2% for those without. Analysts of such experiments note that in order to harm a fetus the metha- qualone dose has to be high enough to poison the pregnant female, so the practical meaning of such results may be that normal doses of the drug are safe during pregnancy. Effects on human fetal development are unclear. Hu- man reports tend to involve combinations with other drugs, making it hard to determine methaqualone’s role. Given the uncertainties, pregnant women are advised to avoid the drug.

Combination products. Mandrax and Toquilone Compositum contain both methaqualone and the antihistamine diphenhydramine. Some research indi-

288 Methaqualone

cates that diphenhydramine boosts the actions of methaqualone; some re- search indicates that the antihistamine lengthens the time that a methaqualone dose lasts. Adverse reactions have occurred when persons take the combina- tion along with tricyclic antidepressants.

Additional information. Methaqualone and diazepam each have the nick- name “Ludes,” but the drugs are different substances.

Additional scientific information may be found in:

Bailey, D.N. “Methaqualone Ingestion: Evaluation of Present Status.” Journal of Ana- lytical Toxicology 5 (1981): 279–82.

Brown, S.S., and S. Goenechea. “Methaqualone: Metabolic Kinetic and Clinical Phar- macologic Observations.” Clinical Pharmacology and Therapeutics 14 (1973): 314–24.

“Evaluation of a Sedative-Hypnotic Agent; Methaqualone (Quaalude).” Journal of the American Medical Association 199 (1967): 749.

Falco, M. “Methaqualone Misuse: Foreign Experience and United States Drug Control Policy.” International Journal of the Addictions 11 (1976): 597–610.

Gerald, M.C., and P.M. Schwirian. “Nonmedical Use of Methaqualone.” Archives of General Psychiatry 28 (1973): 627–31.

Ostrenga, J.A. “Methaqualone—A Dr. Jekyll and Mr. Hyde?” Clinical Toxicology 6 (1973): 607–9.

Perry, C.D., et al. “The South African Community Epidemiology Network on Drug Use (SACENDU): Description, Findings (1997–99) and Policy Implications.” Ad- diction 97 (2002): 969–76.

Roden, S., P. Harvey, and M. Mitchard. “Influence of Alcohol on the Persistent Effects on Human Performance of the Hypnotics Mandrax and Nitrazepam.” Interna- tional Journal of Clinical Pharmacology, Therapy and Toxicology 15 (1977): 350–55.

Wetli, C.V. “Changing Patterns of Methaqualone Abuse. A Survey of 246 Fatalities.” Journal of the American Medical Association 249 (1983): 621–26.


Pronunciation: meth-KATH-i-nun
Chemical Abstracts Service Registry Number: 5650-44-2 Formal Names: Ephedrone, Methylcathinone

Informal Names: Bathtub Speed, C, Cadillac Express, Cat, Crank, Gager, Gagger, Go Fast, Goob, Jeff, Khat, Qat, Quicksilver, Slick Superspeed, Somali Tea, Star, Stat, Tweak, Tweek, Tweeker, Wild Cat (with cocaine), Wonder Star

Type: Stimulant (amphetamine class). See page 12 Federal Schedule Listing: Schedule I (DEA no. 1237) USA Availability: Illegal to possess
Pregnancy Category: None

Uses. The substance is derived from cathinone (the most potent drug in- gredient in khat) and is related to methamphetamine. A U.S. patent was granted for methcathinone in 1957, but because of adverse actions described below the drug never went into commercial medical production.

Despite methcathinone’s many drawbacks noted below, some drug abusers have found appealing aspects in the compound. These users experience eu- phoria accompanied by strong and prolonged feelings of sexual pleasure, along with an ability to use more alcohol than normal. Such characteristics can transform an otherwise unappealing substance into a party drug. Appar- ently these characteristics were discovered in the Soviet Union; at least that is where the drug first surfaced as a popular item, accounting for perhaps one fifth of illicit drug use in that territory during the late 1980s and early 1990s. In the 1990s the drug took hold in Michigan and spread elsewhere in America.

Drawbacks. At high doses the drug exhibits classic amphetamine effects: appetite loss, insomnia, hallucinations, paranoia, restlessness, and impaired ability to focus attention and to get along with people. Users have said meth- cathinone is more prone to produce paranoia than methamphetamine. In animal experiments methcathinone interferes with breathing, promotes trem- bling and epilepticlike seizures, and impedes limb control. In humans a dose may increase body temperature, cause irregular heart rate, excessively reduce blood pressure, bring on nosebleeds, produce red and blue spots in extremities accompanied by cold sweating, promote tics and cramps along with nausea and headaches, generate evidence of liver and kidney damage, and cause in-

290 Methcathinone

fected facial cysts that can leave scars. Heart impairment has been discovered among current users. Examination of former users reveals brain damage that may lead to Parkinson’s disease. Autopsies find widespread blood vessel dam- age throughout the body, from skin to vital organs.

Abuse factors. When effects from a dose ebb, the drug’s initial elevation of mood converts into the opposite, and abusers lacking in self-confidence may rely more and more on additional doses of the drug to restore a positive mood instead of seeking to build and rely upon inner resources. As mental spirits level off or decline, abusers respond with binge behavior—rather than grad- ually increasing their dosage, they alternate between heavy use and no use. They may take the drug every hour or so for days even though users report that effects of a dose can last for almost a week.

A group of 19 users compared methcathinone with other drugs. Those per- sons described methcathinone’s stimulation as more of a physical jolt and cocaine’s as more of a mental jolt. None of cocaine’s physical numbing was noticed with methcathinone. The latter drug was described as stronger, cheaper (at least in the 1990s), and having better duration than cocaine. The 19 persons all misused methcathinone in ways that added turmoil to their lives and said their need for the drug was psychological, not physical. The users mostly said the drug had ruined their lives. Those lives seemed troubled before methcathinone entered, however. Only 4 of the persons were employed when they started using the substance. Relationships with family and friends declined, but that decline was accelerated by explosive anger and by delib- erately avoiding friends and relatives. The employed persons got into conflicts with coworkers or stayed away from the workplace. All lost their jobs. No doubt the drug made things worse, but abusers seemed to be struggling with sad lives before adding methcathinone to other drugs they abused.

Drug interactions. Users claim that eating sugar can worsen methcathi- none’s undesirable psychological effects.

Cancer. Not enough scientific information to report.
Pregnancy. Not enough scientific information to report.
Additional information. “Qat” and “Somali tea” are nicknames for both

methcathinone and khat, but those are different substances. Additional scientific information may be found in:

Calkins, R.F., G.B. Aktan, and K.L. Hussain. “Methcathinone: The Next Illicit Stimulant Epidemic?” Journal of Psychoactive Drugs 27 (1995): 277–85.

Emerson, T.S., and J.E. Cisek. “Methcathinone: A Russian Designer Amphetamine In- filtrates the Rural Midwest.” Annals of Emergency Medicine 22 (1993): 1897–903.

Goldstone, M.S. “ ‘Cat’: Methcathinone—A New Drug of Abuse.” Journal of the Amer- ican Medical Association 269 (1993): 2508.

Zhingel, K.Y., et al. “Ephedrone: 2-Methylamino-1-Phenylpropan-1-One (Jeff).” Journal of Forensic Sciences 36 (1991): 915–20.


Pronunciation: meth-ill-FEN-i-dait
Chemical Abstracts Service Registry Number: 113-45-1. (Hydrochloride form


Formal Names: Concerta, Metadate CD, Metadate ER, Methylin, Ritalin

Informal Names: Pellets, Rities, West Coast. Combination with pentazocine: Crackers, 1s & 1s, Poor Man’s Heroin, Ritz & Ts, Sets, Ts & Rits, Ts & Rs. Combination with heroin: Speedball

Type: Stimulant (amphetamine class). See page 12 Federal Schedule Listing: Schedule II (DEA no. 1724) USA Availability: Prescription
Pregnancy Category: C

Uses. Methylphenidate became available in the 1940s. The drug is fast acting and long lasting. Although not a true amphetamine, methylphenidate has properties similar to dextroamphetamine (including appetite suppression and sleep disruption) but is less potent.

Methylphenidate’s prime medical use is for managing attention deficit hy- peractivity disorder (ADHD), a condition in which people are so excitable that they have severe problems with social interactions. The affliction is more com- mon in children than adults, and methylphenidate seems more effective against ADHD in children, though one study finds the drug to have little influence on long-term outcome. Limited success is seen in experimental usage of the drug to help autistic children. A case report says a regimen of that drug and the antidepressant sertraline (Zoloft) cured a young kleptomaniac. Among adults methylphenidate is typically prescribed for narcolepsy and has also been used successfully against apathy and depression. Despite the drug’s oc- casional tendency to increase blood pressure, studies find the substance prom- ising for rehabilitation of persons recovering from stroke and other brain injuries, not only improving mood but also helping ability to move.

In volume of use, methylphenidate has been called the predominant med- ically prescribed psychoactive drug among American juveniles. A survey of approximately 200,000 prescription records of preschool children found about 1% of them to be receiving stimulants in the 1990s, and almost all those pre- scriptions were for methylphenidate. By the decade’s end, two medical au- thorities put the school-age population’s stimulant prescription figure as high

292 Methylphenidate

as 6%. In the mid-1990s approximately 1.5 million American school-age chil- dren were taking stimulant medications just for ADHD, compared to 50 chil- dren receiving methylphenidate for any purpose in Great Britain in 1991. Another comparison: A 1999 report said 1.65% of students in one South Af- rican urban area were receiving methylphenidate, but none of these children were Afrikaans. Such dramatic differences in prescribing practices suggest strong cultural influence on what is considered acceptable medical treatment. During the mid-1980s great debate arose in the United States about the custom of routinely prescribing methylphenidate to juveniles. The debate was based on ethical values rather than strictly medical concerns, with some persons arguing that the drug was being used as an agent of social control instead of treating disease. After a flurry of lawsuits, the controversy eased.

A review of 23 studies evaluating ADHD drug effectiveness found little distinction among methylphenidate, dextroamphetamine, and pemoline.

Drawbacks. Children with ADHD may also experience muscle tics, which methylphenidate and other stimulants can worsen. Such a dual condition is challenging, but in short-term usage, methylphenidate has been found effec- tive for lessening ADHD without increasing tics, even though one study found that almost 10% of ADHD children may develop temporary tics when taking methylphenidate. A case report notes that a child began stuttering when dos- age started, with the stutter ceasing when dosage ceased.

Amphetamine class drugs can promote psychosis and other psychiatric dis- ability, and such unwanted results have been observed with methylphenidate, including paranoia and hallucinations. In youngsters methylphenidate has been known to bring on obsessive-compulsive behavior.

Among juveniles the compound has caused skin rash, stomach distress, mild headaches, and sleep difficulties. In juveniles the compound can at least temporarily reduce appetite, although in elderly users the drug has been ob- served to increase appetite. Controversy exists about whether the drug affects growth. The substance is associated with stroke suffered by two boys.

Methylphenidate is not recommended for persons suffering from seizures. The drug has been reported to cause anemia and is suspected of worsening allergies. The substance has been known to impair vision and is not recom- mended for persons with glaucoma. Methylphenidate tends to increase im- mune system activity; in theory that might affect vaccinations and also harm HIV (human immunodeficiency virus)-positive persons. In some humans ab- normal liver activity has been seen, but whether the drug caused or revealed the problem is uncertain. The drug appears to cause heart damage in rats and mice, and a human case has been reported.

Despite potential drawbacks, however, with proper precautions the drug is considered generally safe for medical utilization.

Abuse factors. In primates cocaine and methylphenidate seem to work in similar ways; indeed, some illicit substance users have been unable to tell whether they received a dose of cocaine or methylphenidate. Although meth- ylphenidate is a Schedule II substance, abuse of the drug is uncommon. De- mand is small enough that the U.S. Drug Enforcement Administration reports no illicit manufacturing. A large review of scientific literature covering the years 1966 to 1998 was unable to substantiate news media claims about wide

Methylphenidate 293

abuse. A survey of 161 children receiving the medication found none who believed they were at risk of becoming abusers (a belief sustained by general experience nationwide), although about 25 had encountered situations where someone wanted access to their drug supply. The oral format has little ability to produce euphoria. The drug has been called a more potent hallucinogen than LSD, but support for that claim seems nonexistent in scientific journals.

Adults suffering from ADHD are routinely found to be cocaine abusers. An experiment showed methylphenidate effective for improving both problems, but the treatment was also accompanied by several weeks of individual coun- seling, which in itself might have been a major factor in any improvement. Some drug abuse treatments seek to switch abusers from one drug to another. Results of an experiment were unencouraging for shifting cocaine abusers to methylphenidate but had intriguing findings nonetheless. For example, co- caine addicts are generally considered particularly susceptible to addictive properties in other drugs, but methylphenidate had little appeal to subjects in this experiment. The experiment also found mental effects of methylphenidate to include irritability, worry, sadness, and a general mood of dissatisfaction. Physical effects included quivering and accelerated pulse rate. Still, even though these cocaine users found methylphenidate unappealing, methylphen- idate is not recommended for any medical treatment in persons with a history of substance abuse.

Experimenters using methylphenidate to help smokers give up tobacco found the results encouraging.

Methylphenidate abusers sometimes grind up oral tablets and inject the material. A preparation designed to go through the digestive system can have untoward consequences in the circulatory system. The talc in oral methyl- phenidate can lodge in small blood vessels, cutting off blood flow to portions of the lungs, eyes, or brain. Respiratory difficulty, vision damage, and crip- pling paralysis can result. Studies of such injuries sometimes refer to autopsy results; such reference implies that this type of drug abuse is dangerous in- deed.

Tolerance has been noted from illicit usage. Intense depression can emerge when an abuser stops using the drug.

Drug interactions. Apparently methylphenidate interacts with valproic acid, a substance used to treat epilepsy in ADHD children; the interaction can cause teeth grinding and interfere with body movement. Interaction with serotonin reuptake inhibitors found in some antidepressants is suspected of causing heartbeat irregularity in a teenager, and methylphenidate is not recommended for persons taking monoamine oxidase inhibitors (MAOIs, found in some antidepressants). High blood pressure can occur if tricyclic antidepressants are used with methylphenidate, and methylphenidate also seems to reduce time needed for tricyclic antidepressants to show results; lower doses of those drugs are advised when a person is taking methylphenidate. Interactions with phenobarbital have been observed. Methylphenidate has allowed terminal cancer patients to tolerate higher doses of opiates, thereby improving pain management.

Cancer. Scientists looking for evidence that methylphenidate causes cancer in rats and humans have instead found lower-than-normal incidence of the

294 Methylphenidate

disease. In one experiment mice developed liver tumors after receiving many times the therapeutic dose, but the strain of mice used is prone to such tumors, so scientists are uncertain about what the experiment means.

Pregnancy. An experiment using mice found the drug to have no effect on reproduction. Studies of pregnant women abusing methylphenidate find no birth defects associated with the drug, but babies tend to be small and pre- mature. A one-year follow-up found the infants to be in the normal range of development, although some were at the low end of normal. In one study all the pregnant women abusing methylphenidate were cigarette smokers; some were alcoholics; some had sexually transmitted disease; few received much prenatal care. In another study the methylphenidate-abusing mothers’ situa- tions were so grim that over half the infants were put into immediate foster care after delivery and did not go home with their mothers. Such confounding factors cloud any conclusions about the drug’s effect on fetal development. Whether levels in breast milk are safe for infants is unconfirmed.

Additional scientific information may be found in:

Cox, D.J., et al. “Effect of Stimulant Medication on Driving Performance of Young Adults with Attention-Deficit Hyperactivity Disorder: A Preliminary Double- Blind Placebo Controlled Trial.” Journal of Nervous and Mental Disease 188 (2000): 230–34.

Crutchley, A., and J.A. Temlett. “Methylphenidate (Ritalin) Use and Abuse.” South African Medical Journal 89 (1999): 1076–79.

Debooy, V.D., et al. “Intravenous Pentazocine and Methylphenidate Abuse during Pregnancy. Maternal Lifestyle and Infant Outcome.” American Journal of Diseases of Children 147 (1993): 1062–65.

Efron, D., F.C. Jarman, and M.J. Barker. “Child and Parent Perceptions of Stimulant Medication Treatment in Attention Deficit Hyperactivity Disorder.” Journal of Paediatrics and Child Health 34 (1998): 288–92.

Jadad, A.R., et al. “Treatment of Attention-Deficit/Hyperactivity Disorder.” Evidence Report/Technology Assessment, no. 11 (1999): 1–341. Issue no. 11 is available online at: http:/

Llana, M.E., and M.L. Crismon. “Methylphenidate: Increased Abuse or Appropriate Use?” Journal of the American Pharmaceutical Association 39 (1999): 526–30. Parran, T.V., Jr., and D.R. Jasinski. “Intravenous Methylphenidate Abuse. Prototype

for Prescription Drug Abuse.” Archives of Internal Medicine 151 (1991): 781–83. Scarnati, R. “An Outline of Hazardous Side Effects of Ritalin (Methylphenidate).” In-

ternational Journal of the Addictions 21 (1986): 837–41.


Pronunciation: meth-ill-tess-TOSS-ter-ohn
Chemical Abstracts Service Registry Number: 58-18-4 Formal Names: Android, Estratest, Methitest, Testred, Virilon Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000)
USA Availability: Prescription
Pregnancy Category: X

Uses. Methyltestosterone is a synthetic drug manufactured from testoster- one. Methyltestosterone’s medical uses include supplementation of testoster- one in males with low levels of that hormone and treatment of female breast cancer. Scientists report unsatisfactory results from a test of whether the com- pound might work as a male contraceptive and mixed results when the sub- stance was used to treat male impotence. Impotence improvement was better when methyltestosterone was taken in combination with a yohimbe prepa- ration. Methyltestosterone has provided pain relief and occasionally fertility enhancement to women suffering from a reproductive disorder called endo- metriosis externa. Therapeutic regimens to build up bone strength in older women may include methyltestosterone, as may therapies designed to com- pensate for hormonal changes caused by menopause. In research projects height increase occurred when the drug was administered to boys of short stature. Experimenters describe the drug as effective treatment for hereditary angioedema, an affliction involving tissue swelling. The drug also has agri- cultural uses such as illegally promoting pig and cattle growth.

Drawbacks. Volunteers who took methyltestosterone in an experiment showed slight changes in thinking ability, and 2 of the 20 subjects had man- iclike episodes that might be attributable to the drug. A report noted that someone receiving the drug experienced visual and auditory hallucinations, and a case report indicated that methyltestosterone and methandrostenolone were likely causes of psychotic incidents experienced by two bodybuilders. A human experiment attempted to document the drug’s psychological effects but was unable to correlate behavioral changes with volunteers’ usage of the substance. The substance is suspected of causing liver damage, sometimes resulting in jaundice, lesions, tumors, or other conditions. The compound may cause fluid retention, which can be risky for persons with kidney, liver, or

296 Methyltestosterone

heart malfunction. Like many drugs of this type, methyltestosterone can cause females to develop masculine characteristics such as facial hair or coarser voice. Such effects can become permanent if dosage is not swiftly stopped upon first appearance of the changes. Other unwanted actions of the drug can include acne, headache, uneasiness, burning or prickling sensations, menstrual disturbances, nausea, and high blood levels of calcium and cholesterol. In rats high blood pressure has been traced to methyltestosterone.

Abuse factors. Methyltestosterone is banned from athletic competitions, but some athletes are tempted to use it, nonetheless. Claims that the compound produces gains in weight and muscle strength have been difficult to document in humans, partly because experimenters cannot subject humans to experi- mental conditions that are as brutal as can be used with laboratory animals. A robust experiment on rats demonstrated increased strength and stamina from methyltestosterone.

Drug interactions. A case report mentions that a person using the hormone along with the anticholesterol medicine clofibrate developed extremely low levels of high-density lipoprotein (the so-called good cholesterol), a develop- ment attributed to methyltestosterone. A similar result occurred in an exper- iment tracking women using this anabolic steroid along with female hormones called esterified estrogens. Methyltestosterone interferes with blood clotting, which can be a serious problem for persons taking anticlotting medicine. A case report indicates that the substance interacts badly with cyclosporine, an immunosuppressive agent used to fight rejection of organ transplants. A small experiment using methyltestosterone to increase benefits from the tricyclic an- tidepressant imipramine went awry when almost all patients became para- noid, a condition that rapidly disappeared when methyltestosterone dosage stopped.

Cancer. Researchers have noted liver cancer in mice that received methyl- testosterone. Other case reports indicate strong suspicion that the drug causes human liver cancer. The substance has been associated with a person’s de- velopment of prostate cancer, but “association” is not the same as cause.

Pregnancy. Women are advised to avoid the drug during pregnancy be- cause the substance may masculinize a female fetus, a discovery made in the 1950s when methyltestosterone was a standard medication for reducing the likelihood of miscarriage. Nursing mothers are advised to avoid the drug be- cause it might pass into milk and masculinize a female infant. These effects of the drug are powerful enough that methyltestosterone is used in tilapia farming to change females of this fish into males. The drug has also been used to change female flounder into male fish. Research on rats has demonstrated that masculinizing effects on females can persist into a subsequent generation that did not receive the drug. Human males who use the substance may pro- duce more male offspring than usual.

Additional scientific information may be found in:

Black, J.A., and J.F. Bentley. “Effect on the Fetus of Androgens Given During Preg- nancy.” Lancet 1 (1959): 21–24.

Greene, R., and L.S. Carstairs. “Effect of Anabolic Hormones on the Growth of Un- dersized Boys.” British Journal of Clinical Practice 27 (1973): 3–7.

Methyltestosterone 297

Regestein, Q.R., et al. “Neuropsychological Effects of Methyltestosterone in Women Using Menopausal Hormone Replacement.” Journal of Women’s Health & Gender- Based Medicine 10 (2001): 671–76.

Richardson, J.H., and S. Smith. “A Comparison of the Effects of Dianabol and Meth- yltestosterone on Muscle Contraction and Fatigue.” Journal of Sports Medicine and Physical Fitness 21 (1981): 279–81.

Simon, J.A. “Safety of Estrogen/Androgen Regimens.” Journal of Reproductive Medicine 46 (2001 Supp. 3): 281–90.

Su, T.P., et al. “Neuropsychiatric Effects of Anabolic Steroids in Male Normal Volun- teers.” Journal of the American Medical Association 269 (1993): 2760–64.

Westaby, D., et al. “Liver Damage from Long Term Methyltestosterone.” Lancet 2 (1977): 261–63.

Wilson, I.C., A.J. Prange, and P.P. Lara. “Methyltestosterone with Imipramine in Men: Conversion of Depression to Paranoid Reaction.” American Journal of Psychiatry 131 (1974): 21–24.


Pronunciation: mid-AZ-ah-lam
Chemical Abstracts Service Registry Number: 59467-70-8. (Hydrochloride form

59467-96-8; maleate form 59467-94-6)
Formal Names: Dormicum, Hypnovel, Versed
Type: Depressant (benzodiazepine class). See page 21 Federal Schedule Listing: Schedule IV (DEA no. 2884) USA Availability: Prescription
Pregnancy Category: D

Uses. This quick-acting drug’s common medical uses are to reduce anxiety, calm people, and help them sleep. Naturalists use the substance to knock out wildlife ranging from foxes to aardvarks. Effects do not last a long time, typ- ically making the substance a good choice for weakened persons or animals who would be strained by a longer-acting drug. For example, weary moun- taineers climbing Mt. Everest have used the drug to improve quality of sleep.

One study found the drug could help workers who must alter their sleep schedules for reporting to different work shifts. Experiments show the drug having potential for treating muscle spasms. Midazolam has been used suc- cessfully to alleviate status epilepticus, in which people have continual sei- zures, and to control seizures caused by high fevers in children. The U.S. Army has tested midazolam experimentally, but with limited success, to coun- teract seizures and other poisonous effects from the chemical warfare sub- stance soman. A case report about treating a cobra snake bite victim notes that midazolam worked when another drug faltered. Midazolam reduces blood pressure. The compound is routinely given to people before surgical, dental, or uncomfortable medical procedures and is used to relieve pain in afflictions and after surgery. Midazolam can produce amnesia about events that occurred while under the drug’s influence and may be able to interfere with remembering things that occurred shortly before the drug was received. That amnesia action can be beneficial in reducing stress from medical treat- ments but might also be used by unscrupulous persons wanting to exploit someone.

Drawbacks. When injected intravenously the drug can be so hazardous that in some instances a resuscitation specialist must be on hand with the exclusive duty of monitoring the patient’s condition at all times. Without that precaution

Midazolam 299

people have suffered crippling brain damage or death from respiratory arrest caused by the drug while a medical procedure was being performed. Respi- ratory emergencies have also occurred from oral dosage. Midazolam is not recommended for persons suffering from breathing trouble. Nonetheless, de- spite the drug’s potential hazards, examination of 5,439 records of patients receiving the drug at one hospital revealed only 3 instances of respiratory arrest. Examination of 9,842 medical records of persons who received mida- zolam in 14 hospitals did not reveal serious respiratory events caused by the drug; indeed, the study concluded that people were more likely to die from diazepam. That conclusion, of course, was based on administration of the drugs in a medical setting, not misuse on the street.

A rat study found the drug to have “minimal” ability to cause brain dam- age, and then only in older rats, even after four months of daily dosing. In a subsequent and related report investigators stated flatly that the drug does not cause brain damage, although once again slight differences were observed when older rats were compared to others.

Researchers have noted that midazolam harms white blood cells. Other un- wanted effects include headache, coughing and hiccups, nausea, and vomit- ing. Less commonly, the drug can prompt euphoria, hallucinations, tremor, rapid heartbeat, discomposure, and aggression. Two researchers tracking vi- olent deaths in Finland concluded that the drug was found in victims more often than would be expected through chance occurrence. Hallucinations by surgical patients have occurred often enough and can be realistic enough (such as patients perceiving imaginary sexual assault by medical personnel) that medical staff have been advised to have someone witness all contact with patients receiving the drug.

Midazolam lengthens reaction times, although two experiments found that users performed normally 4 hours after a dose such as a patient would receive for outpatient surgery. Those findings are supported by other studies as well, including one using test equipment to measure performance of commercial airline pilots. Nonetheless, persons are supposed to avoid activity requiring careful vigilance (such as driving) for at least 24 hours after taking midazolam.

A small study found that a dose of midazolam produces higher blood levels of the drug and lasts longer in ethnic Mexicans than in ethnic whites.

Abuse factors. Among monkeys dependence has been established with the drug after 5 to 10 weeks of steady dosage. Sudden cessation of dosage can provoke a withdrawal syndrome: perspiration, tremors and cramps, vomiting, convulsions, and hallucinations. The syndrome can be avoided by gradually reducing drug use instead of stopping all at once. Some researchers believe tolerance has been demonstrated. The substance is considered to have at least the same addiction potential as diazepam, which is three or four times weaker than midazolam.

Drug interactions. In some circumstances midazolam can lower blood pres- sure drastically and cause seizures; administering the drug with fentanyl or other opiates can increase the likelihood of such severe actions. Rat experi- ments unexpectedly found that the stimulant caffeine boosts difficulties in movement caused by midazolam, and cocaine also worsened that perfor- mance. Opiates or alcohol can deepen some midazolam effects in humans,

300 Midazolam

and rat experiments find that midazolam makes alcohol more appealing. The HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syn- drome) drug saquinavir and the antibiotic erythromycin increase midazolam levels in the body and make effects last longer. The antacid and ulcer medi- cation cimetidine (such as Tagamet) can lengthen sedation from a midazolam dose. Some research indicates that drinking grapefruit juice increases mida- zolam’s ability to act upon a person, but other research does not support that finding. The tuberculosis medicine rifampin and the epilepsy drugs phenytoin and carbamazepine diminish midazolam’s effectiveness.

Cancer. Rat and mice experiments have produced no cancer even when midazolam was given daily for two years at 25 times the recommended hu- man dose. The same usage of the drug at about 225 times the recommended human dose, however, produced liver and thyroid tumors. Relevance of the latter outcome to human medical use, involving normal dosage and typically using the drug for one day, is unclear. Gene mutations are considered an element in causing cancer, and midazolam did not produce mutations in as- sorted standard tests, nor were they observed in a study of patients receiving the drug.

Pregnancy. The drug has been given to mice, rats, and rabbits at 5 to 32 times the normal human dose without producing birth defects. Researchers conducting one experiment concluded, however, that the drug altered behav- ior of mice after fetal exposure (making males more uneasy and females less uneasy) while slowing their development. Tests indicate that the drug will pass from a pregnant woman into the fetus. The substance has been success- fully used to treat eclampsia, a serious disease of late pregnancy involving convulsions, but midazolam is generally not desirable for pregnant women. The drug passes into the milk supply of nursing mothers, and caution is rec- ommended about breast-feeding in such circumstances.

Additional scientific information may be found in:

Curran, H.V., and B. Birch. “Differentiating the Sedative, Psychomotor and Amnesic Effects of Benzodiazepines: A Study with Midazolam and the Benzodiazepine Antagonist, Flumazenil.” Psychopharmacology 103 (1991): 519–23.

Dundee, J.W. “Fantasies during Sedation with Intravenous Midazolam or Diazepam.” Medico-Legal Journal 58 (1990, pt. 1): 29–34.

Gupta, A., et al. “The Effects of Midazolam and Flumazenil on Psychomotor Function.” Journal of Clinical Anesthesia 9 (1997): 21–25.

Kelly, D.J., et al. “The Effects of Midazolam on Pure Tone Audiometry, Speech Audi- ometry, and Audiological Reaction Times in Human Volunteers.” Anesthesia and Analgesia 88 (1999):1064–68.

Langlois, S., et al. “Midazolam: Kinetics and Effects on Memory, Sensorium, and He- modynamics.” British Journal of Clinical Pharmacology 23 (1987): 273–78.

“Midazolam.” Medical Letter on Drugs and Therapeutics 28 (1986): 73–74.
Nordt, S.P., and R.F. Clark. “Midazolam: A Review of Therapeutic Uses and Toxicity.”

Journal of Emergency Medicine 15 (1997): 357–65.


Pronunciation: moh-DA-fih-nill
Chemical Abstracts Service Registry Number: 68693-11-8 Formal Names: Alertec, Modiodal, Provigil
Type: Stimulant. See page 11
Federal Schedule Listing: Schedule IV (DEA no. 1680) USA Availability: Prescription
Pregnancy Category: C

Uses. This drug is a medical treatment for narcolepsy and other conditions involving difficulty in staying awake. The substance also improves vigilance. In the 1990s U.S. Air Force researchers called for exploration of the drug’s potential in assisting military missions. Investigators have found that the com- pound may assist aircraft pilots in maintaining a better performance level when deprived of sleep for extended periods. An experiment indicated that the drug can help military personnel engage in sustained operations for 64 hours without sleep, with fewer unwanted effects than amphetamine has. A French military experiment showed the drug could be used along with short naps to permit extended operations without normal sleep periods. Additional study has shown, however, that people using the compound are less aware of reduced quality of performance; in comparison, sleep-deprived individuals who use dextroamphetamine or a placebo have a more accurate assessment of their capabilities. Thus, from a practical standpoint, sleep-deprived persons using modafinil may be overconfident and try to do things that should not be attempted.

Modafinil is used against obstructive sleep apnea, in which people have temporary breathing stoppages while asleep and which can make them sleepy the next day. Experiments find that although modafinil helps people stay awake, it does not interfere with the quality of their sleep, as dextroamphet- amine does. Modafinil has helped patients respond better to antidepressant therapy while also reducing their feelings of weariness. Favorable results have been seen in experiments using the drug against attention deficit hyperactivity disorder (ADHD) and against organic brain problems caused by alcoholism. An animal study indicates the substance may have potential for treating Par- kinson’s disease. Some authorities speculate that the compound may reduce brain problems caused by aging. Modafinil makes animals more active.

302 Modafinil

Drawbacks. Modafinil can produce euphoria in humans. Headache, dry mouth, sore throat, appetite loss, nausea, diarrhea, uneasiness, depression, insomnia, fever, infection, and weakness have been reported by modafinil users. Among cardiac patients, unwanted actions may include heart palpita- tions, chest pain, and breathing difficulty. High doses have caused tremors, faster pulse rate, high blood pressure, peevishness, confusion, and aggression. Although the compound is a stimulant, it has a risk of adversely affecting skills needed for operating dangerous machinery such as automobiles.

A modafinil dose lasts a shorter time in young females than in young males.

Abuse factors. Modafinil’s chemical properties reduce or even eliminate its effects if injected or smoked, reducing its convenience for abuse. Studies in- dicate the drug has less abuse potential than many other stimulants, but mon- keys will self-administer modafinil, a traditional sign of addictive potential in a substance. Scientists running one monkey experiment noted, however, that only massive doses would interest the animals; even an amount of modafinil 200 times the size of a dextroamphetamine dose was not enough to get them to self-administer the two drugs at the same rate. In a rat test the rodents acted like modafinil has some effects reminiscent of cocaine. In one scientific study persons with a history of drug abuse found modafinil’s actions plea- surable and similar to those of methylphenidate. People using modafinil daily for 9 weeks showed no dependence; and a study of 140 patients who used the drug for varying amounts of time, ranging from 1 month to almost 10 years, revealed no dependence. Tests of humans taking modafinil daily for 40 weeks indicated no development of tolerance.

Drug interactions. Modafinil can make birth control pills and implants less effective. A laboratory test indicated that the drug may reduce blood levels of cyclosporine, an immunosuppressant used to help organ transplant patients. Modafinil may raise blood levels of diazepam, tricyclic antidepressants, the anti–blood clot medicine warfarin, and the epilepsy medicine phenytoin.

Cancer. Laboratory tests have not found indications that modafinil causes cancer.

Pregnancy. Fetal injury emerged in pregnant rats receiving 10 times the normal maximum human dose of modafinil, but pregnant rabbits receiving the same dosage did not show fetal damage attributable to the substance. At lower doses rat offspring appeared normal, and milk from nursing rats re- ceiving the drug did not seem to harm the pups. Effects on human pregnancy and milk are uncertain.

Additional scientific information may be found in:

Akerstedt, T., and G. Ficca. “Alertness-Enhancing Drugs as a Countermeasure to Fa- tigue in Irregular Work Hours.” Chronobiology International 14 (1997): 145–58.

Baranski, J.V., and R.A. Pigeau. “Self-Monitoring Cognitive Performance during Sleep Deprivation: Effects of Modafinil, D-Amphetamine and Placebo.” Journal of Sleep Research 6 (1997): 84–91.

Lyons, T.J., and J. French. “Modafinil: The Unique Properties of a New Stimulant.” Aviation, Space, and Environmental Medicine 62 (1991): 432–35.

“Modafinil for Narcolepsy.” Medical Letter on Drugs and Therapeutics 41 (1999): 30–31. Rugino, T.A., and T.C. Copley. “Effects of Modafinil in Children with Attention- Deficit/Hyperactivity Disorder: An Open-Label Study.” Journal of the American

Academy of Child and Adolescent Psychiatry 40 (2001): 230–35.

Morning Glory

Pronunciation: MOR-neen GLOH-ree

Chemical Abstracts Service Registry Number: None

Formal Names: Ipomoea hederacea, Ipomoea purpurea, Ipomoea sidaefolia, Ipomoea tricolor, Ipomoea violacea

Informal Names: Flying Saucers, Heavenly Blue, Pearly Gates, Tlitliltzin, Yaxce’lil Type: Hallucinogen. See page 25
Federal Schedule Listing: Unlisted
USA Availability: Nonprescription natural product

Pregnancy Category: None

Uses. Morning glory is a familiar flower. Many varieties exist, and some have drug properties. Although morning glory is an uncontrolled substance, the hallucinogenic varieties contain lysergic acid amide, a Schedule III de- pressant.

Seeds and roots of the Ipomoea hederacea morning glory are used medicinally. The natural product works as a laxative and as a treatment against intestinal worms. Traditional applications include combating flatulence, easing excessive feelings of fullness after a meal, and treating scabies (a skin disease caused by a parasite).

Albert Hofmann, the discoverer of LSD, became intrigued by accounts of seed called ololiuqui by the Aztecs. Folk medicine used its ointments or potions to treat flatulence, tumors, and venereal disease. Ingesting the seeds allowed Aztecs to commune with their gods, and native peoples still used ololiuqui for that purpose during the twentieth century. Hofmann found that the ololiuqui seeds of Mexico came from two kinds of morning glory: from Ipomoea sidaefolia (also called Rivea corymbosa) and from Ipomoea violacea (also called Ipomoea tricolor, whose seeds are also known as badoh negro). Seeds from both plants contained ergot chemicals resembling LSD.

Although Ipomoea violacea is often viewed in a drug context, the plant has agricultural usage as a natural means of weed control. Ipomoea purpurea is sensitive enough to airborne chemicals that researchers use it to measure air pollution.

Drawbacks. Morning glory seeds have been publicized as a substitute for LSD, but no less an authority than Hofmann himself found LSD and morning glory to have different effects. In particular he noted that morning glory emp-

304 Morning Glory

tied thoughts from the mind and made the world seem meaningless, while promoting unease, depression, and a weariness that transformed into sleep. In addition to being a hallucinogen, LSD has powerful stimulant actions, but when morning glory seed was tested on rats, they became less active than normal and, contrary to what would be expected with a hallucinogen, they showed no change in perceptual abilities. A team of researchers who studied reactions of volunteers described morning glory’s active chemicals as unlike LSD. Those volunteers nonetheless felt some euphoria; they also had a dis- torted sense of time and a crossover of senses (in which colors might be smelled or sounds might be seen), but hallucinations or alteration of con- sciousness did not seem to develop. The research team likened morning glory to the drug ibogalin (which lacks significant psychological effect despite its close relation to ibogaine) and to the drug scopolamine found in belladonna. A case report about a person being treated for morning glory seed overdose said no hallucinations were present.

Those kinds of observations seem to differ from the effects experienced by the Aztecs and modern native peoples. Indeed, some recreational users (and their medical caregivers) report morning glory experiences quite similar to those of LSD, from hallucinations to philosophical insights—although one short series of case reports about such reactions argued that every instance involved a psychologically abnormal person. Some users describe cold extrem- ities, a possible sign of ergot poisoning. A case report noted other physical reactions: red face and abdominal discomfort eased by “explosive diarrheic bowel movements.” The patient also had lowered blood pressure and heart rate, opposite to accounts about LSD.

Morning glory seeds purchased from garden stores are not intended for human consumption and may contain fungicides that could harm a person who ingests them, although one investigator doubts a human stomach can hold enough morning glory seeds to cause fatal poisoning from the fungicide coating. Experimenters have fed uncontaminated seed to rats as various per- centages of their diet, from less than 1% up to 8%. After 90 days animals receiving the greatest amount showed a higher death rate than normal, with males more affected than females. Although the animals had less weight gain than would be expected on an ordinary diet, various internal organs enlarged. In addition, liver damage occurred, and blood abnormalities appeared.

Abuse factors. In the 1960s the British government concluded that morning glory seeds were harmless, but American researchers did not reach a consen- sus about whether danger existed. Some authorities state that Ipomoea purpurea morning glory seeds lack psychedelic properties, but other authorities say otherwise.

Drug interactions. Not enough scientific information to report.

Cancer. The Ames test, a laboratory screen used to test substances for cancer-causing potential, reveals that morning glory seeds have that potential. Pregnancy. Lysergic acid amide has damaged embryo development in mice. Pregnant women are advised to avoid Ipomoea hederacea because it is suspected

of causing birth defects.
Additional scientific information may be found in:

Morning Glory 305

Blum, O., et al. “Ambient Tropospheric Ozone in the Ukrainian Carpathian Mountains and Kiev Region: Detection with Passive Samplers and Bioindicator Plants.” Environmental Pollution 98 (1997): 299–304.

Dungan, G.M., and M.R. Gumbmann. “Toxicological Evaluation of Morning Glory Seed: Subchronic 90-Day Feeding Study.” Food and Chemical Toxicology 28 (1990): 553–60.

Fink, P.J., M.J. Goldman, and I. Lyons. “Morning Glory Seed Psychosis.” Archives of General Psychiatry 15 (1966): 209–13.

Heim, E., H. Heimann, and G. Lukacs. “Psychotomimetic Effects of the Mexican Drug ‘Ololiuqui.’ ” Psychopharmacologia 13 (1968): 35–48.

Hofmann, A. “Teonanacatl and Ololiuqui, Two Ancient Magic Drugs of Mexico.” Bul- letin on Narcotics 23, no. 1 (1971): 3–14.

Ingram, A.L., Jr. “Morning Glory Seed Reaction.” Journal of the American Medical As- sociation 190 (1964): 1133–34.

“Morning Glory and Hallucinosis.” South African Medical Journal 40 (1966): 1015–16.


Pronunciation: MOR-feen

Chemical Abstracts Service Registry Number: 57-27-2

Formal Names: Astramorph, Duramorph, Infumorph, Kadian, Kapanol Sevredol, Morphine Sulfate, MS Contin, MSIR, MST Continus, MXL, Oramorph, Roxanol

Informal Names: Cube Juice, Dope, Dreamer, Emsel, First Line, God’s Drug, Hard Stuff, Hocus, Hows, Lydia, Lydic, M, Miss Emma, Mister Blue, Monkey, Morf, Morph, Morphide, Morphie, Morpho, Mother, MS, Ms. Emma, Mud, New Jack Swing (with heroin), Sister, Tab, Unkie, Unkie White, Stuff

Type: Depressant (opiate class). See page 22
Federal Schedule Listing: Schedule II (DEA no. 9300) USA Availability: Prescription
Pregnancy Category: C

Uses. Morphine was identified as opium’s main active ingredient in the early 1800s. The body transforms a heroin dose into morphine. If stored too long in a water solution, morphine will eventually transform into other chem- icals including morphine-N-oxide, a Schedule I controlled substance. Al- though pharmaceutical supplies of morphine come from opium harvests, mammals produce small amounts of morphine in their bodies. Thus the sub- stance is a natural product in both the plant and animal kingdoms. The drug can also be created entirely in a laboratory.

Morphine’s role in medicine did not become prominent until the hypoder- mic needle was introduced in the 1850s. Injection was long the main means of administration, but other delivery systems (such as absorption by the nasal lining and through rectal suppositories) have since been developed. Oral dos- age formats are also available.

Morphine is widely used to sedate people and to ease anxiety. The drug is commonly given to treat acute pain from injury or surgery and chronic pain from assorted afflictions. The hurting does not actually go away, but people become less aware of it. In addition to pain control, morphine also has anti- inflammatory actions and can suppress coughing.

The drug tends to produce better pain relief in women than in men. A small study examined whether Chinese men respond to morphine differently than white men do: Doses lasted longer in the whites, interfered more with their breathing, and produced greater reduction in their blood pressure.

Morphine 307

Drawbacks. When used to reduce continual pain in serious disease, too much morphine can increase discomfort rather than relieve it and cause a condition in which a patient experiences pain from activity that should not be uncomfortable.

Morphine can make people drowsy, so they should avoid operating an au- tomobile or other hazardous machinery until they know how the drug affects them. Despite morphine’s safety in a medical context, it can be hazardous when injected into fluid circulating through the spinal cord and brain, and if hospital staffs use this technique, they are advised to have resuscitation equip- ment on hand.

Nausea and vomiting are common unwanted effects from morphine. It pro- motes constipation and urine retention. Itching and hives can occur. The drug interferes with sexual activity by male rats and lowers testosterone levels in human males. Morphine can impede breathing and often is avoided if a per- son suffers from asthma. Rats dosed with morphine for six weeks developed a weakened immune system. People can experience seizures and accelerated heart activity from a strong dose.

Abuse factors. After several weeks of medical dosage a person can experi- ence noticeable dependence with morphine. Such development should take longer with adulterated street supplies. Medical patients who were surveyed about their experience with morphine claimed to have experienced no diffi- culty in stopping the drug. Addiction from medical use is almost unheard of. Normally withdrawal symptoms are a mild version of the opiate withdrawal syndrome. Tolerance is normally described as evidence of drug abuse, but morphine tolerance can develop in persons receiving the drug medically for pain relief. Symptoms of such tolerance include a need to take doses more often and at a higher strength in order to produce the same amount of pain relief. This is notable because tolerance to medical effects of a drug tends to be unusual; perhaps the development indicates a substantial psychological component in morphine’s pain management. Tolerance is commonly observed among addicts, but they do not continually increase their dosage. At some point they generally reach a level adequate to maintain the sensations they seek. In the 1980s a mice experiment indicated that vitamin C may prevent morphine tolerance and dependence, but judging from subsequent absence of this technique in treating humans, apparently initial hopes for the therapy have not been fulfilled.

One of the main appeals in illicit use of morphine is the drug’s ability to induce calmness. People making unauthorized use of the drug for this purpose are not so much using the drug for recreation as for relieving mental suffering. In some people the drug can cause euphoria, a characteristic that can have appeal strictly for recreation but also for self-medication. In these and other respects, morphine and heroin will appeal to the same sorts of people for the same sorts of reasons.

For decades morphine addiction was portrayed as the classic kind of drug abuse. Although the substance was unwelcome in the workplace as the twenty-first century began, a century earlier some workers used the drug to increase productivity in both manual and intellectual tasks by relieving ten- sion that otherwise diminished performance. Other pharmaceuticals later su-

308 Morphine

perseded that antianxiety function of morphine. Somewhat surprisingly, given morphine’s depressant actions, researchers have found the drug can improve performance on a test of response time in decision making. Other researchers have found no effect on performance in tests of memory, reasoning, muscular coordination, and various additional skills basic to everyday living. Few ill effects seem to come from chronic use of pure morphine (as opposed to adul- terated street supplies). Addicts with access to the pure product have lived healthy and productive lives into old age. As drug laws tightened over the past century, use of morphine by ordinary middle-class people declined, shift- ing the prevalence of nonmedical morphine usage from law-abiding persons into populations with more social deviance. Consequently, illicit use of mor- phine became more associated with society’s outcasts. That association, how- ever, was caused by changes in laws and social attitudes (changes in setting), not by any chemical effect of the drug.

Drug interactions. Animal and human experiments show that more pain relief can come from morphine if ephedrine is taken at the same time. Dex- troamphetamine can improve pain relief provided by morphine. Alcohol, tri- cyclic antidepressants, and monoamine oxidase inhibitors (MAOIs, found in some antidepressants and other medicine) can boost morphine effects. Rat experiments indicate that benzodiazepine class depressants lengthen the effect from a morphine dose. Researchers find that morphine and nicotine have cross-tolerance in mice.

Cancer. Morphine is not known to cause cancer. Some laboratory tests and some studies of human users, however, detect cell damage that could lead to cancer. Some people smoke morphine, and the smoke is suspected of causing esophageal cancer. Evidence exists that naturally occurring morphine in lung tissue may constrain development of lung cancer, that nicotine counteracts such protection, and that tobacco smokers have more naturally occurring mor- phine in their lung tissue than nonsmokers (perhaps because the body in- creases morphine production when challenged by nicotine). All this evidence, however, involves minute levels of naturally occurring morphine in the body and does not support taking the drug in hopes of avoiding lung cancer.

Pregnancy. When given in amounts exceeding normal human medical doses by hundreds of times, morphine has caused animal birth defects. Malforma- tions involving bones and soft tissues have been observed in animals. Preg- nant rats and hamsters dosed on morphine produce male offspring that exhibit feminized behavior. When morphine was routinely given to male adolescent rats, the drug seemed to interfere with sexual maturation. As their offspring reached adulthood, they appeared normal but had hormone abnormalities.

In humans no increase in birth defects has been observed in offspring of women who used morphine during pregnancy. A morphine dose quickly passes from the woman into the fetus, however, and reaches a blood level similar to the woman’s. A dose lasts longer in the fetus than elsewhere in a woman’s body. The drug reduces fetal motions. A baby born to a chronic morphine user can have dependence on the drug and exhibit withdrawal symptoms after birth. One study found that infants receiving morphine for medical purposes soon after birth show no ill effects five years later in con- duct, muscular coordination, or intelligence.

Morphine 309

Morphine apparently passes into a mother’s milk. One case report described the amount as minimal and found no effect on the nursing infant, but another report tells of an infant receiving so much morphine from milk that depen- dence developed.

Additional scientific information may be found in:

Hamilton, G.R., and T.F. Baskett. “In the Arms of Morpheus, the Development of Mor- phine for Postoperative Pain Relief.” Canadian Journal of Anaesthesia 47 (2000): 367–74.

Hill, J.L., and J.P. Zacny. “Comparing the Subjective, Psychomotor, and Physiological Effects of Intravenous Hydromorphone and Morphine in Healthy Volunteers.” Psychopharmacology 152 (2000): 31–39.

O’Neill, W.M., et al. “The Cognitive and Psychomotor Effects of Morphine in Healthy Subjects: A Randomized Controlled Trial of Repeated (Four) Oral Doses of Dex- tropropoxyphene, Morphine, Lorazepam and Placebo.” Pain 85 (2000): 209–15.

Walker, D.J., and J.P. Zacny. “Subjective, Psychomotor, and Analgesic Effects of Oral Codeine and Morphine in Healthy Volunteers.” Psychopharmacology 140 (1998): 191–201.

Zacny, J.P., et al. “Comparing the Subjective, Psychomotor and Physiological Effects of Intravenous Pentazocine and Morphine in Normal Volunteers.” Journal of Phar- macology and Experimental Therapeutics 286 (1998): 1197–207.


Pronunciation: MOTH-ballz
Chemical Abstracts Service Registry Number: None
Formal Names: Naphthalene, Paradichlorobenzene
Type: Inhalant. See page 26
Federal Schedule Listing: Unlisted
USA Availability: Generally available nonprescription product Pregnancy Category: None

Uses. Mothballs typically contain naphthalene or paradichlorobenzene. Nei- ther persons who use mothballs recreationally nor their medical caregivers are always aware of which kind of mothballs have been used. Diaper pail and toilet deodorizers may contain one or the other of those chemicals. Naphtha- lene varieties look dry, and paradichlorobenzene products appear oily. Nor- mally people inhale fumes, but cases of oral ingestion are known. Naphthalene can also be absorbed through the skin; an infant died from using diapers and blankets contaminated with the substance. Some glues contain naphthalene, but sensations from glue sniffing are normally considered a result of toluene.

Drawbacks. Naphthalene may create agitation and tiredness, fever, skin paleness, headache, appetite loss, abdominal discomfort, nausea and vomiting, diarrhea, cataracts, and kidney failure. Blood disorders serious enough to pre- vent the body from utilizing enough oxygen from the lungs may arise. The kidney failure can create excessive blood potassium levels, which in turn can cause heart failure. Seizures and coma may also occur. Jaundice is a known affliction from naphthalene, and a case report notes fatal liver damage.

A case report tells about difficulty with control of fingers due to inhaling mothball fumes. Paradichlorobenzene is not associated with such an affliction, so the problem is assumed to have come from naphthalene mothballs. Com- pared to naphthalene, harm from paradichlorobenzene normally takes longer to appear but may include liver and kidney malfunction. A case of anemia is known from eating two paradichlorobenzene toilet freshener blocks per week.

Abuse factors. One person experienced tremors and weariness upon stop- ping daily oral ingestion of paradichlorobenzene mothballs (which suggests dependence may have developed).

Drug interactions: Not enough scientific information to report.
Cancer. Naphthalene has not been found to cause cancer. Paradichloroben-

Mothballs 311

zene fumes failed to produce cancer in a short animal test. The disease did develop in mice and rats that received oral dosage, and paradichlorobenzene caused cell mutations (a possible indication of cancer-causing potential) in fungi but not in bacteria. Human risk is unknown.

Pregnancy. A normal infant was born to a woman who ate one or two paradichlorobenzene toilet fresheners a week during her pregnancy. A preg- nant woman who sniffed naphthalene, however, produced a child with skin color typical of naphthalene poisoning and an enlarged liver and spleen. The organs became normal after treatment.

Additional scientific information may be found in:

Athanasiou, M., et al. “Hemolytic Anemia in a Female Newborn Infant Whose Mother Inhaled Naphthalene Before Delivery.” Journal of Pediatrics 130 (1997): 680–81.

Santucci, K., and B. Shah. “Association of Naphthalene with Acute Hemolytic Anemia.” Academic Emergency Medicine 7 (2000): 42–47.

Siegel, E., and S. Wason. “Mothball Toxicity.” Pediatric Clinics of North America 33 (1986): 369–74.

Weintraub, E., D. Gandhi, and C. Robinson. “Medical Complications Due to Mothball Abuse.” Southern Medical Journal 93 (2000): 427–29.


Pronunciation: nal-BYOO-feen
Chemical Abstracts Service Registry Number: 20594-83-6. (Hydrochloride form

Formal Names: Nubain
Type: Depressant (opioid class). See page 24 Federal Schedule Listing: Unlisted
USA Availability: Prescription
Pregnancy Category: B

Uses. This opioid is considered about as effective as morphine at pain relief and is also used in anesthesia and for sedation. Nalbuphine is used to control substantial pain in conditions ranging from surgery and broken bones to heart attack and sickle cell anemia crisis. Women seem to get more pain relief from the drug than men do. The compound’s anesthetic capabilities have been used in military medicine; one scientific report1 blandly describes nalbuphine usage in cases of “large, multiple gunshot wounds of the trunk and extremities, as well as injuries caused by fragments of projectiles and explosive devices.” The drug is also used in dentistry.

Nalbuphine is a narcotic agonist-antagonist, meaning it has opiate proper- ties itself but can counteract other opiates/opioids, a counteraction sometimes strong enough to cause a withdrawal syndrome if someone has dependence on the other opiate/opioid.

The drug’s safety for administration to children is considered unproven in the United States, but nalbuphine is given to youngsters in America and else- where.

Drawbacks. Unwanted effects include dizziness, perspiration, itching, con- stipation, nausea, vomiting, and breathing impairment. Hallucinations and euphoria are reported. The drug may interfere with physical and mental abil- ities needed to operate automobiles or other dangerous devices; tests have demonstrated slower reaction times and impaired decision making among users. The drug can make a person act drunk.

Abuse factors. Research indicates that nalbuphine injections briefly increase blood levels of growth hormone, an increase that may lead some people to think the drug promotes muscle mass. Reports circulating in bodybuilder cir- cles claim the drug can promote muscle mass in another way also, by reducing

Nalbuphine 313

blood levels of a hormone called cortisol. In the 1990s nalbuphine was popular among bodybuilders using anabolic steroids. These individuals mainly used nalbuphine to reduce pain caused by exercise regimens. Interviews with such users revealed that many were suffering unwanted physical and mental effects from nalbuphine and that many of these persons were abusing other drugs as well. A case report tells of illicit nalbuphine injection causing muscle dam- age—the opposite of what bodybuilders seek.

In low amounts nalbuphine can produce morphine effects. High doses tend to make users feel nervous and uncomfortable, however, reducing nalbu- phine’s attractiveness for illicit recreational use. At those higher dosage levels people can experience vision trouble, sleep disturbance, weird dreams, and thoughts running out of control. The drug is generally considered to have a low potential for abuse, lower than propoxyphene or codeine. Some research- ers, however, describe the abuse liability as about equivalent to pentazocine, a drug with a notorious reputation for illicit misuse and that has effects similar to those of nalbuphine. Tolerance and dependence may develop if a person uses nalbuphine in amounts higher than normal medical doses. Withdrawal symptoms are described as those of mild opiate withdrawal.

Drug interactions. Not enough scientific information to report.

Cancer. Standard laboratory tests do not indicate the drug has potential for causing cancer. Long-term experiments with rats and mice have failed to pro- duce cancer.

Pregnancy. Animal research using nalbuphine at high doses has not pro- duced birth defects attributable to the drug. It passes from a pregnant woman into the fetus and can build up there; one study found that newborn levels could be six times higher than maternal levels. Due to effects on the newborn’s heartbeat and breathing, controversy exists about the drug’s appropriateness for easing pain of childbirth. Some researchers believe the substance is risky during childbirth; some believe nalbuphine is safer than combinations of other drugs. Nalbuphine passes into milk of nursing mothers but is not believed to harm breast-feeding infants.

Additional scientific information may be found in:

Jasinski, D.R., and P.A. Mansky. “Evaluation of Nalbuphine for Abuse Potential.” Clin- ical Pharmacology and Therapeutics 13 (January–February 1972): 78–90.

Miller, R.R. “Evaluation of Nalbuphine Hydrochloride.” American Journal of Hospital Pharmacy 37 (1980): 942–49.

Saarialho-Kere, U. “Psychomotor, Respiratory and Neuroendocrinological Effects of Nalbuphine and Haloperidol, Alone and in Combination, in Healthy Subjects.” British Journal of Clinical Pharmacology 26 (1988): 79–87.

Schmidt, W.K., et al. “Nalbuphine.” Drug and Alcohol Dependence 14 (1985): 339–62. Stambaugh, J.E. “Evaluation of Nalbuphine: Efficacy and Safety in the Management of Chronic Pain Associated with Advanced Malignancy.” Current Therapeutic Re-

search: Clinical and Experimental 31 (1982): 393–401.
Wines, J.D., et al. “Nalbuphine Hydrochloride Dependence in Anabolic Steroid Users.”

American Journal on Addictions 8 (1999): 161–64.
Zacny, J.P., K. Conley, and S. Marks. “Comparing the Subjective, Psychomotor and

Physiological Effects of Intravenous Nalbuphine and Morphine in Healthy

314 Nalbuphine

Volunteers.” Journal of Pharmacology and Experimental Therapeutics 280 (1997): 1159–69.


1. Rakaric-Poznanovic, M., Z. Boljevic, and D. Marcec. “Anestezija Nalbufin/Pro- pofol u Kirurskom Zbrinjavanju Ratnih Ozljeda [Nalbuphine/Propofol Anesthesia in the Surgical Treatment of War Injuries].” Lijecnicki Vjesnik 115 (1993): 303–305. Abstract in English.


Pronunciation: NAN-droh-lohn
Chemical Abstracts Service Registry Number: 434-22-0. (Decanoate form 360-

70-3; furylpropionate form 7642-64-0; phenpropionate form 62-90-8)

Formal Names: Anabolin LA-100, Androlone D, Deca-Durabolin, Demalon, Dex- atopic, Durabolin, Hybolin Decanoate, Nandrolin, Nortestosterone

Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000) USA Availability: Prescription
Pregnancy Category: X

Uses. Nandrolone is used to treat breast cancer and anemia, and the drug has improved asthma and Sjo ̈gren’s syndrome, a disease that destroys sali- vary, sweat, and tear glands. Healing action on cornea afflictions has been observed, and rat experiments have explored nandrolone’s potential for speeding recovery from tooth extractions. A skin cream containing nandrolone is used against eczema. Human research indicates that the drug can improve osteoporosis, a disease causing brittle bones, although results conflict on how long the improvement lasts. Among some diabetics with a kidney condition called Kimmelstiel-Wilson syndrome, nandrolone has helped both renal and eyesight difficulties. In kidney dialysis, patients’ experimental use of nandro- lone was able to improve weariness, increase muscle mass, and fight mal- nutrition. The compound has helped AIDS (acquired immunodeficiency syndrome) patients build up weight, muscles, and strength. The substance has also been given in hopes of stimulating appetite in malnourished cancer pa- tients, although animal cancer research indicates that any weight gain may simply be due to water retention rather than improved nutrition (in contrast to research with healthy animals that produced weight increase associated with protein gain—some livestock raisers illegally dose animals with nandro- lone to promote growth). After administration of the drug, improvement oc- curred in a case of anorexia nervosa, a psychological condition in which people with normal or low weight misperceive themselves as fat.

Drawbacks. Typically, but not always, studies of humans who use nandro- lone have measured declines in cholesterol levels (including HDL, the so- called good cholesterol) and elevation of triglycerides (associated with body processes leading to heart attack and stroke). In monkeys, coronary artery

316 Nandrolone

damage appeared after long-term administration of nandrolone. After the drug was given for a year or more to female monkeys they showed abnor- malities in the uterus. Female reproductive behavior was disrupted in a rat experiment using doses comparable to what humans take. In humans the sub- stance can promote male characteristics in females (such as facial hair and deeper voice), and in men it can enlarge breasts while diminishing sexual organs. Other unwanted effects may include acne, aggressive conduct, urinary difficulty, and fluid retention causing tissues to swell. Nandrolone is supposed to be avoided by males suffering from breast or prostate cancer and by anyone with porphyria, liver disease, heart failure, or kidney failure. The drug may interfere with children’s growth and their gender differentiation.

Taking nandrolone without watchful medical supervision can be hazardous. A bodybuilder’s use of nandrolone and other steroids is suspected of trans- forming a routine case of chickenpox into a nearly fatal experience, requiring over a month of hospitalization in an intensive care unit. Daily nandrolone is suspected of leading to kidney and bone marrow disease that paralyzed a 29- year-old bodybuilder, although eventually he recovered enough to walk with- out help.

Abuse factors. Nandrolone can improve muscle mass, and some athletes use it for that purpose even though sports regulatory agencies forbid use of the compound by competitors. Among athletes tested by the International Olympic Committee in the 1980s nandrolone was the most frequently found illicit anabolic steroid. The sports ban extends beyond human competitions and includes horse racing; however, an experiment testing thoroughbred rac- ing performance found no effect from the drug.

Research demonstrates that consuming boar meat or taking the nonpre- scription steroid androstenedione can produce false-positive tests for nandro- lone. In theory consumption of horse meat might also produce a false positive, as natural body processes in a horse may produce enough nandrolone to be measurable.

Drug interactions. The substance can alter the amount of insulin needed by diabetics. Some experimentation on rats found that nandrolone can boost heart rate acceleration caused by cocaine; in other rat work the combination appar- ently lowered pulse rate. Nandrolone boosts actions of anti–blood clot medi- cines, putting patients at risk of excessive bleeding.

Cancer. Judging from decades of medical experience, the compound does not seem to cause cancer.

Pregnancy. Due to danger of masculinization of offspring, nandrolone is supposed to be avoided by women who are pregnant or nursing.

Additional scientific information may be found in:

Gerritsma, E.J., et al. “Virilization of the Voice in Post-Menopausal Women Due to the Anabolic Steroid Nandrolone Decanoate (Decadurabolin). The Effects of Medi- cation for One Year.” Clinical Otolaryngology and Allied Sciences 19 (1994): 79–84.

Gold, J., et al. “Safety and Efficacy of Nandrolone Decanoate for Treatment of Wasting in Patients with HIV Infection.” AIDS 10 (1996): 745–52.

Johansen, K.L., K. Mulligan, and M. Schambelan. “Anabolic Effects of Nandrolone De-

Nandrolone 317

canoate in Patients Receiving Dialysis: A Randomized Controlled Trial.” Journal

of the American Medical Association 281 (1999): 1275–81.
“Nandrolone Decanoate.” In Therapeutic Drugs, ed. C. Dollery. 2d ed. New York: Chur-

chill Livingstone, 1999. N28–N30.
Radis, C.D., and K.P. Callis. “Systemic Lupus Erythematosus with Membranous Glom-

erulonephritis and Transverse Myelitis Associated with Anabolic Steroid Use.” Arthritis and Rheumatism 40 (1997): 1899–1902.


Pronunciation: NIK-uh-teen (also pronounced NIK-uh-tin)

Chemical Abstracts Service Registry Number: 54-11-5

Formal Names: Habitrol, Nicoderm, Niconil, Nicorette, Nicotiana rustica, Nico- tiana tabacum, Nicotrol, Prostrop, Tobacco

Informal Names: Chip (cigarette mixed with PCP), Fry Daddy (cigarette mixed with crack cocaine)

Type: Stimulant (pyridine alkaloids class). See page 18

Federal Schedule Listing: Unlisted

USA Availability: Generally available to adults as a component of tobacco prod- ucts; nonprescription and prescription in pharmaceutical format

Pregnancy Category: C or D (depending on pharmaceutical format)

Uses. Tobacco’s history is mentioned on page 18. Nicotine is the addictive drug component of tobacco and is found in other plants as well. Nicotine is one of the more hazardous drugs, and dosage via tobacco smoke adds still more peril. Although nicotine has medical uses, characteristics of the natural product tobacco fall within the criteria of a Schedule I controlled substance. Nonetheless, federal law explicitly excludes tobacco from such control, making the tobacco industry legal. At the time this book was written debate was under way about limiting adult access to nicotine products, a restrictive effort re- quiring changes in law.

Traditional medical uses of the drug include treatment of insect bites, skin and intestinal parasites, vomiting, earache, toothache, runny nose, hernia, and heart pain. Although tobacco smoking worsens a gastrointestinal inflamma- tion called Crohn’s disease, medical practice uses nicotine skin patches, oral capsules, or suppositories to treat inflammation of the colon and rectum caused by ulcerative colitis. Nicotine chewing gum has been used successfully to treat finger or toe sores deriving from Buerger’s disease, an affliction in which blood vessels get blocked off (and which, despite the usefulness of pharmaceutical nicotine, seems to be worsened by smoking). Pharmaceutical nicotine helps some persons suffering from the tics of Tourette’s syndrome. Researchers have found cigarette smoking to reduce the likelihood of getting preeclampsia, a potentially serious disease of late pregnancy in which women suffer fluid retention, high blood pressure, and too-high urine protein levels. Cigarette smoking is also associated with a lower probability of getting Par-

Nicotine 319

kinson’s or Alzheimer’s disease. Even though “association” does not demon- strate cause and effect, some experiments using pharmaceutical nicotine to treat those afflictions show positive results. Such results, however, have not yet given nicotine a generally accepted role in treating those diseases. Nicotine reduces hunger pains and raises blood sugar, effects that help users eat less (Native Americans have traditionally chewed tobacco to better endure circum- stances involving little food, water, or rest). Nicotine initially raises blood pressure, but continued dosage will lower it.

Drawbacks. Tobacco smoking can lead to lung cancer and heart disease. Many other afflictions are attributed to tobacco smoking: bronchitis, emphy- sema, cataracts, mouth cancer, pancreas cancer, bone density loss (making broken bones more likely), abdominal aortic aneurysm (a sac ballooning out from the blood vessel wall), brain aneurysm, and gastroesophageal reflux (re- current backward flow of acid and partially digested food from the stomach to the esophagus, making esophageal cancer more likely). One study noted that smoking tends to produce changes causing women to go through men- opause at a younger age than nonsmokers. Laboratory tests imply that smoke- less tobacco promotes tooth decay. Still more unwanted actions are known, partly because tobacco has simply been studied so intensively that more is known about it than is known about many other substances. Whether nicotine itself causes afflictions produced by tobacco is uncertain. For example, some investigators suspect that heart disease in smokers comes from carbon mon- oxide and tar constituents of smoke rather than the nicotine.

In adults 40 mg to 100 mg of pharmaceutical nicotine can produce fatal poisoning; an equivalent dose through cigarettes would require a person to quickly smoke several packs. Smaller dosages can be dangerous for children who play with nicotine patches or gum or who consume tobacco.

Abuse factors. As with many drugs, persons often find nicotine unpleasant at first but learn to ignore bad sensations and focus upon effects that are enjoyed. Experiments examining differences that users perceive in various drugs find that some sensations from nicotine, amphetamine, and cocaine are similar, so similar that in one experiment persons receiving injections of nic- otine typically identified it as cocaine. A user can establish a physical de- pendence with nicotine, causing withdrawal symptoms if dosage stops: nervousness, tenseness, crankiness, lightheadedness, broken sleep, weariness, distractedness, tremors. These symptoms often last a few days, sometimes longer, and can relate to a person’s expectations (a psychosomatic component).

Debate exists about how addictive nicotine is. A study published in 1994 noted that about 33% of tobacco smokers become addicted. A study published in 2000 found that 20% to 60% of adolescent smokers are addicted. Many smokers with no interest in quitting can nonetheless substantially reduce their cigarette consumption with little difficulty. In contrast, many smokers wanting to stop find themselves unable to cease, and for them even pharmaceutical nicotine can be an insufficient replacement for tobacco. Among such persons the persistence of a smoking habit suggests that something more than the drug nicotine is involved. Tobacco smoke contains thousands of chemical ingredi- ents besides nicotine; perhaps some of the less-studied ones are important. In addition, the paraphernalia and mechanics of cigarette smoking provide a

320 Nicotine

psychological buffer to users, allowing continual brief respites in interactions with other persons (such as breaking eye contact during a puff). Nicotine itself is a mild stimulant able to release adrenaline and increase pulse rate and blood pressure, with the physiological arousal produced by the drug masking phys- ical arousal provoked by life’s tensions, thereby making smokers feel less ner- vous despite the stimulant effects. Smokers tend to have lower levels of body chemicals that are supplemented by antianxiety and antidepressant drugs. Such pharmaceuticals, unfortunately, seemingly have little ability to help smokers quit their tobacco addiction.

As with any addiction, the power of nicotine and tobacco depends upon needs met by those substances. People do not smoke simply to avoid tem- porary withdrawal symptoms. If a person’s life is filled with situations that smoking eases like nothing else can, breaking the addiction is hard. If a person finds other ways of dealing adequately with those situations, desire for ciga- rettes can go away and never be bothersome again. Contrary to expectations of researchers, a laboratory test found nicotine to be no more appealing to ex- smokers than to persons who have never smoked—a finding implying that life circumstances, and not just chemistry, determine this drug’s appeal.

Alcohol and illicit drug abusers reliably tend to be tobacco cigarette smok- ers, so reliably that the amount of tobacco use can be used to estimate the amount of cocaine and opiate usage by persons in drug abuse treatment pro- grams. An experiment found that persons smoked less tobacco when they had access to marijuana, suggesting that those persons used the two substances for similar purposes. Nonsmokers tend to avoid drug abuse, implying that smokers and nonsmokers use different strategies to cope with life’s challenges. Cigarette smoking is more prevalent among schizophrenics, seriously de- pressed persons, and persons with low-grade psychiatric disturbance that may lack outward symptoms. Almost two thirds of smokers in one research project turned out to have a history of present or past psychiatric abnormality. Among such individuals smoking may be a strategy of self-medication. One study found that withdrawal symptoms can depend on the extent to which the drug is used for self-medication.

Improvement has been measured in alertness, energy, and happiness as cigarette smokers start their day’s consumption in the morning. Conversely, cutting off a smoker’s supply of cigarettes produces measurable increases in fatigue, irritation, sadness, stress, and disorientation. New users do not get favorable effects sought by experienced users but instead have measurable nausea and general uneasiness. Among new users nicotine reduces job per- formance skills such as physical coordination and accuracy in memory tasks— the opposite of what happens with experienced users.

Although pharmaceutical nicotine has various medical applications, its main use is for treatment of addiction to tobacco smoking. One authority aptly described nicotine chewing gum as the methadone of cigarettes, meaning that such a treatment strategy is intended to switch addicts from tobacco to phar- maceutical nicotine, just as treatment personnel seek to switch heroin addicts to methadone. Although such programs may have an official goal of elimi- nating a person’s addiction, in practice simply switching a person from a more harmful drug to a less harmful drug is often considered a success.

Nicotine 321

Drug interactions. Nicotine interacts with commonly used medical drugs. Antipsychotic drugs and the anti–blood clot medicine heparin flush from the body faster if a person uses nicotine. Nicotine also reduces the sedative effect of benzodiazepines and reduces pain relief from various opioids. Cigarette smoke acts as a monoamine oxidase inhibitor (MAOI), a type of chemical found in some antidepressants and that can have serious adverse effects when used simultaneously with some medicines (though acute danger from ciga- rette interactions may be small). Caffeine seems to make nicotine more plea- surable. Rat studies show that nicotine increases alcohol’s appeal and worsens pancreas inflammation caused by both drugs. Birth control pills increase the boost that nicotine gives to pulse rate, and some researchers speculate that such increase is related to the elevated risk of heart disease found among smokers who use birth control pills.

Cancer. Tests indicate that pure nicotine (as opposed to smoke containing nicotine) does not cause cancer.

Pregnancy. Smoking reduces female fertility according to most studies of the topic, and studies of Canadian farm couples and of men in the Netherlands found an apparent reduction in male fertility as well. Pregnant women who smoke tobacco increase the chance of miscarriage, premature birth, smaller full-term infants, and sudden infant death syndrome (SIDS or “crib death”). The children are more likely to have muscle tone abnormalities. Smoking harms male and female gametes, damages chromosomes, and can change DNA in ways linked with childhood cancer. Nicotine usage by a pregnant woman changes movements and heart action of a fetus. One researcher warns that nicotine patches or chewing gum may deliver even more nicotine to a fetus than smoking would. Nicotine enters the milk of nursing mothers. Rat experiments indicate that fetal exposure to nicotine combined with newborn exposure to nicotine in milk increases the risk of offspring developing lung trouble similar to emphysema. Human birth defects have been attributed to tobacco smoking. Although a study of teenage tobacco smokers did not see any increased incidence of birth defects in their infants, research based on animal experimentation and published in 1998 declared that nicotine causes defects in fetal brain development leading to problems in thinking and learn- ing that may not become apparent until years after birth. The children tend to have lower scores on psychological measurements, somewhat reminiscent of “cocaine babies,” deficits that continue for years. Some investigators see a link between pregnant smokers and offspring with psychological problems. Investigators tracking mothers and daughters for three decades found that daughters were more likely to take up smoking if their mothers smoked dur- ing pregnancy.

Additional information. Scientific studies find that “passive smoking” threatens health of bystanders who inhale smoke from tobacco products and exhalations of smokers. A study of spontaneous abortions found them more likely in pregnant nonsmoking women who inhale environmental smoke and use a lot of caffeine or a moderate amount of alcohol. Infants from nonsmoker women who were exposed to tobacco smoke during pregnancy are more likely to have lower birth weight and persistent pulmonary hypertension. Offspring also exhibit the same kinds of lower psychological test scores that are seen in

322 Nicotine

children of active smokers. Inhalation of smoke by infants is suspected of contributing to SIDS. For sure, compared to children in nonsmoking house- holds, infants of smokers are hospitalized more often for pneumonia and bron- chitis. The level of environmental smoke necessary for ill effects is often unclear in scientific studies; a person working in a poorly ventilated smokey bar for eight hours a day will have a considerably different exposure than someone in a nonsmoking household who sits outside once a week with a friend who smokes a couple of cigarettes.

Additional scientific information may be found in:

Brown, C. “The Association between Depressive Symptoms and Cigarette Smoking in an Urban Primary Care Sample.” International Journal of Psychiatry in Medicine 30 (2000): 15–26.

Brown, K.G. “Lung Cancer and Environmental Tobacco Smoke: Occupational Risk to Nonsmokers.” Environmental Health Perspectives 107 (1999, Suppl. 6): 885–90.

Colby, S.M., et al. “Are Adolescent Smokers Dependent on Nicotine? A Review of the Evidence.” Drug and Alcohol Dependence 59 (2000, Suppl. 1): S83–S95.

Dursun, S.M., and S. Kutcher. “Smoking, Nicotine and Psychiatric Disorders: Evidence for Therapeutic Role, Controversies and Implications for Future Research.” Med- ical Hypotheses 52 (1999): 101–9.

Haustein, K.O. “Cigarette Smoking, Nicotine and Pregnancy.” International Journal of Clinical Pharmacology and Therapeutics 37 (1999): 417–27.

Parrott, A.C., and F.J. Kaye. “Daily Uplifts, Hassles, Stresses and Cognitive Failures: In Cigarette Smokers, Abstaining Smokers, and Non-smokers.” Behavioural Phar- macology 10 (1999): 639–46.

Robinson, J.H., and W.S. Pritchard. “The Role of Nicotine in Tobacco Use.” Psycho- pharmacology 108 (1992): 397–407.

Stolerman, I.P., and M.J. Jarvis. “The Scientific Case That Nicotine Is Addictive.” Psy- chopharmacology 117 (1995): 2–10.

Van Gilder, T.J., P.L. Remington, and M.C. Fiore. “The Direct Effects of Nicotine Use on Human Health.” Wisconsin Medical Journal 96 (1997): 43–48.


Pronunciation: NIGH-tright
Chemical Abstracts Service Registry Number: 8017-89-8 (amyl nitrite); 542-56-3

(isobutyl nitrite)

Formal Names: Amyl Nitrite, Butyl Nitrite, Cyclohexyl Nitrite, Isoamyl Nitrite, Isobutyl Nitrite, Nitrous Acid

Informal Names: Aimes, Aimies, Ames, Amys, Army, Aroma of Men, Blackjack, Blue Heaven, Bolt, Boppers, Buds, Bullet, Buzz Bomb, Climax, Dixcorama, Hardware, Heart-On, High Ball, Liquid Gold, Liquid Incense, Locker Room, Man Aroma, Oz, Ozone, Pearls, Poppers, Quicksilver, Ram, Rush, Snappers, Thrust, Whiteout

Type: Inhalant. See page 26
Federal Schedule Listing: Unlisted, but may be in state schedules
USA Availability: Prescription for some formats; nonprescription for others Pregnancy Category: X (amyl nitrite, also called isoamyl nitrite)

Uses. Various chemical subvarieties of nitrite inhalants exist. Isobutyl nitrite is popular in some teenager circles and has been called “the cocaine of poor people.” Although anyone is physically free to use any drug, authorities find that nitrite sniffing has particular appeal to male homosexuals, especially dur- ing sexual activity. Aphrodisiac qualities are claimed for the substance. Amyl nitrite sniffers report euphoria and muscle relaxation. Isobutyl nitrite users report losing their sense of who they are and also becoming calm or, in con- trast, becoming prone to wild conduct—differences that may illustrate the impact that someone’s personality and surroundings have on drug experi- ences. Regardless of exact content of a nitrite experience, sensations are brief. Some persons have confused nitrites with nitrates; they have a similar spelling but are different substances.

Drawbacks. Nitrite inhalants have brief action but may incapacitate a per- son during that time and thus should not be used while engaged in dangerous activity such as driving a car. Unwanted actions of nitrites include feelings of falling and spinning, headache, facial flushing, rapid heartbeat, generalized throbbing feelings, and low blood pressure (low enough to make a person faint). Less common are nausea, vomiting, agitation, sweating, loss of energy and strength, and loss of bladder and rectal control. In mice experiments in- volving single and multiple exposures, inhaling isobutyl nitrite can cause ane-

324 Nitrite

mia, harm the immune system, create nose and lung abnormalities, and disturb the spleen. Similar results are seen with rats. Blood and spleen ab- normalities developed in a mice experiment using cyclohexyl nitrite. In a hu- man patient, sniffing isobutyl nitrite caused bronchitis severe enough to affect the trachea. Amyl nitrite (which has a long medical history as a heart medi- cine) and isobutyl nitrite may each cause methemoglobinemia, a sometimes fatal blood disease interfering with the body’s use of oxygen; this affliction is particularly likely if a person drinks isobutyl nitrite instead of inhaling the vapor. Isobutyl nitrite interference with the body’s ability to use oxygen may be perilous for persons with inadequate oxygen supply to the heart.

In the early days of AIDS (acquired immunodeficiency syndrome) research, scientists noticed that many victims were nitrite sniffers. Because of this as- sociation, at one time nitrite sniffing was suspected to be the cause of AIDS, an excellent example of why association of a chemical with a disease cannot be assumed to demonstrate a cause-effect relationship. The substance is still, however, suspected of worsening the progression of AIDS once the disease strikes. In addition, damage to the immune system caused by nitrite inhalation is suspected of making a user more susceptible to AIDS and to a type of cancer called Kaposi’s sarcoma.

Abuse factors. Tolerance to amyl nitrite can develop.

Drug interactions. Although amyl nitrite is used as an antidote for cyanide poisoning, isobutyl nitrite can interact with coffee in a way that produces enough cyanide to poison someone who drinks the combination beverage. Using amyl nitrite with alcohol can cause heart failure. Nitrites are flammable, making them hazardous around flames or lit cigarettes. Persons with glau- coma are supposed to avoid amyl nitrite. People report burns caused by iso- butyl nitrite splashing on skin.

Cancer. Laboratory tests and animal experiments (the latter involving long- term exposure) indicate that isobutyl nitrite liquid and vapor each cause cancer.

Pregnancy. In the body nitrite breaks down into chemicals that may pro- mote birth defects. The lower blood pressure produced by amyl nitrite is be- lieved harmful to a fetus. Whether amyl nitrite passes into the milk of nursing mothers is unknown.

Additional scientific information may be found in:

Bradberry, S.M., et al. “Fatal Methemoglobinemia Due to Inhalation of Isobutyl Ni- trite.” Journal of Toxicology: Clinical Toxicology 32 (1994): 179–84.

Covalla, J.R., C.V. Strimlan, and J.G. Lech. “Severe Tracheobronchitis from Inhalation of an Isobutyl Nitrite Preparation.” Drug Intelligence and Clinical Pharmacy 15 (1981): 51–52.

Haverkos, H.W., and J. Dougherty. “Health Hazards of Nitrite Inhalants.” American Journal of Medicine 84 (1988): 479–82.

Haverkos, H.W., et al. “Nitrite Inhalants: History, Epidemiology, and Possible Links to AIDS.” Environmental Health Perspectives 102 (1994): 858–61.

Israelstam, S., S. Lambert, and G. Oki. “Use of Isobutyl Nitrite as a Recreational Drug.” British Journal of Addiction to Alcohol and Other Drugs 73 (1978): 319–20.

Nitrite 325

Lange, W.R., and J. Fralich. “Nitrite Inhalants: Promising and Discouraging News.” British Journal of Addiction 84 (1989): 121–23.

Soderberg, L.S. “Immunomodulation by Nitrite Inhalants May Predispose Abusers to AIDS and Kaposi’s Sarcoma.” Journal of Neuroimmunology 83 (1998): 157–61.

Nitrous Oxide

Pronunciation: NIGH-truhs OX-eyed

Chemical Abstracts Service Registry Number: 10024-97-2

Formal Names: Dinitrogen Monoxide, Dinitrogen Oxide, Entonox

Informal Names: Fall Down, Gas, Hippie Crack, Hysteria, Laughing Gas, Nitro, Nitrous, Nitrous Acid, Noss, Pan, Shoot the Breeze, Tanks, Thrust, Whippets

Type: Inhalant. See page 26

Federal Schedule Listing: Unlisted

USA Availability: Nonprescription, but sales and usage are controlled in some jurisdictions

Uses. This drug has been known since the 1720s. Some authorities describe nitrous oxide as an opioid; some persons even use the gas to counteract effects from stimulants. Nitrous oxide actions and its recreational use are similar to those of other inhalants. Recreational use is illegal in some jurisdictions but has a venerable history. The writer Samuel Taylor Coleridge, thesaurus com- piler Peter Mark Roget, and potter Josiah Wedgwood were all eighteenth- century notables who relaxed with nitrous oxide.

Although this substance is a pharmaceutical product, it also occurs natu- rally. For instance, eating lettuce generates enough nitrous oxide that scientists can measure it in a person’s breath. Large quantities are produced by wild prairie grass. Humans do not receive enough nitrous oxide from such natural sources to be affected, however. The substance is also produced by the human body. One study found the amount to increase as oral hygiene declined. As with the amounts produced by grass and lettuce, the level created by the body is too small to have any known effect on a person. From a global environ- mental perspective, however, nitrous oxide is a gas that promotes the green- house effect and ozone layer destruction, and concern exists about medical usage affecting the world’s climate. Medical sources are estimated to create 2% of the atmosphere’s supply. Such usage may seem insignificant in that regard, but the gas is so durable in the atmosphere that any artificial source has been described as an environmental hazard.

Medically this drug is used as an anesthetic and to relieve pain ranging from dental work to migraine headache and cancer. In a medical context nitrous oxide is considered a reliable sedative. Experimental usage to treat anxiety has been successful, and one authority has noted a therapeutic anti-

Nitrous Oxide 327

depressant action. The substance has been used to help persons break pen- tazocine addiction. Researchers report success in using the gas to ease alcohol, nicotine, and opioid withdrawal and to reduce craving for alcohol, tobacco, and marijuana among addicts. The latter three substances are so different from one another that nitrous oxide’s ability to reduce craving for all of them is remarkable. Some medical practitioners claim that a single dose of the gas actually eliminates craving for those substances, but that claim sounds much like those made for other “miracle cure” addiction treatments over the years but that turned out to be overly optimistic.

In former times, nitrous oxide was used to fight ear afflictions. For many years the substance was believed to make hearing more acute, but tests of hearing ability while using the compound show no improvement—and vol- unteers in those tests even felt they had lesser ability to detect soft sounds. Nitrous oxide can increase pressure in the middle ear, and a case report tells of treatable hearing loss caused by the drug. Hearing defect has been reported from recreational use as well.

Typical nitrous oxide actions are tingling, numbness, dreaminess, euphoria, dysphoria (the opposite of euphoria), altered sensory perceptions, changed awareness of the body, and different experience of time flow. Although ni- trous oxide is not classified as a hallucinogen, some descriptions of experiences are indistinguishable from hallucinations, particularly if a user is talented at creating internal imagery. Some persons claim to achieve mystical insight while under the drug’s influence. Intoxication from a dose lasts only a few minutes.

Drawbacks. The substance disrupts learning ability. That action has been exploited medically to promote amnesia of unpleasant procedures. In a typical experiment volunteers who inhaled a low dose of the drug showed worsened reaction time, worsened ability to do arithmetic, and general sedation accom- panied by nervous system depression (as opposed to stimulation). Interference with driving ability has been noted one-half hour after a dose. In another experiment volunteers felt stimulated; in still another experiment some indi- viduals were sedated, and others became stimulated. One group became weary, uneasy, and confused. Short-term exposure can cause dizziness, nau- sea, vomiting, and breathing difficulty. Some recreational users quickly inhale as much nitrous oxide as possible and hold their breath. This technique causes a sudden change of pressure inside the lungs and can rupture small interior structures needed for breathing. Blood pressure can go up or down, depend- ing on dosage. Users can lose consciousness, which may be hazardous in a recreational context due to falls or inability to shut off the gas source. The substance deactivates vitamin B12, an effect that can cause numbness and dif- ficulty in moving arms and legs. Other results can be impotence and invol- untary discharge of urine and feces. Nitrous oxide interferes with blood clotting, and long-term exposure has caused blood abnormalities. Persons with chronic industrial exposure have more kidney and liver disease than usual. Nitrous oxide can become very cold when released as a gas from a pressurized container, cold enough to cause frostbite upon meeting skin or throat. Breathing nitrous oxide without an adequate supply of oxygen can be fatal; a little in a closed space or a lot from a face mask can suffocate a user. Although

328 Nitrous Oxide

nitrous oxide is called nonflammable, when inhaled it can seep into the ab- dominal cavity and bowels, mixing with body gases to create a flammable combination. If ignited the result would be like setting off an explosive inside the body; the danger is real enough that surgical personnel administering nitrous oxide as an anesthetic have been warned about it.

As with many other drugs, effects of nitrous oxide can be influenced by changes in setting. For example, volunteers who knew what to expect per- formed better on tests than persons who had no information about what ni- trous oxide would do to them.

Abuse factors. In tests of the drug’s appeal, people in general chose nitrous oxide no more often than placebo; such lack of preference is a classic sign of low addictive potential. One experiment revealed a catch to such findings, however: Volunteers who enjoyed nitrous oxide effects chose it more often than placebo, and volunteers who disliked the drug actions chose it less often than placebo. Thus, overall in the general population the drug might be no more attractive than placebo, but nonetheless some persons may find it cap- tivating. Such a finding is consistent with drugs having high abuse potential, such as heroin; so the fact that persons typically find no attraction in nitrous oxide does not prove low abuse potential for nitrous oxide. Its nickname “hip- pie crack” suggests that users have recognized an abuse potential. Nonethe- less, a medical practitioner who administered the gas as a drug addiction treatment said that in 15,000 cases not a single addict indicated subsequent craving for nitrous oxide; such a patient population would be expected to show particular susceptibility if given a substance with abuse potential. The same practitioner notes that regardless of theoretical possibilities, 200 years of experience demonstrate that nitrous oxide is among the least abused drugs.

Tolerance develops in rats. Human experimentation documents tolerance developing to some effects (such as euphoria and pain relief) but not neces- sarily to all.

Drug interactions. In an experiment comparing light drinkers of alcohol to moderate drinkers, the moderate drinkers found nitrous oxide more appeal- ing. One group of researchers found that alcohol boosts nitrous oxide effects and that the drug combination creates effects produced by neither substance alone. Those researchers concluded, however, that the combination was not potent enough to have more appeal than nitrous oxide alone. That conclusion assumes, of course, that drug abusers base their conduct on rational analysis of scientific findings. In a similar experiment comparing users and nonusers of marijuana, when given a choice neither group preferred nitrous oxide more than a placebo, but nitrous oxide effects felt stronger to marijuana users. In rats ketamine boosts effects from nitrous oxide. In a human medical context that combination is routine and appears safe, but the combination causes brain damage in rats. Persons using morphine or other opiates can experience mus- cle rigidity when inhaling nitrous oxide, a situation that can interfere with breathing.

Cancer. Studies do not indicate that nitrous oxide causes cancer in animals. Whether the drug causes cancer in humans is unknown. Genetic damage sim- ilar to the amount from daily smoking 10 to 20 cigarettes has been found in

Nitrous Oxide 329

health care workers routinely exposed to minuscule amounts of nitrous oxide; such damage might have a potential for causing cancer.

Pregnancy. Fertility is lower in female rats exposed to nitrous oxide than in rats having no exposure. Lower fertility has also been observed among female health care workers with occupational exposure to the gas, and reduced fer- tility is also reported for males. Offspring of male mice exposed to nitrous oxide have weighed less than normal and have not matured as fast as normal. Birth defects resulted from an experiment exposing pregnant rats to the gas for 24 hours. When given to pregnant women during childbirth the drug builds up in the fetal blood and brain; one authority recommends adminis- tering oxygen to any newborn whose mother received nitrous oxide while giving birth. As the twenty-first century began researchers reported that the gas might cause permanent fetal and newborn brain damage, a finding in contrast to previous understanding of the drug. Occupational exposure to ni- trous oxide is associated with smaller infants and lower birth weight and may increase likelihood of spontaneous abortion. Pregnant and breast-feeding health workers are advised to avoid rooms where nitrous oxide residues may contaminate the air. Sperm abnormalities and lower fertility have been noted in male rats exposed to nitrous oxide. Wives of men exposed to the gas have shown a higher spontaneous abortion rate, compared to wives of men with no exposure. The compound is not detected in milk of nursing mothers.

Additional information. “Nitrous acid” is an unstable nitrite substance. The nickname “nitrous acid” is sometimes used for nitrous oxide, but they are different substances.

Additional scientific information may be found in:

Block, R.I., et al. “Psychedelic Effects of a Subanesthetic Concentration of Nitrous Ox- ide.” Anesthesia Progress 37 (1990): 271–76.

Danto, B.L. “A Bag Full of Laughs.” American Journal of Psychiatry 121 (1964): 612–13. Dohrn, C.S., et al. “Subjective and Psychomotor Effects of Nitrous Oxide in Healthy

Volunteers.” Behavioural Pharmacology 3 (1992): 19–30.
Linden, C.H. “Volatile Substances of Abuse.” Emergency Medicine Clinics of North Amer-

ica 8 (1990): 559–78.
Temple, W.A., D.M. Beasley, and D.J. Baker. “Nitrous Oxide Abuse from Whipped

Cream Dispenser Chargers.” New Zealand Medical Journal 110 (1997): 322–23. Yagiela, J.A. “Health Hazards and Nitrous Oxide: A Time for Reappraisal.” Anesthesia

Progress 38 (1991): 1–11.
Zacny, J.P., et al. “Examining the Subjective, Psychomotor and Reinforcing Effects of

Nitrous Oxide in Healthy Volunteers: A Dose-Response Analysis.” Behavioural Pharmacology 7 (1996): 194–99.


Pronunciation: NUT-mehg
Chemical Abstracts Service Registry Number: 84082-68-8 Formal Names: Mace, Myristica fragrans
Type: Hallucinogen. See page 25
Federal Schedule Listing: Unlisted
USA Availability: Nonprescription (food)
Pregnancy Category: None

Uses. Nutmeg is a familiar spice, but when used in larger amounts, it can act as a drug. Nutmeg originated in the Spice Islands of Indonesia. It is a seed coming from an evergreen tree that can reach 45 feet in height. Folk medicine uses nutmeg for treating insomnia, mouth sores, stomach inflammation, gas, diarrhea, and vomiting. Animal research verifies the antiinsomnia and anti- diarrhea properties; they have been observed among humans undergoing for- mal medical care, and recreational users mention sleep-inducing action. The substance is also used as an aphrodisiac, and laboratory tests show that it kills headlice. Nutmeg may be able to help improve dysentery, infections, and rheumatism. In rabbit experiments, nutmeg lowered cholesterol levels and aided in coughing up mucus. Nutmeg, like many other spices, has antimicro- bial actions that appear to retard spoilage of unrefrigerated food.

Nutmeg can produce false positives for marijuana in a field test that law enforcement officers have used to identify an unknown substance, but of course more sophisticated laboratory examination can correct such an error.

Drawbacks. A nutmeg dose sufficient to produce hallucinations is also suf- ficient to produce headache, thirst, nausea, constipation, rapid heartbeat, diz- ziness, and a miserable hangover. Muscular discoordination can be severe enough to mimic multiple sclerosis. Research on cats produced liver destruc- tion. All these results are from dosage quantities much higher than the small amounts used for spicing foods.

Abuse factors. Nutmeg is not considered addictive, although a case report notes a patient hospitalized for nutmeg poisoning, who craved the substance so much that he had a supply smuggled to him during his hospital stay. The report said he was never able to go beyond two weeks without nutmeg.

Some researchers are skeptical that nutmeg possesses hallucinogenic qual- ities, but for centuries numerous users have said otherwise. Betel chewers

Nutmeg 331

sometimes add nutmeg to a quid for extra sensations, and mixing tobacco with nutmeg is a practice reported in Asia. Research indicates that human body chemistry converts part of a nutmeg dose into substances related to amphetamine, affecting mood and sometimes causing hallucinations. The ef- fects from a dose can last three days. Overdose requiring medical intervention is possible, although only one fatality is recorded. Nutmeg has received mixed reviews as a recreational drug. Some people call it incomparable; others resort to it only as an act of desperation when nothing else is available. A favorable description says nutmeg is “capable of removing one completely from the world of reality in a hypnotic trance accompanied by golden dreams and euphoric bliss.”1 In contrast, someone who used nutmeg together with mari- juana received emergency hospital treatment for gagging, hot and cold flashes, numbness, blurred vision, double vision, triple vision, and difficulty in con- trolling movements—among other complaints. Persons who use nutmeg by itself have also reported bad experiences.

Drug interactions. In a mice experiment nutmeg boosted actions of alcohol and reduced those of dextroamphetamine. One authority describes nutmeg as a weak monoamine oxidase inhibitor (MAOI), and MAOIs interact badly with many drugs described in this book.

Cancer. A laboratory test using a nutmeg extract found evidence that it might cause cancer, and a nutmeg experiment with mice produced DNA changes that might be related to eventual cancer.

Pregnancy. Male mice that received nutmeg in an experiment did not show chromosome damage. A case report notes a normal full-term infant born to a woman who had experienced nutmeg poisoning during pregnancy, but preg- nant women are advised to avoid using nutmeg as a drug.

Additional information. As with many other natural products, nutmeg’s effects may be produced by the combination of hundreds of chemicals found in the substance. Researchers have identified several chemicals as likely causes of nutmeg’s effects: elemicin, eugenol, myristicin, and safrole. Under labora- tory conditions myristicin can be chemically converted to MDMA and safrole to MDA, but this conversion has never been detected in animals or humans. Body chemistry does convert myristicin into substances resembling amphet- amine. Myristicin is found not only in nutmeg but in plants related to carrots. An experiment testing myristicin on rats found no poisonous result. Research- ers found no evidence of cancer after dosing mice with the substance, but the study did not last long enough to reveal whether cancer would eventually develop. Myristicin’s potential for causing birth defects is unknown. Safrole has a faint ability to promote cancer; pregnant women are advised to avoid using it as a drug.

Mace comes from the same seed as nutmeg does, but is a different spice. Folk medicine uses mace to reduce inflammation and pain; research indicates it can protect against some chemically caused cancers. Mace is routinely added to areca nut quids.

Additional scientific information may be found in:

Fras, I., and J.J. Friedman. “Hallucinogenic Effects of Nutmeg in Adolescent.” New York State Journal of Medicine 69 (1969): 463–65.

332 Nutmeg

Lewis, P.W., and D.W. Patterson. “Acute and Chronic Effects of the Voluntary Inha- lation of Certain Commercial Volatile Solvents by Juveniles.” Journal of Drug Issues 4 (1974): 172.

Lewis, W.H., and M.P.F. Elvin-Lewis. Medical Botany: Plants Affecting Man’s Health. New York: John Wiley & Sons, 1977. 408–10.

Panayotopoulos, D.J., and D.D. Chisholm. “Hallucinogenic Effect of Nutmeg.” British Medical Journal 1 (1970): 754.

Sjoholm, A., A. Lindberg, and M. Personne. “Acute Nutmeg Intoxication.” Journal of Internal Medicine 243 (1998): 329–31.

Van Gils, C., and P.A. Cox. “Ethnobotany of Nutmeg in the Spice Islands.” Journal of Ethnopharmacology 42 (1994): 117–24.

Weiss, G. “Hallucinogenic and Narcotic-Like Effects of Nutmeg.” Psychiatric Quarterly 34 (1960): 346–56.


1. W.H. Lewis and M.P.F. Elvin-Lewis, Medical Botany: Plants Affecting Man’s Health (New York: John Wiley & Sons, 1977), 408.


Pronunciation: OH-pi-uhm
Chemical Abstracts Service Registry Number: 8008-60-4 Formal Names: Papaver album, Papaver somniferum, Poppy

Informal Names: Ah-pen-yen, Aunti, Aunti Emma, Big O, Black, Blackjack, Black Pill, Black Stuff, Chandoo, Chandu, Chinese, Chinese Molasses, Chinese To- bacco, Chocolate, Cruz, Dopium, Dover, Dover’s Deck, Dover’s Powder, Dreamer, Dream Gun, Dreams, Dream Stick, Easing Powder, Emma, Fi-Do-Nie, Garden-Poppy, Gee, God’s Medicine, Goma, Gondola, Gong, Goric, Great To- bacco, Gum, Guma, Hard Stuff, Hocus, Hop, Indonesian Bud, Joy, Joy Plant, Mawseed, Midnight Oil, Mira, Mud, O, Oil, OJ, OP, Ope, Pen Yan, Pen Yen, PG, Pin Gon, Pin Yen, Plant, PO, Pox, Skee, Tar, Tongs, Tox, Toxy, Toys, When- Shee, Winshee, Yen Shee Suey, Ze, Zero

Type: Depressant (opiate class). See page 22
Federal Schedule Listing: Schedule II (DEA no. 9600) USA Availability: Prescription
Pregnancy Category: C

Uses. Many opium products are discussed elsewhere in this book, but here we are dealing with the substance from which all those products originate. Opium has long been used to relieve pain, fight coughs, cure diarrhea, and control spasms. Traditionally, opium is dried sap harvested from the seed- producing portion of opium poppy plants. At harvest time fields of poppies can have a strong smell, and children in the fields can be overcome by those airborne chemicals. A modern opium variety is “poppy straw,” composed of dry or liquid extracts from the plant. The natural product can be used by itself or can be refined to produce various drugs known as “opiates,” valued for their medicinal effects.

Archaeologists have found evidence of opium poppy cultivation dating from 15,000 years ago, but examination of historical records has not proven that ancient peoples understood opium’s medicinal benefits; the product may have been used traditionally but without understanding how or even whether it worked. Opium may have been used in Roman Empire religious ceremonies, perhaps exploiting the drug’s effects to symbolize a process of death and re- incarnation, and even older records imply that ancients may have believed

334 Opium

that opium could produce happiness, although evidence of ancient recrea- tional use is nonexistent.

The Opium War from 1840 to 1842 was the first drug war, followed by the second Opium War of 1856 to 1860. These military conflicts were fought against China by England and other European powers in order to force the Chinese government to legalize the opium trade (certainly a goal different from that of the “drug war” familiar to Americans as the twenty-first century began).

Opium and its morphine component were widely used to treat wounded soldiers in the American Civil War, and later historians have routinely said that addiction became so common that it was called “the soldier’s disease.” Such illness may have existed, but an investigator who diligently examined medical writings from that time found none that attributed postwar addictions to war-related medical use. In that era the opium trade was legal, and some- one who analyzed opium import statistics found no evidence that consump- tion rose due to Civil War addictions; a distinguished authority has noted that people of that era called dysentery “the soldier’s disease.”

Just before World War I an article in the Journal of the American Medical Association declared, “If the entire materia medica at our disposal were limited to the choice and use of only one drug, I am sure that a great many, if not the majority, of us would choose opium; and I am convinced that if we were to select, say half a dozen of the most important drugs in the Pharmacopeia, we should all place opium in the first rank.”1 Although many useful drugs have been discovered since then, opium is still the basis for many standard medications. Because opium is a natural product, its morphine content can vary greatly from batch to batch. Opium commercially processed for medical use is adjusted so that 10% of any given amount of medical opium is com- posed of morphine.

Although medical opinion about opium has changed little, public opinion has changed a lot. Reasons for that shift go beyond the scope of this book, but in the nineteenth century, use of opium and its derivatives had wide social approval in America. Alcohol was considered more hazardous to health and home. One of the most telling measures of approval came from the life in- surance industry in India, which freely granted policies to known opium users, as mortality statistics showed opium having no effect on life span. A life insurance official reported similar experience in China, although older users in China had higher mortality than older nonusers (probably many users took the drug for diseases that nonusers did not have, with the death rate related more to those diseases than to opium). Some of those statistics would change as the twentieth century progressed because drug laws would change the kinds of people who used opium, thereby associating opium with popu- lations having higher mortality for reasons unrelated to opium’s drug prop- erties.

Although identified with China, opium has been grown in the United States. In the late eighteenth century Benjamin Franklin used laudanum (typically wine laced with opium) to treat himself for kidney stones. During the nine- teenth century Americans used opium mainly as an ingredient in laudanum and paregoric. Paregoric is a liquid including anise, camphor, and opium.

Opium 335

Paregoric was first produced in the eighteenth century as an asthma medicine. The compound is no longer used for that purpose but can reduce lung con- gestion by helping people to cough up mucus. Paregoric is a standard diarrhea remedy and is used to help infants suffering from drug withdrawal syn- dromes. In the 1960s the compound had a flurry of popularity among opiate addicts who would process the product in hopes of isolating the opium, then inject the substance they produced. The outcomes were typical of what hap- pens when oral medications are injected, resulting in lung damage and dis- figuring injuries to injection sites.

Less familiar modern opium preparations include home remedy mixtures of the substance with caffeine, aspirin, and acetaminophen (Tylenol or other brands). In America opium preparations were once a standard method of qui- eting noisy infants and children, and that practice is still followed in some parts of the world. One hazard in that custom is the possibility of fatal over- dose, as people administering such concoctions do not always understand pediatric dosage.

Drawbacks. Although some opium users have generally unhealthy life- styles, few ailments have been attributed solely to the drug. Those ailments tend to be in the gastrointestinal tract, such as problems with the small intes- tine’s bile duct. “Cauliflower ear,” in which an ear thickens and becomes mis- shapen, was once associated with opium smoking. The affliction, however, apparently came not from the drug but rather from the habit of lying down for hours in a comatose condition with an ear pressing against a hard surface.

Abuse factors. Recreational use of opium is harder to define than we might think, because even if persons take the drug in a social setting, they can be seeking to reduce mental anxiety or physical pain, which is not the same as using a drug for fun. Some people swallow dry opium or drink tea made with seed or with dried heads of poppy flowers. In the nineteenth century poppy tea was a common medicinal drink, but in the early twenty-first century the habit tends to be limited to opiate addicts. The traditional recreational way to use opium is to inhale its smoke. Heating opium enough to make it smoke can reduce the drug content, and opium is already far weaker than substances refined from it (such as morphine and heroin). One authority estimates that the amount of active drug inhaled by someone who smokes a given weight of opium will typically be 300 to 400 times less than the drug content in the same weight of injected heroin. Moreover, while an entire dose of heroin might be ingested in a few seconds, a pipeful of opium is smoked over a much longer period to slowly savor its effects, further reducing the opium’s impact. The English poet Samuel Taylor Coleridge started out using opium for medical purposes, as did Thomas De Quincey, and both men produced classic accounts of hallucinations and creative inspiration occurring under opium’s influence. Those accounts and later ones may well be true, but for such results people need to be particularly sensitive to the drug and also be prone to such experiences regardless of pharmaceutical encouragement. Ar- senic is sometimes added to opium to increase smokers’ interest in sexual activity, a practice generating reports of arsenic poisoning among users.

Drug interactions. Not enough scientific information to report about the

336 Opium

natural product, although many studies have examined drug interactions with opiates and opioids.

Cancer. Laboratory tests find that opium smoke may cause cancer, as may opium dross (waste products, such as scrapings from the inside of an opium pipe, which some persons chew or suck). Opium is suspected of causing esophageal and bladder cancer.

Pregnancy. A pregnant woman using paregoric can give birth to an infant having dependence with opium.

Additional information. Seed from opium poppies is a food product com- monly used in breads, cakes, and candies. Consumption of amounts found in a normal meal can cause a false opiate positive in drug screens; controversy exists about whether further analysis of results from such testing can show that poppy seed was the cause. Poppy seed oil is a comparatively unfamiliar product, but animal tests indicate it has good potential for human nutrition. In some parts of the world iodized poppy seed oil has been used instead of iodized salt to treat goiter and has been suggested as a means of preventing nervous endemic cretinism caused by iodine deficiency in the diet of pregnant women. Iodized poppy seed oil is taken up by cancerous portions of a liver, giving the substance clinical usefulness if anticancer drugs are blended into it, as the drugs then concentrate exactly where they are needed in the liver. Results from animal research have led investigators to speculate that consum- ing normal poppy seed oil may help prevent cancer.

Opium lettuce is not related to opium but can produce mild sensations similar to opium. Sedative and pain relief qualities of opium lettuce have been used for centuries. Lung and urinary tract afflictions have been treated with it. Opium lettuce is smoked for recreational purposes, but results have not caused the practice to gain popularity. A case report tells of individuals who received medical care after injecting a preparation made from the plant. It has other names including Acrid Lettuce, Bitter Lettuce, Compass Plant, Great Lettuce, Green Endive, Lactucarium, Lactuca virosa, Poison Lettuce, Prickly Lettuce, Strong-Scented Lettuce, and Wild Lettuce.

Additional scientific information may be found in:

Aurin, M. “Chasing the Dragon: The Cultural Metamorphosis of Opium in the United States, 1825–1935.” Medical Anthropology Quarterly 14 (2000): 414–41.

Gharagozlou, H., and M.T. Behin. “Frequency of Psychiatric Symptoms among 150 Opium Addicts in Shiraz, Iran.” International Journal of the Addictions 14 (1979): 1145–49.

Goodhand, J. “From Holy War to Opium War? A Case Study of the Opium Economy in North-Eastern Afghanistan.” Disasters 24 (2000): 87–102.

Haller, J.S. “Opium Usage in Nineteenth Century Therapeutics.” Bulletin of the New York Academy of Medicine 65 (1989): 591–607.

Kalant, H. “Opium Revisited: A Brief Review of Its Nature, Composition, Non-Medical Use and Relative Risks.” Addiction 92 (1997): 267–77.

Lerner, A.M., and F.J. Oerther. “Characteristics and Sequelae of Paregoric Abuse.” An- nals of Internal Medicine 65 (1966): 1019–30.

Quinones, M.A. “Drug Abuse during the Civil War (1861–1865).” International Journal of the Addictions 10 (1975): 1007–20.

Opium 337

Strang, J. “Lessons from an English Opium Eater: Thomas De Quincey Reconsidered.” International Journal of the Addictions 25 (1990): 1455–65.


1. 64 (February 6, 1915): 477.


Pronunciation: ok-SAN-droh-lohn

Chemical Abstracts Service Registry Number: 53-39-4

Formal Names: Anatrophill, Anavar, Lipidex, Lonavar, Oxandrin, Provitar, Vaso- rome

Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000) USA Availability: Prescription
Pregnancy Category: X

Uses. This drug is used to encourage return of adequate heaviness in per- sons who have lost too much weight from illness, injury, or medical therapy. Experiments with AIDS (acquired immunodeficiency syndrome) patients mea- sured substantial improvement in weight and strength. Oxandrolone may di- minish pain from a bone disease called osteoporosis, although the drug has potential for worsening the underlying bone affliction. In rats and in humans the drug has hastened healing of wounds. Experimental therapy using oxan- drolone against Duchenne muscular dystrophy has been successful.

Drawbacks. Nausea and diarrhea are among the less serious reports of un- wanted effects. The substance can masculinize female users and interfere with menstrual periods. In immature rats oxandrolone has drastically interfered with the male reproductive system, a finding that may be relevant to young athletes using the compound without medical supervision. In humans the sub- stance can promote prostate disease and should be avoided by men with breast cancer and generally by anyone with kidney disease (although doctors sometimes give oxandrolone to dialysis patients). The drug has been used to treat hepatitis in alcoholics despite its ability to interfere with bile flow and to cause jaundice or liver malfunction. Fluid retention can occur and be a serious problem for heart patients. Other unwanted effects may include over- all higher cholesterol levels (accompanied by reduction of the HDL “good cholesterol”), although unlike some other drugs of this type, oxandrolone has been seen to reduce levels of triglycerides (which are associated with increased risk of heart attack and stroke), and in some cases oxandrolone reduced over- all cholesterol as well. Such effects may, however, depend upon what causes the original levels. Oxandrolone can bring about premature bone maturation in children, preventing attainment of normal adult height. Nonetheless, the

Oxandrolone 339

compound is used to treat delayed puberty in boys, increasing their height and weight. Turner’s syndrome interferes with height and sexual maturation in girls, deficits that have improved with oxandrolone therapy.

Abuse factors. Sports competitors are forbidden to use the substance. Vio- lation of the ban may risk punishment for nothing: Even though oxandrolone can promote muscle mass, a study examining users and nonusers of oxandro- lone found no difference between the two groups in muscle mass, strength, and general fitness. Athletes who abuse oxandrolone may suffer bad psycho- logical effects. In one case a person became hyperactive and had racing thoughts. In another case someone abusing this and other steroids became suspicious of other people, rageful, and occasionally suicidal.

An addiction case report mentioned not only psychological craving for ox- androlone and other anabolic steroids but physical dependence as well. When the bodybuilder in question received a dose of a substance that provokes withdrawal symptoms in opiate addiction, he responded with classic opiate withdrawal signs.

Drug interactions. Oxandrolone can alter insulin needs of diabetics and boost actions of anti–blood clot medicines. The steroid can help rats survive an overdose of meprobamate or nicotine.

Cancer. Potential for causing cancer is unknown. A case report associates oxandrolone with development of colon cancer in a 27-year-old bodybuilder. Pregnancy. Potential for causing birth defects is unknown. In animal studies testing oxandrolone at nine times the normal human dose, fetal injury has occurred, including introduction of male characteristics into a female fetus. Pregnant women are advised to avoid the drug. Oxandrolone’s ability to pass

into milk of nursing mothers is unknown. Additional scientific information may be found in:

Frasier, S.D. “Androgens and Athletes.” American Journal of Diseases of Children 125 (1973): 479–80.

Freinhar, J.P., and W. Alvarez. “Androgen-Induced Hypomania.” Journal of Clinical Psychiatry 46 (1985): 354–55.

Levien, T.L., and D.E. Baker. “Reviews of Trimetrexate and Oxandrolone.” Hospital Pharmacy 29 (1994): 696–702.

Mendenhall, C.L., et al. “Short-Term and Long-Term Survival in Patients with Alco- holic Hepatitis Treated with Oxandrolone and Prednisolone.” New England Jour- nal of Medicine 311 (1984): 1464–70.

Rosenfeld, R.G., et al. “Six-Year Results of a Randomized, Prospective Trial of Human Growth Hormone and Oxandrolone in Turner Syndrome.” Journal of Pediatrics 121 (1992): 49–55.

Taiwo, B.O. “HIV-Associated Wasting: Brief Review and Discussion of the Impact of Oxandrolone.” AIDS Patient Care and STDs 14 (2000): 421–25.

Wilson, D.M., et al. “Oxandrolone Therapy in Constitutionally Delayed Growth and Puberty.” Pediatrics 96 (1995): 1095–1100.


Pronunciation: ox-A-zeh-pam (also pronounced ox-AZ-eh-pam) Chemical Abstracts Service Registry Number: 604-75-1
Formal Names: Anxiolit, Serax, Serenid D
Type: Depressant (benzodiazepine class). See page 21

Federal Schedule Listing: Schedule IV (DEA no. 2835) USA Availability: Prescription
Pregnancy Category: C

Uses. This substance is a metabolite of diazepam, temazepam, chlordiaze- poxide, and clorazepate dipotassium. Oxazepam’s primary medical usage is to fight insomnia, hostility, and anxiety. Some researchers have found the drug also works against depression. Studies show oxazepam, diazepam, and fluni- trazepam to have about the same therapeutic effects, though not the same strengths (oxazepam being the weakest). In the 1990s a survey of pharmacies in Cracow, Poland, illustrated oxazepam’s worldwide popularity; around 14% of benzodiazepine prescriptions were for oxazepam, predominantly to women. One advantage of the drug is its safe “therapeutic ratio,” meaning that the amount needed to produce a desired medical effect is far below the amount needed to produce a poisonous effect. Thus medical practitioners have considerable flexibility in adjusting dosage to an exact amount needed by a patient.

Experimental use against tinnitus (ringing in the ears) has been promising. Sometimes oxazepam is the preferred antianxiety medicine for alcoholics suf- fering from cirrhosis, because a fully functioning liver is unnecessary to flush the substance from the body. Oxazepam is used to alleviate alcohol with- drawal syndrome and has been used to treat neuroses and schizophrenia. Oxazepam is considered appropriate for short-term treatment of agitation in elderly persons suffering from dementia. Tests indicate the drug can reduce hostility as well as anxiety, an ability that would set oxazepam apart from other benzodiazepines. In a cat experiment, however, the drug increased pred- ator behavior. The drug makes mice more combative. Rats kill more mice when dosed with oxazepam, but researchers interpret that result as illustrating potency of the drug rather than indicating it would promote aggression in humans. Human oxazepam reactions that increase hostility and combativeness are unusual and unexplained, although factors may include size and fre-

Oxazepam 341

quency of dose along with inherent personalities of users. Hostile human re- actions are “paradoxical” effects, meaning they are the opposite of what normally happens after taking an oxazepam dose.

Drawbacks. While under the drug’s influence people exhibit memory trou- ble. Oxazepam lowers body temperature in mice and rats. Case reports tell of oxazepam causing blisters or other skin eruptions on people. In mice the sub- stance boosts the poisonous action of the cancer medicine ifosfamide. Some experiments using oxazepam to induce sleep find no hangover effect on per- sons’ performance the next day, but that result is not invariable; size of dose appears relevant. An experiment testing the drug’s effect on vigilance (an important ability when driving a car) found normal ability while persons were under the influence of a low dose. Another experiment using a dose four times greater did find vigilance impairment. Still another experiment showed slower movements.

Abuse factors. One reviewer of the drug’s characteristics reported that it may have less addictiveness than diazepam. In one study opiate addicts found oxazepam no more attractive than a placebo. In another study sedative abus- ers judged the drug less attractive than diazepam and indeed mistakenly iden- tified oxazepam as a placebo one third of the time (a mistake they almost never made with diazepam) and even considered a placebo more appealing than oxazepam about one fifth of the time (a preference never occurring with diazepam). A similar experiment in which drug abusers compared oxazepam, diazepam, and placebo produced comparable results.

An animal research study found no tolerance produced by the drug. Mon- keys, however, exhibit signs of tolerance, dependence, and withdrawal after taking the drug for a week or two. One human study found tolerance but no withdrawal symptoms. Nonetheless, melancholy, mood swings, confusion, anxiousness, panic, and seizures have been observed when doses of the drug stopped abruptly. Some of those “withdrawal symptoms,” however, are also conditions for which the drug is prescribed; so emergence of those conditions upon stopping the drug may simply mean the underlying conditions were not cured. A case report recounts a rare instance of someone having visual hal- lucinations while undergoing oxazepam withdrawal. Tapering oxazepam does not necessarily prevent abstinence symptoms, but symptoms have been con- trolled by substituting another drug. One authority warns that stopping ox- azepam can be as touchy as stopping barbiturates. In the 1980s a health official in Australia portrayed oxazepam dependence as a growing problem. In con- trast, another authority reviewing oxazepam’s history for a medical journal found only four accounts of human dependence on the drug and declared withdrawal symptoms to be unusual upon sudden stoppage. This reviewer speculated that oxazepam’s slow delivery of drug effects and its tendency to make people dizzy if a lot is consumed help discourage abuse.

Drug interactions. A driving skills test showed that oxazepam worsens im- pairment induced by alcohol. Cigarette smoking shortens the time span that an oxazepam dose stays in the body. A mouse study found that animals could withstand higher doses of morphine and methadone if oxazepam was also used.

Cancer. Findings about oxazepam’s potential for causing human cancer

342 Oxazepam

have been inconclusive. Gene mutations would be a possible sign that cancer might eventually emerge; some laboratory tests show that the drug does not cause gene mutations, but genetic mutations were apparent after a six-month administration of the drug to mice. Oxazepam is described as causing liver cancer in mice. Researchers testing the drug on rats concluded that an unclear potential for causing cancer exists, but their uncertain conclusion was partly based on some dosages so high that apparently they were fatal to various individual animals.

Pregnancy. Experiments have exposed mice to oxazepam during fetal de- velopment, and assorted differences in their behavior (compared to mice with no exposure) have been documented, including decreased sociability and de- creased interaction with surroundings. What those differences might mean in a human context is unclear. Experimental evidence indicates that prenatal ex- posure to oxazepam may harm a mouse’s learning ability and temporarily slow growth. In humans the drug passes from a pregnant woman into the fetus. A survey of 4,014 instances of birth defects in the Netherlands from 1981 to 1994 found an association between oxazepam and cleft lip. The same association was found in Finland a few years earlier. Mice experiments have also produced head and mouth malformations, but the doses involved were far higher than humans would be expected to take.

Oxazepam is considered to have less impact than other benzodiazepines on a nursing mother’s milk supply. Two nursing mothers who had measurable levels of oxazepam in their blood had no evidence of the substance in their milk. A case report tells of a nursing mother whose milk contained about 4.7% of her oxazepam dosage, with no apparent effect on the infant. In other cases, not even 0.001% of the oxazepam dose taken by a mother passed into her milk.

Additional scientific information may be found in:

Ayd, F.J., Jr. “Oxazepam: Update 1989.” International Clinical Psychopharmacology 5 (1990): 1–15.

Bliding, A. “The Abuse Potential of Benzodiazepines with Special Reference to Oxa- zepam.” Acta Psychiatrica Scandinavica. Supplementum, no. 274 (1978): 111–16.

Bucher, J.R., et al. “Toxicity and Carcinogenicity Studies of Oxazepam in the Fischer 344 Rat.” Toxicological Sciences 42 (1998): 1–12.

Fouks, L., et al. “The Clinical Activity of Oxazepam.” Acta Psychiatrica Scandinavica. Supplementum, no. 274 (1978): 99–103.

Griffiths, R.R., et al. “Comparison of Diazepam and Oxazepam: Preference, Liking and Extent of Abuse.” Journal of Pharmacology and Experimental Therapeutics 229 (1984): 501–8.

Mewaldt, S.P., M.M. Ghoneim, and J.V. Hinrichs. “The Behavioral Actions of Diazepam and Oxazepam Are Similar.” Psychopharmacology 88 (1986): 165–71.

Vaisanen, E., and E. Jalkanen. “A Double-Blind Study of Alprazolam and Oxazepam in the Treatment of Anxiety.” Acta Psychiatrica Scandinavica 75 (1987): 536–41.


Pronunciation: ox-i-KOH-dun
Chemical Abstracts Service Registry Number: 76-42-6 (Hydrochloride form 124-


Formal Names: Endocet, Endocodone, Endodan, M-Oxy, Oxycet, Oxycocet, OxyContin, OxyFast, OxyIR, Percocet, Percodan, Percodan-Demi, Percolone, Roxicet, Roxicodone, Roxilox, Roxiprin, Supeudol, Tylox

Informal Names: Oxicotten, Oxy, Oxycotton, Oxy 80s, Percs Type: Depressant (opiate class). See page 19
Federal Schedule Listing: Schedule II (DEA no. 9143)
USA Availability: Prescription

Pregnancy Category: B

Uses. This drug is considered more addictive than codeine, from which oxycodone is derived. Some authorities say oxycodone comes from thebaine, which is correct also, because thebaine is the parent chemical that yields co- deine. Oxycodone is anywhere from 7 to 12 times stronger than codeine and about 0.3 to 2.2 times the strength of morphine, depending on the way the drugs are used. Body chemistry transforms part of an oxycodone dose into oxymorphone. Patients have found pain relief from oxycodone to be as sat- isfactory as relief from ketamine and morphine. Oxycodone has been used successfully to reduce pain from dentistry, surgery, cancer, and osteoarthritis (a painful disease of a person’s joints). The drug is also used as a sedative and as a cough suppressant. It is sometimes prescribed for “restless leg syn- drome,” an affliction in which persons keep moving their arms and legs around. The drug has also reduced tics associated with Tourette’s syndrome. Oxycodone can relax people and at times even create euphoria. Some re- searchers speculate that oxycodone’s euphoric effects may improve patients’ sensation of pain relief, making the substance more effective for that purpose than a drug that lacks euphoric effects. The drug works an antidepressant for some persons.

Blood levels from a given dose of oxycodone tend to be about 25% higher in females than in males. The cause is unknown, but the difference apparently has no impact on medical usage.

Drawbacks. Unwanted effects include nausea, vomiting, constipation, itch- ing, sweating, sleepiness, reduced sex drive, general weakness, impairment of

344 Oxycodone

breathing, and momentary low blood pressure when a person stands up. One study found the drug to impair breathing more than various other opiates do, and in another study, doses of oxycodone had to be stopped lest the volun- teers be harmed by further breathing difficulty. Normally the drug should be avoided if a person suffers from pancreatitis, enlarged prostate, difficulty with urination, or poorly functioning thyroid or adrenal glands. Experimenters have demonstrated that the drug reduces physical and mental abilities needed for driving automobiles.

Abuse factors. The drug’s potential for abuse is considered the same as morphine’s, and oxycodone is a sought-after product among opiate abusers. A study that reviewed medical records found no evidence of tolerance de- veloping in a medical context. Regardless of whether people use the drug medically or recreationally, dependence can develop, followed by withdrawal symptoms if dosage stops suddenly. Withdrawal symptoms are described as minor and can be avoided by gradually discontinuing the drug instead of suddenly stopping it or by administering clonidine, a substance normally used to control high blood pressure.

Drug interactions. People should use oxycodone cautiously if they are also taking antihistamines, various antidepressants, or a monoamine oxidase in- hibitor (MAOI, found in some antidepressants and other medicine). Combin- ing those sorts of drugs with oxycodone can produce excessive effects. The same is true of alcohol. Oxycodone also seems to interact with cyclosporine, a substance used to suppress an individual’s immune system (an effect useful in preventing rejection of organs in transplant patients).

Cancer. Oxycodone’s potential for causing cancer is unknown.

Pregnancy. Oxycodone is believed to pose a small risk of causing birth de- fects, but safety for administration during pregnancy has not been determined. An examination of medical records found a slightly higher likelihood of birth defects if pregnant women use oxycodone, but, unlike most drugs associated with malformations, no particular type of birth defect appeared after using oxycodone. That suggests the drug might not be responsible for the observed abnormalities.

Newborns may have dependence on the drug if their mothers have been taking it during pregnancy. Enough of the drug can pass into a woman’s milk to cause dependence in a breast-feeding infant.

Combination products. Tylox contains sodium metabisulfite, to which asth- matics and other persons may have a serious allergic reaction, and should be used cautiously if the user is sensitive to sulfites.

Additional scientific information may be found in:

Kalso, E., and A. Vainio. “Morphine and Oxycodone Hydrochloride in the Manage- ment of Cancer Pain.” Clinical Pharmacology and Therapeutics 47 (1990): 639–46.

Saarialho-Kere, U., M.J. Mattila, and T. Seppala. “Psychomotor, Respiratory and Neu- roendocrinological Effects of a Mu-Opioid Receptor Agonist (Oxycodone) in Healthy Volunteers.” Pharmacology and Toxicology 65 (1989): 252–57.

Schick, B., et al. “Preliminary Analysis of First Trimester Exposure to Oxycodone and Hydrocodone.” Reproductive Toxicology 10 (1996): 162.

Oxycodone 345

Stoll, A.L., and S. Rueter. “Treatment Augmentation with Opiates in Severe and Re- fractory Major Depression.” American Journal of Psychiatry 156 (1999): 2017.

Walters, A.S., et al. “Successful Treatment of the Idiopathic Restless Legs Syndrome in a Randomized Double-Blind Trial of Oxycodone versus Placebo.” Sleep 16 (1993): 327–32.

Ytterberg, S.R., M.L. Mahowald, and S.R. Woods. “Codeine and Oxycodone Use in Patients with Chronic Rheumatic Disease Pain.” Arthritis and Rheumatism 41 (1998): 1603–12.


Pronunciation: ok-see-METH-ah-lohn
Chemical Abstracts Service Registry Number: 434-07-1
Formal Names: Adroyd, Anadrol, Anapolon, Anasteron, Oxymethalone Type: Anabolic steroid. See page 24
Federal Schedule Listing: Schedule III (DEA no. 4000)
USA Availability: Prescription
Pregnancy Category: X

Uses. This drug’s main medical usage is for treatment of anemia and other blood disorders. The compound has also seen success against hereditary an- gioedema, a condition involving painful swelling of body tissues. Discourage- ment of blood clots and encouragement of weight gain are other medical applications. Particular success has been noted in weight gain with HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syndrome) pa- tients, accompanied by general improvement in quality of life. Cancer patients have also benefitted from the drug’s weight-gain property. An experiment indicated that short-term dosage can help persons suffering from heart failure. In another experiment the drug improved bone density in bedridden people. Still another experiment showed that oxymetholone can boost height and weight in boys and girls who are small for their age; such usage requires careful monitoring, as the substance has potential for stopping bone growth and thereby preventing attainment of normal adult height.

Drawbacks. Oxymetholone can produce masculine physical characteristics in women (facial hair, deeper voice) and disrupt the menstrual cycle; some authorities indicate that such masculinization is uncommon. Experimentation with male rats lowered their blood levels of testosterone and halted sexual activity. In human males oxymetholone may promote enlargement of the pros- tate gland. Men with prostate or breast cancer should avoid the drug, as should women who have both breast cancer and signs of a bone-weakening disease called osteoporosis. Oxymetholone can damage the liver and, in un- usual circumstances, is associated with fatal harm to the spleen. Cholesterol levels can rise, increasing the risk of conditions leading to heart attack and stroke; kidney dialysis patients are considered to be at special risk for such outcomes. Case reports attribute stroke to oxymetholone. The drug may cause fluid retention, a possible hazard for persons with heart, liver, or kidney dis-

Oxymetholone 347

ease. Other unwanted effects have included nausea, vomiting, chills, acne, and painful testicles. Case reports have noted severe changes in several persons’ ability to handle blood sugar levels. Another case report noted mental con- fusion that developed in a patient receiving oxymetholone and that continued for weeks after the therapy stopped.

Abuse factors. Some athletes use the compound with the hope it will im- prove their sports performance. A case report attributed rupture of the triceps tendon to a regimen of oxymetholone, nandrolone, and testosterone, although analysts have noted that a nonanabolic steroid called cortisone may have pro- moted the injury. Another case report told of a 20-year-old athlete developing persistent balance problems after taking oxymetholone and two other steroids; investigators of that case felt that steroids were a likely cause, given their ability to promote brain damage (stroke) and mental difficulties (mood and thinking). A case report notes manic activity in a person using oxymetholone. Another case report notes an even-tempered person who became rageful and violent after beginning a regimen of oxymetholone. Researchers tested one group of athletes who were using that compound and other steroids, a second group composed of former users, and a third group that had never used these drugs. Compared to the other groups, current users perceived themselves as more antagonistic, but investigators found only slight psychological differ- ences among the groups. Chickenpox is a childhood disease that adults can suffer, and a bodybuilder who used oxymetholone and other anabolic steroids came down with a severe case requiring extended hospitalization; the case report did not blame the steroids but considered his drug use important enough to emphasize.

A case report speaks of oxymetholone “dependency” but in the context of persons needing the drug to maintain good health, not dependency in the traditional terminology of drug abuse. Another case report, however, does describe dependence in a bodybuilder who was taking oxymetholone and other anabolic steroids. A noteworthy aspect of this case was the person’s sudden development of opiate withdrawal symptoms when he received a drug that provokes opiate withdrawal.

Drug interactions. Not enough scientific information to report, although anabolic steroids as a drug class tend to boost effects from medicines intended to reduce blood clotting.

Cancer. Oxymetholone gives negative results in assorted laboratory tests designed to detect cell mutations that may lead to cancer and gives mixed results in tests involving animals dosed on the substance. Oxymetholone is suspected of causing human cancer, with liver cancer a particular risk. Sci- entists have been unsure about any connection between the substance and human cancer, but the high level of suspicion is illustrated by numerous pub- lished case reports noting development of cancer by patients using oxymeth- olone.

Pregnancy. The drug may reduce fertility. In rat experiments the substance masculinized female fetuses even more than methyltestosterone. Whether ox- ymetholone passes into human milk is uncertain, but nursing mothers are advised to avoid the substance.

Additional scientific information may be found in:

348 Oxymetholone

Alexanian, R., and J. Nadell. “Oxymetholone Treatment for Sickle Cell Anemia.” Blood 45 (1975): 769–77.

Barker, S. “Oxymethalone and Aggression.” British Journal of Psychiatry 151 (1987): 564. Bond, A.J., P.Y. Choi, and H.G. Pope, Jr. “Assessment of Attentional Bias and Mood in Users and Non-Users of Anabolic-Androgenic Steroids.” Drug and Alcohol

Dependence 37 (1995): 241–45.
Hengge, U.R., et al. “Oxymetholone Promotes Weight Gain in Patients with Advanced

Human Immunodeficiency Virus (HIV-1) Infection.” British Journal of Nutrition

75 (1996): 129–38.
Keele, D.K., and J.W. Worley. “Study of an Anabolic Steroid: Certain Effects of Oxy-

metholone on Small Children.” American Journal of Diseases of Children 113 (1967):

Murchison, L. “Uses and Abuses of Anabolic Steroids.” Prescribers’ Journal 26 (1986):

“Oxymetholone.” IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals

to Man: Some Miscellaneous Pharmaceutical Substances 13 (1977): 131–39.


Pronunciation: ox-i-MOR-fohn
Chemical Abstracts Service Registry Number: 76-41-5. (Hydrochloride form 357-

Formal Names: Numorphan
Type: Depressant (opioid class). See page 24
Federal Schedule Listing: Schedule II (DEA no. 9652) USA Availability: Prescription
Pregnancy Category: C

Uses. Medically this drug is used to ease pain and assist in anesthesia. It is about 9 to 13 times stronger than morphine, with similar actions. Oxymor- phone has been likened to heroin. Because body chemistry transforms part of an oxycodone dose into oxymorphone, scientists wondered if oxycodone’s therapeutic actions actually came from oxymorphone; upon investigation, ex- perimenters concluded that oxycodone does produce effects apart from those of oxymorphone. Allowing hospitalized patients to control their own oxy- morphone dosage for pain relief has caused no problems. Hydromorphone can sometimes be used as a substitute. A case report indicates oxymorphone can have antidepressant actions.

Drawbacks. Unwanted effects of oxymorphone can include nausea, vomit- ing, and breathing difficulty. Euphoria has been noted in horses that receive the drug.

Abuse factors. Not enough scientific information to report, but the drug is legally classified as highly addictive.

Drug interactions. Other depressants should generally be avoided, and monoamine oxidase inhibitors (MAOIs, found in some antidepressants and other medicine) should also be avoided.

Cancer. Not enough scientific information to report.

Pregnancy. Birth defects appeared after experimenters gave pregnant ham- sters 1,500 times the recommended human dose. Effects on human pregnancy are unknown. The drug can influence fetal heartbeat if used in childbirth. Oxymorphone has been found effective for easing pain after caesarean section.

Additional scientific information may be found in:

350 Oxymorphone

Heiskanen, T.E., et al. “Morphine or Oxycodone in Cancer Pain?” Acta Oncologica (Stockholm, Sweden) 39 (2000): 941–47.

Johnstone, R.E., et al. “Combination of Delta-9-Tetrahydrocannabinol with Oxymor- phone or Pentobarbital: Effects on Ventilatory Control and Cardiovascular Dy- namics.” Anesthesiology 42 (1975): 674–84.

Sinatra, R.S., and D.M. Harrison. “Oxymorphone in Patient-Controlled Analgesia.” Clinical Pharmacy 8 (1989): 541, 544.

Sinatra, R.S., et al. “A Comparison of Morphine, Meperidine, and Oxymorphone as Utilized in Patient-Controlled Analgesia Following Cesarean Delivery.” Anes- thesiology 70 (1989): 585–90.

Stoll, A.L., and S. Rueter. “Treatment Augmentation with Opiates in Severe and Re- fractory Major Depression.” American Journal of Psychiatry 156 (1999): 2017.


Pronunciation: pee-see-pee
Chemical Abstracts Service Registry Number: 77-10-1. (Hydrochloride form 956-


Formal Names: Phencyclidine

Informal Names: Ace, Ad, Alien Sex Fiend (with heroin), Amoeba, Angel, Angel Dust, Angel Hair, Angel Mist, Angel Poke, Animal Trank, Animal Tranq, Animal Tranquilizer, Aurora Borealis, Belladonna, Black Dust, Black Whack, Blotter Acid, Blue Madman, Boat, Bohd, Bush, Busy Bee, Butt Naked, Cadillac, Can- nabinol, Cigarrode Cristal, CJ, Clicker, Clickum, Cliffhanger, Columbo, Cozmo’s, Crazy Coke, Crazy Eddie, Crystal, Crystal Joint, Crystal T, Cycline, Cyclone, D, Detroit Pink, Devil’s Dust, Dipper, DMT, DOA, Do It Jack, Domex, Drink, Dummy Dust, Dust, Dusted Parsley, Elephant, Elephant Trank, Elephant Tranquilizer, Elysion, Embalming Fluid, Energizer, Erth, Fake STP, Flake, Flying Saucer, Fresh, Fuel, Good, Goon, Goon Dust, Gorilla Biscuit, Gorilla Tab, Green, Green Leaves, Green Tea, Happy Sticks, HCP, Heaven & Hell, He-Man, Herms, Hinkley, Hog, Hog Dust, Horse Tracks, Horse Tranquilizer, Ice, Ill, Illy Momo, Jet Fuel, Juice, K, Kap, Kay Jay, K-Blast, Killer, KJ, Kool, Koolly High, Krystal, KW, LBJ, Leaky Bolla, Leaky Leak, Lemon Drop, Lemon 714, Lenos, Lethal Weapon, Little One, Live One, Log, Loveboat, Lovely, Mad Dog, Mad- man, Magic, Magic Dust, Magic Mist, Mean Green, Mint Dew, Mint Leaf, Mint Weed, Missile, Mist, Monkey Dust, Monkey Tranquilizer, More, New Acid, New Magic, Niebla, Octane (mixed with gasoline), Oil, Omen, OPP, Orange Crystal, Ozone, P, Parsley, Paz, PCPA, Peace, PeaCe Pill, Peace Weed, Peep, Peter Pan, Pig Killer, Pikachu (mixed with MDMA), Pit, Polvo, Polvo de Angel, Polvo de Estrellas, Puffy, Purple Rain, Red Devil, Rocket Fuel, Scaffle, Scuffle, Selma, Sernyl, Sernylan, Sheets, Sherm, Sherman, Sherm Stick, Skuffle, Smok- ing, Snort, Soma, Space Base (mixed with crack cocaine), Space Cadet (with crack), Space Dust (with crack), Speedboat (with crack and marijuana), Spore, Squirrel (with crack and marijuana), Stardust, Stick, STP, Super, Super Grass (with marijuana), Super Joint, Super Kool, Super Weed, Surfer, Synthetic Co- caine, Synthetic THT, TAC, T-Buzz, Tea, Tic, Tic Tac, Tish, Titch, Trank, Wac, Wack, Water, Weed, Wet (alone or with marijuana), Wet Daddy, Whack (with crack or heroin), Whacky Weed, White Devil, White Horizon, White Powder, Wicky Stick (with crack and marijuana), Wobble Weed, Wolf, Wooly (with marijuana), Worm, Yellow Fever, Zimbie, Zombie Dust, Zombie Weed, Zoom

Type: Depressant. See page 19

352 PCP

Federal Schedule Listing: Schedule II (DEA no. 7471) USA Availability: Prescription

Uses. This substance was invented in the 1920s, but not until the 1950s was it introduced as a drug, intended as a human and veterinary anesthetic. Hu- man medical use soon ended because of psychological effects discovered dur- ing tests on patients. PCP is related to ketamine and, like that substance, has hallucinogenic qualities. Depending on how PCP is used, it can have stimu- lant, depressant, or hallucinogenic actions. In monkeys PCP is about 10 times stronger than ketamine.

Drawbacks. PCP can make people feel aloof from the world around them, cause numbness, interfere with movement, and distort perception of time. Hallucinations, floating sensations, euphoria, and mania can occur. People may forget what they did while under the drug’s influence; such amnesia can last for 24 hours after a dose. Although euphoric effects are well documented, one group of researchers noted bouts of depression brought on by chronic use of the substance, though not by intermittent use. Yet the same researchers also found people successfully using the drug as an antidepressant, and animal studies suggest PCP may have antianxiety properties. The substance reduces appetite in dogs. Rats lost weight when they chronically received PCP.

Law enforcement authorities say the drug can make people hostile and give them extra physical strength, and the same has been experienced by medical personnel dealing with overdose emergencies. Researchers, however, have generally not observed such results from PCP (although one of the very first studies in the 1950s noted violent reactions from about 5% of surgery patients who received the drug as an anesthetic). A study examining PCP cases at a Los Angeles psychiatric hospital emergency room explicitly noted that wild conduct among PCP patients was uncommon. Perhaps police simply have more dealings with hostile individuals; for example, alcohol can embolden belligerent persons, but violence is not considered an inherent effect of alcohol. Persons who become violent after taking PCP already have such a history without the substance, and during a police encounter they may well be under the influence of alcohol or other drugs as well. Military research found that PCP hostility did not occur unless persons were under stress, and not all stressed individuals reacted that way. The military study also found that psy- chotic episodes did not occur with normal persons; someone had to be prone to psychosis in order for such behavior to occur while using the drug (a find- ing supported by other studies as well). In mice research PCP reduces violent behavior. Most species, including monkeys, act more docile after taking the drug. Some violent human episodes are described as coming not from ag- gression but from a PCP user’s panic when police or medical personnel try to restrain the person. One group of addicts spoke of the substance lowering inhibitions, which is not the same as causing violence, although an already enraged person who loses inhibitions may engage in stormy behavior. In ad- dition, users who attract attention from police or emergency medical person- nel are not necessarily representative of recreational users in general, either in personality or size of dose or reaction to the dose.

PCP 353

PCP’s physical effects include increased salivation, body temperature, pulse rate, and blood pressure. Case reports about humans indicate that PCP can raise blood pressure so high that a medical emergency occurs. The drug can bring on dizziness and double vision, create seizures, and cause muscle dis- coordination and damage. Numbness caused by PCP can promote injury due to lack of pain signals that ordinarily warn a person to stop doing something. Cases of kidney failure and liver destruction have been associated with the substance.

The higher one rises in the traditional evolutionary scale (for example, from mice to rats to humans), the lower the dose necessary for PCP to create an- esthesia. Two observers who noted that trend concluded that human brains are exquisitely sensitive to PCP. Animal experiments reveal brain damage when the substance is used chronically for as little as five days. PCP addicts have complained of memory trouble. A small human study found impaired ability for abstract thinking and for physical movement in response to signals, impairment measured years after the persons said they had stopped using PCP. Moreover, users of the drug may have normal scores on intelligence tests but have emotional disabilities and be crippled in their ability to cope with problems. Those latter defects may be caused by the drug or may instead be reasons why people resort to the drug.

Abuse factors. Initially PCP was a Schedule III drug, but in 1978 government authorities shifted it to Schedule II because of recreational use. At about that time a Los Angeles psychiatric hospital emergency room tested 145 consecu- tive patients for PCP; 63 were positive (over 40%).

A study of 200 recreational users found differences in effects reported by persons who took a little of the drug once a month and by persons who took a lot every day for years. Heavy users felt more pepped-up, violent, and su- icidal. Regular users of PCP are known for self-destruction; one study found that 24% of regular users had tried to commit suicide, and 36% had overdosed on other drugs. A study of PCP users who were treated at a charity hospital found no behavioral difference between black or white males, but black fe- males acted much stranger and more aggressively than white females. The meaning of that finding is unclear—it could be racial, could be cultural, could be a statistical oddity that would disappear after more research.

When monkeys were given a choice between water or PCP, the animals showed no preference; such indifference is a sign of low addictive potential. An experiment measuring rats with prenatal exposure to PCP found the ani- mals were more sensitive to the drug than were rats lacking prenatal expo- sure—the opposite of tolerance. Dependence has been reported in monkeys that receive PCP. Pigeons that received the drug every day for 215 days did not develop dependence. Human research has found tolerance but not depen- dence among users, although dependence is suspected.

Various cold remedies contain doxylamine succinate, which can cause a false-positive drug test for PCP.

Drug interactions. In a rat experiment neither alcohol nor PCP affected blood pressure, but blood pressure rose when they were used simultaneously. They also speeded up the heart. One human study found that PCP may be more likely to induce excitability in alcoholics than in nonalcoholics, possibly

354 PCP

meaning that alcohol increases the likelihood of a manic reaction. In mice marijuana has reduced hyperactivity caused by PCP.

Cancer. Not enough scientific information to report.

Pregnancy. Two studies published only a few months apart in the 1980s gave different impressions about the prevalence of PCP use among pregnant women. In one study a group of 2,327 pregnant women were tested for PCP use; 19 were taking the drug. Those 19 were typically polydrug abusers. A different study of 200 pregnant women found 24 using PCP, a rate 15 times higher than in the other group.

If a pregnant woman uses PCP, it passes into the fetus. Reports exist of PCP being detected in newborns three months after the mothers claimed to have stopped using the drug during pregnancy, which would mean that the drug remains in a fetus months after a pregnant woman stops taking PCP. Whether the women’s claims of abstinence were confirmed by laboratory testing during those months of pregnancy is unclear, however. In mice and pigs PCP builds up in the fetus, reaching levels 7 to 10 times higher than in the female’s blood- stream.

The drug is suspected of causing birth defects. At dosage levels high enough to poison the pregnant female, birth defects have been produced in rats and mice. Rats with prenatal exposure to PCP show defective memory and learn- ing ability. The substance is suspected of harming fetal brain development in humans. Pregnant women who use the drug tend to produce infants who are smaller than normal. In a group of 83 infants with prenatal PCP exposure, almost half had a head circumference below the 25th percentile (meaning that 75% of infants in the general population have bigger heads and, by implica- tion, larger brains). Some were below the 10th percentile. Smaller-than-normal infant skulls may interfere with physical growth of the brain. People who abuse one drug tend to abuse others as well; one study of 41 women who used PCP during pregnancy found that most had also been using cocaine. Two studies of women who used PCP during pregnancy found that all were poor; most were unmarried, were in an ethnic minority, and had received inadequate prenatal care. Such factors confound efforts to confirm what effect PCP alone has on pregnancy.

Offspring of mothers who have been using PCP can exhibit symptoms sim- ilar to those seen in infants undergoing opiate withdrawal—even though the drug is not an opiate, and research has yet to demonstrate that PCP depen- dence occurs. Infant distress may be real, but the newborn may be responding to the unpleasant effects of the drug itself rather than responding to sudden absence of the drug.

A year after birth, a group of 57 babies with prenatal PCP exposure showed normal development in mental ability and physical coordination, although almost half were ill-tempered. About 15% had trouble sleeping, and the same percentage lacked normal emotional attachment. Those findings are consistent with other studies. Home environment, of course, may influence behavior as much or more than prenatal drug exposure. Factors noted above (lack of money, absent father, being in a disadvantaged ethnic minority) can weaken home life. Still, the kinds of brain function damage seen in animal studies are the kinds of damage that should interfere with children’s abilities to socialize

PCP 355

normally—exactly the kind of deficit seen in children who have prenatal ex- posure to PCP.

In mice PCP not only passes into maternal milk, but milk levels are 10 times higher than maternal blood levels.

Additional information. PCP is related to the Schedule I hallucinogens PCE (CAS RN 2201-15-2), PCPy (2201-39-0), TCP (21500-98-1), and TCPy (22912- 13-6). Rat experimentation measured PCPy as about the same strength as PCP. Other laboratory measurement shows TCP as stronger than PCP, and PCE as stronger than TCP. French military experiments found that TCP could protect rats and guinea pigs from the chemical warfare agent soman.

“Cannabinol” is a nickname for PCP and refers to THC, which is the active chemical in marijuana and dronabinol, but PCP is not THC. Likewise “DMT” and “STP” (DOM) are nicknames for PCP, but they are all different drugs.

Additional scientific information may be found in:

Baldridge, E.B., and H.A. Bessen. “Phencyclidine.” Emergency Medicine Clinics of North America 8 (1990): 541–50.

Brecher, M., et al. “Phencyclidine and Violence: Clinical and Legal Issues.” Journal of Clinical Psychopharmacology 8 (1988): 397–401.

Giannini, A.J., R.K. Bowman, and J.D. Giannini. “Perception of Nonverbal Facial Cues in Chronic Phencyclidine Abusers.” Perceptual and Motor Skills 89 (1999): 72–78. Graeven, D.B., J.G. Sharp, and S. Glatt. “Acute Effects of Phencyclidine (PCP) on Chronic and Recreational Users.” American Journal of Drug and Alcohol Abuse 8

(1981): 39–50.
Harry, G.J., and J. Howard. “Phencyclidine: Experimental Studies in Animals and

Long-term Developmental Effects on Humans.” In Perinatal Substance Abuse: Re- search Findings and Clinical Implications, ed. T.B. Sonderegger. Baltimore, MD: Johns Hopkins University Press, 1992. 254–78.

Khajawall, A.M., T.B. Erickson, and G.M. Simpson. “Chronic Phencyclidine Abuse and Physical Assault.” American Journal of Psychiatry 139 (1982): 1604–6.

Pradhan, S.N. “Phencyclidine (PCP): Some Human Studies.” Neuroscience and Biobehav- ioral Reviews 8 (1984): 493–501.

Schuckit, M.A., and E.R. Morrissey. “Propoxyphene and Phencyclidine (PCP) Use in Adolescents.” Journal of Clinical Psychiatry 39 (1978): 7–13.

Sioris, L.J., and E.P. Krenzelok. “Phencyclidine Intoxication: Literature Review.” Amer- ican Journal of Hospital Pharmacy 35 (1978): 1362–67.


Pronunciation: PEM-oh-leen
Chemical Abstracts Service Registry Number: 2152-34-3 Formal Names: Cylert
Informal Names: Popcorn Coke
Type: Stimulant. See page 11
Federal Schedule Listing: Schedule IV (DEA no. 1530) USA Availability: Prescription
Pregnancy Category: B

Uses. In the United States pemoline became available for medical purposes during the 1970s. It is used to treat depression, weariness, and attention deficit hyperactivity disorder (ADHD). The drug’s stimulant effects are described as greater than caffeine but less than amphetamine. Unlike many scheduled stimulants, pemoline is unrelated to amphetamine.

Studies find pemoline useful in reducing symptoms of depression, and ex- perimental usage of pemoline with monoamine oxidase inhibitor (MAOI) an- tidepressants has helped depressed persons who obtain insufficient relief with other drugs.

Pemoline has eliminated drowsiness felt by persons taking antihistamines. The drug has been proposed for workplace usage to reduce fatigue but has not been tested extensively for that purpose. Tests have found that the drug improves ability to perform arithmetic when users are tired. In a different but more robust experiment, members of the U.S. Navy Special Warfare group stayed awake 64 hours around the clock while using pemoline. Though their performance appeared to decline as the experiment continued, they not only did better than participants who used placebos, but they also did better than persons using methylphenidate. In England, Royal Air Force experimenters concluded that pemoline can help keenness and capabilities during long shifts of duty. A Russian report endorses the drug’s usefulness for “urgent increase” of functioning but notes that persons using pemoline cannot maintain initial ability if body temperature rises and oxygen supply declines, nor does the drug help persons push past emotional strain or fulfill complicated task re- quirements. During the 1980s and 1990s sports officials in Belgium found the drug was frequently used by cyclists seeking a competitive edge. Multiple sclerosis patients using pemoline sometimes report less exhaustion than those

Pemoline 357

using a placebo, but investigators who rigorously reviewed studies about mul- tiple sclerosis fatigue found no evidence of pemoline improving weariness. An instance is known of an elderly man taking pemoline to help him stay awake during lectures, but the regimen seemed to promote prostate trouble. Pemoline has been successfully used against narcolepsy.

Studies find pemoline about as effective as either dextroamphetamine or methylphenidate in helping children with ADHD. Pemoline has been used successfully against ADHD in teenagers and adults as well. Growth rates are below normal in some youngsters with ADHD, and pemoline itself can tem- porarily hold back such development but without long-term harm—young- sters develop normal adult weight and height. Those deficient growth rates may be treated with growth hormone. One study found, however, that pemo- line seems to make the hormone treatment less effective in some patients. As the age of ADHD patients grows, so can unwanted effects that they experience from pemoline.

Animal experiments in the 1960s indicated that pemoline boosts learning ability. The lure of a “smart pill” had understandable appeal to suffering stu- dents and teachers, but when the drug was tested on college students, no improvement in learning ability occurred. The same dismal outcome occurred when elderly persons received the drug; indeed, some performed worse than elderly persons receiving a placebo. Group results in still another experiment showed either no improvement or worsening of learning scores when people used the drug. In contrast, long-term daily administration of the drug seemed to improve memory in some persons entering senility.

A review covering 10 years of pemoline reports found none attributing eu- phoria to the drug, a lack that sets it apart from other scheduled stimulants. Unlike some other stimulants, pemoline also seems to have little effect on pulse rate or blood pressure.

Drawbacks. The drug can bring on tics and partial muscle movements, in a particularly severe way if an overdose occurs. An instance is known of muscle damage in an adult misusing pemoline. Pemoline is also known to reduce appetite and salivation, increase crankiness, bring on headaches and stomachaches, cause skin rash, and interfere with sleep. Hallucinations from pemoline have been reported.

In rats and mice pemoline can cause self-harm behavior, and the amount needed to induce such behavior declines when a certain kind of brain damage is present, damage that is often seen in mentally retarded humans. Those findings suggest that such persons receiving pemoline may need monitoring to guard against self-injury. Long-term excessive usage may generate tempo- rary psychotic behavior, but such an outcome appears untypical.

Probably the most serious unwanted results of taking pemoline can be hep- atitis and other liver injury, injury so severe as to require a transplant. Damage can continue to worsen after the drug is stopped, and people have died from liver failure induced by pemoline. Victims tend to be children. Such an ad- verse effect is particularly disquieting because it occurs at therapeutic dosage, rather then being created by reckless abuse. A child can take pemoline for months before harm is apparent, or alarming symptoms can arise after just a week of use. Methylphenidate is suspected of contributing to liver trouble in

358 Pemoline

persons who are also taking pemoline. Debate exists about how dangerous pemoline is to liver function when no other drugs are being taken, but the debate has limited practical significance because many patients taking pemo- line receive other drugs as well. Because of concern about liver damage, par- ents are supposed to sign a written consent form before their children begin pemoline therapy.

Abuse factors. Although pemoline is a scheduled substance, a review of reports covering the first 10 years of its medical availability in the United States found little evidence of addiction or abuse. A Norwegian review of pemoline use boldly described it as “a stimulant which cannot be abused.”1 When given a choice of drugs, animals show no particular interest in pemo- line, a sign of low abuse potential. Nonetheless, a case report does exist of a pemoline addict who developed a paranoid psychosis that went away after stopping the drug. A British medical practitioner reported that drug misusers were supplementing their amphetamine habit with pemoline.

An experiment tested pemoline’s ability to help reduce cocaine usage among persons receiving methadone treatment (meaning the persons were addicted to cocaine and heroin both). Results were unencouraging. In contrast, favorable response in an ADHD alcoholic caused researchers to predict that pemoline may be useful for treating alcohol addiction. Mice experimentation shows that pemoline reduces effects produced by THC, considered the pri- mary drug in marijuana.

Drug interactions. Pemoline is suspected of interfering with epilepsy med- icines. It can boost mono amine oxidase inhibitor (MAOI) antidepressants and urinary acidifers (the latter action interfering with pemoline’s psychostimulant effects).

Cancer. Rat experiments do not indicate any cancer risk from pemoline.

Pregnancy. Experiments with rabbits and rats reveal no harm to fetal de- velopment, but influence on human fetal development is unknown.

Additional information. When tested on mentally handicapped workers, magnesium pemoline (CAS RN 18968-99-5) brought on the kinds of temper- ament modification associated with caffeine but failed to increase either pro- ductivity or time worked. Two cocaine addicts who appeared to have mild ADHD were able to reduce their intake of cocaine while receiving magnesium pemoline, a result leading the scientific investigators to wonder if magnesium pemoline might have potential for helping to break cocaine addiction. Animal experiments have shown that both pemoline and magnesium pemoline can provide protection against atomic radiation.

Additional scientific information may be found in:

Bostic, J.Q., et al. “Pemoline Treatment of Adolescents with Attention Deficit Hyper- activity Disorder: A Short-Term Controlled Trial.” Journal of Child and Adolescent Psychopharmacology 10 (2000): 205–16.

Elizur, A., I. Wintner, and S. Davidson. “The Clinical and Psychological Effects of Pemoline in Depressed Patients—A Controlled Study.” International Pharmaco- psychiatry 14 (1979): 127–34.

Honda, Y., and Y. Hishikawa. “Long Term Treatment of Narcolepsy and Excessive

Pemoline 359

Daytime Sleepiness with Pemoline (Betanamin).” Current Therapeutic Research:

Clinical and Experimental 27 (1980): 429–41.
Langer, D.H., et al. “Evidence of Lack of Abuse or Dependence Following Pemoline

Treatment: Results of a Retrospective Survey.” Drug and Alcohol Dependence 17

(1986): 213–27.
Newlands, W.J. “The Effect of Pemoline on Antihistamine-Induced Drowsiness.” The

Practitioner 224 (1980): 1199–1201.
Shevell, M., and R. Schreiber. “Pemoline-Associated Hepatic Failure: A Critical Anal-

ysis of the Literature.” Pediatric Neurology 16 (1997): 14–16.
Sternbach, H. “Pemoline-Induced Mania.” Biological Psychiatry 16 (1981): 987–89. Valle-Jones, J.C. “Pemoline in the Treatment of Psychogenic Fatigue in General Prac-

tice.” The Practitioner 221 (1978): 425–27. Note

1. N. Lie, “Sentralstimuleren Midler ved AD/HD Hos Voksne. Kan De Misbrukes? [Central Stimulants in Adults with AD/HD. Can They Be Abused?],” Tidsskrift for den Norske Laegeforening 119 (1999): 82–83. Abstract in English.


Pronunciation: pen-TAZ-oh-seen
Chemical Abstracts Service Registry Number: 359-83-1. (Hydrochloride form


Formal Names: Fortral, Fortralgesic, Fortralin, Fortwin, Liticon, Pentgin, Sosegon, Sosenyl, Talacen, Talwin, Talwin Nx

Informal Names: 4 4s, Teacher, Ts, Yellow Footballs. Combination with meth- ylphenidate: Crackers, 1s & 1s, Poor Man’s Heroin, Ritz & Ts, Ts & Rits, Ts & Rs, Sets. Combination with tripelennamine: Ts & Blues, Ts & Bs

Type: Depressant. See page 19
Federal Schedule Listing: Schedule IV (DEA no. 9709) USA Availability: Prescription
Pregnancy Category: C

Uses. Pentazocine became available in the 1960s. Some authorities classify the drug as an opioid; some do not. Rather than having cross-tolerance with opiates and opioids, pentazocine can provoke a withdrawal syndrome from them. Volunteers who receive pentazocine have been uncertain about what sort of drug it is; some say it is a hallucinogen; some think they are receiving alcohol.

Pentazocine has about the same pain relief strength as codeine. An exper- iment using oral surgery patients found pentazocine’s pain relief to be the same as aspirin’s. After drug abusers began grinding down Talwin tablets and injecting the powder to get morphine and heroin sensations, the manufacturer introduced Talwin Nx tablets, which include a chemical designed to block those sensations if the substance is injected. Dispute exists about whether the Nx version of Talwin actually prevents effects sought by illicit users.

Research indicates that women surgical patients tend to get better pain relief from pentazocine than male patients. Research also indicates that the drug’s surgical pain control is more effective for older patients and less effective for neurotics and for individuals with outgoing personalities. The drug has been routinely used to ease cancer pain and has had success in reducing joint pain caused by various afflictions, including arthritis. After noting that pentazocine does not prolong bleeding times, researchers called it suitable to fight pain from hemophilia, a blood disease that promotes bleeding. The substance has also been given as a treatment for stubborn cases of hiccups.

Pentazocine 361

Investigators have documented that people can briefly experience euphoria after taking the drug. Some users feel more amiable and serene after a dose.

Drawbacks. Unwanted pentazocine actions include rapid heartbeat, blood pressure changes (up or down), fainting, sweating, confusion, sleepiness, blurred vision, nausea, vomiting, and constipation. Studies have found that 1% to 10% of persons receiving the drug (especially an injectable pharmaceu- tical version) have odd psychological reactions such as hallucinations, delu- sions, or a sense of unreality about the world. The substance can interfere with decision making and physical movement. Research has shown that driving skills decline when a person uses the drug, and users should avoid operating motor vehicles or other dangerous machinery. Because pentazocine has oc- casionally been associated with seizures, it should be used cautiously by pe