B eta blockers and diabetes

Beta cells secrete insulin

Beta-blockers are the other major class of blood-pressure-lowering drugs that have been implicated in causing diabetes or worsening diabetes control. The several large studies that have looked at the risk of diabetes associated with beta-blockers include the Nurses Health Studies I and II and the ongoing ARIC (Atherosclerosis Risk in Communities) study. In these two studies, the risk of developing diabetes in people originally without it who took beta-blockers was approximately 20% to 28% greater than in those who did not take beta-blockers.

This may seem counterintuitive since people with diabetes are often warned that beta-blockers can cause problems with low blood glucose, not high blood glucose. Beta-blockers cause these two problems in distinct ways. First, they may harm a person’s ability to recognize and respond to low blood glucose, mainly by keeping the heart rate slow, which can dampen symptoms of hypoglycemia. They may also inhibit the release of glucose from the liver. But beta-blockers also block the release of insulin by interacting with nerve signals to the pancreas and can thus lower insulin levels even when blood glucose is high.

There is some evidence that not all beta-blockers affect insulin secretion. Beta-blockers work by interacting with proteins in the body called beta receptors. There are several distinct types of beta receptors in the body. Beta-1 receptors are predominantly in the heart, while beta-2 receptors are in the heart as well as the arteries, muscles, liver, and pancreatic beta cells. This means that beta-1–selective drugs are less likely to interfere with the secretion and regulation of insulin.

Several studies have shown that a combination of beta-blockers and thiazide diuretics, as expected, also produces an increase in the risk of developing diabetes, by approximately 20%. The National Institute for Health and Clinical Excellence in the United Kingdom, an advisory group that develops national health policy, has placed a limited caution against the combined use of beta-blockers and thiazide diuretics for people at high risk for diabetes (because of family history, impaired glucose tolerance, or obesity, for example). While the risk of diabetes-related complications for the population as a whole is relatively low, these drugs may be a source of preventable diabetes or of diminished blood glucose control in individual cases.

Of note, ACE inhibitors and calcium channel blockers have not been strongly linked to diabetes.

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