In this cross-sectional population-based study examining the association between diet and the high-prevalence mental disorders, the hypothesized association between habitual diet quality and these disorders was largely supported by the data. A dietary pattern comprising vegetables, fruit, beef, lamb, fish, and whole-grain foods (traditional) was associated with a lower likelihood of depressive and anxiety disorders, whereas a dietary pattern comprising processed and “unhealthy” foods (western) was associated with a higher likelihood of psychological symptoms and disorders. Better diet quality, as measured by the diet quality score, was associated with a lower level of psychological symptoms. Associations were apparent after adjustments for a wide range of possible confounding variables, including age, socioeconomic status, education, physical activity, and other lifestyle factors.
These results are concordant with previous research demonstrating associations between the quality of habitual diet and a range of other common noncommunicable diseases, risk factors, and medical outcomes. In the Nurses Health Study and the Health Professionals Follow-Up Study, those in the top quintile of diet quality scores had an approximately 25% lower risk for major chronic diseases, such as cardiovascular disease and cancer, over 8—12 years of follow-up compared to the lowest quintile (22), and diet quality measured by dietary pattern analyses predicted cardiovascular disease risk in both studies (23, 24). Diet quality was also inversely associated with overall and cancer mortality in a study of 42,000 older women over nearly 10 years of follow-up (25). Recent results from the 52-country INTERHEART study demonstrated a 30% higher risk for acute myocardial infarction in individuals with higher scores on a measure of dietary “risk” (26).
In this study, the observed attenuation of the positive relationship between the western dietary pattern and depressive disorders by adjustment for overall energy intake may indicate that the absolute amount of unhealthy food consumed in the diet is more relevant to mental health than the quantity as a proportion of overall diet. As it is also a healthy dietary pattern, the tendency for a modern dietary pattern to be associated with a higher, rather than lower, likelihood of depression was unexpected. This may be a consequence of reverse causality, wherein younger, more educated women, who had higher scores on the modern dietary factor, changed their diet in an attempt to improve their symptoms. Another explanation is that components of the traditional dietary pattern, such as vegetables, red meat, whole-grain foods, and high-fat dairy products, are particularly pertinent to the outcomes in question. Alternatively, this association may represent a type I error. We are conducting further studies to examine individual dietary components in relation to mental health outcomes.
The main limitation of this study is the cross-sectional design, which prevents conclusions being reached regarding the direction of the relationship between diet and mental health. Appetite changes are a common feature of depressive illness, and a poor-quality diet may be a result of mental health symptoms, rather than a causative factor. Thus, without a prospective study design, it is not possible to preclude reverse causality as an explanation for our findings. However, in our study there was little evidence that the energy intakes of individuals with psychopathology were markedly different from those of the other subjects.
Diet is an indicator of overall lifestyle patterns, and health-related behaviors are influenced by mental illness, as well as influencing the risk for depressive illness (27). Smoking, alcohol consumption, and physical activity levels are all indicators of self-care (28) and were adjusted for in our analyses. Nevertheless, the possibility exists that we did not account for these adequately or that other unmeasured confounders were a factor in the results. Moreover, in studies examining diet as a risk factor for medical outcomes, confounding by socioeconomic status must be considered (29). In this study, socioeconomic status and education had little impact on the reported associations, but it is not possible to rule out residual confounding or reporting bias by socioeconomic status as a factor in these results.
The strengths of this study include the use of gold-standard assessment tools for the diagnosis of depressive and anxiety disorders, the inclusion of a wide range of likely confounding variables, the testing of body habitus as a possible confounding or mediating factor, and comprehensive dietary assessments with a tool appropriate for the population under study. Diet quality was also operationalized by using both a priori measures (diet quality score) and naturalistic observations (factor analysis). Moreover, the study cohort was randomly selected, population based, and representative of the wider female Australian population (30).
Depressive illness is influenced by genetic, hormonal, immunological, biochemical, and neurodegenerative factors. Diet modulates each of these factors and, as a result, has a plausible impact on the development and course of this illness (4).
Inflammatory processes are thought to play an etiological role in the onset and maintenance of depressive disorders (31), as well as being of central importance in the high-prevalence noncommunicable diseases, such as cardiovascular disease, diabetes (32, 33), and cancer (34). Inflammation may, in part, explain the association between these medical illnesses, depression, and mortality, as well as the associations with diet. Adherence to a Mediterranean diet, high in vegetables, fruits, legumes, whole grains, fish, olive oil, and low-fat dairy products, correlates with lower levels of inflammatory markers (35), whereas western-type diets and diets high in refined carbohydrates are associated with higher levels of C-reactive protein, a marker of low-grade inflammation (5).
Nutritional factors also exert a direct and potent influence on neural physiology (7). In experimental studies a western-style diet lowered brain-derived neurotrophic factor (BDNF) levels within a short time, an effect that was independent of obesity or nutritional deficits (6). BDNF protects neurons from oxidative stress and promotes neurogenesis (36) and is believed to play a central role in depressive illness (37). Thus, by modulating the expression of BDNF, diet may influence psychiatric status.
Finally, diet influences oxidative processes, which may also be implicated in the pathophysiology of depressive illnesses (38). For example, antioxidant-rich diets appear to be effective in slowing or preventing age-associated pathophysiological and cognitive changes (39) and reducing the risk of age-associated diseases (9). In this way, dietary factors may modulate the risk for neurostructural and cognitive changes in the brain that affect psychological symptoms across the life course (38, 40).
The potential impact of diet on pathogenesis of depression may compound the impact of depressive illness on appetite and self-care. Thus, mental illness, dietary inadequacy, and nutrient depletion exacerbating mental illness may be linked in a vicious circle. This model remains to be tested but mirrors and overlaps with what is already known about the course of depressive illness (41).
To our knowledge, this study is the first to present data suggesting that the significant impact of diet quality on common chronic noncommunicable diseases extends to the high-prevalence mental illnesses. We have reported associations between diet quality and mental health cross-sectionally; however, this relationship requires further examination in well-designed prospective studies in order to determine the direction of the relationships and to rule out residual or unrecognized confounding. Confirmation of a causal relationship between diet and mental health would afford the possibility for an evidence-based preventive health care strategy incorporating dietary improvement. Such an approach would overlap with existing strategies for other medical conditions and could be implemented at a population level. Given that diet, unlike many other risk factors, is theoretically a modifiable environmental exposure, the development of an evidence base seems worthy of pursuit.
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