Abstract
We are gratified that Drs Wilson and Brakoulias are in agreement with us regarding the potential importance of dietary factors in the high prevalence psychiatric disorders, and the necessity to develop a population-based primary prevention strategy for these disorders [1].
As they correctly point out, there are a multitude of actions and interactions involved in the relationship between dietary intake and health outcome, and the study of such relationships is not straightforward. The decision to examine magnesium intake, in isolation from that of other nutrients, was originally made in order to test a specific hypothesis on the basis of the existing literature, as well as for pragmatic reasons. Studying individual nutrients in relation to disease, however, has limitations, given the multiplicity of combinations and interactions among nutrients in the daily diet. Nutrient intakes are also associated with particular dietary patterns, which may act as confounders in these analyses.
These facts point to the importance of examining diet as a whole, in addition to individual nutrients, when investigating diet as an aetiological factor in psychiatric illnesses. We are currently examining the association between overall diet quality, measured by diet quality scores and dietary pattern analyses, and mental health outcomes in a range of high-quality epidemiological studies in adolescents and adults. Initial findings from these studies point to an independent association between overall diet quality and the common mental disorders in men and women across the age range. Results of these various analyses are currently being prepared for publication.
It is also important in the examination of nutrition against disease outcome to consider the metabolic effects of acute illness; in individuals with mental illness nutrient deficiencies can be a result of the disorder itself. Stress and acute illness result in significant alterations in nutrient homeostasis, and reduced concentrations of numerous nutrients are evident in those with acute illnesses, secondary to the effects of the acute phase response [2]. As an example, low serum folate is described in those with depressive illnesses in the absence of differences in dietary consumption [3]. As such, in studies examining serum or tissue concentrations of nutrients as factors in psychiatric or other illnesses, dietary intakes need to also be measured in order to tease apart the relative contributions of both diet and illness to nutrient status.
Why would one examine diet in relation to the high-prevalence mental disorders in the first place? The first reason relates to the potential of diet to modulate the biological systems and factors underpinning depressive illness: gene expression, the stress response system, the immune system, neurodegeneration, and biochemistry [4]. The second reason relates to dietary changes evident in the community over the last decade or more. For example, data from the Australian National Nutrition Surveys between 1983 and 1995–96 demonstrate an increase in the consumption of pastries, cakes, biscuits, pizza, desserts, and saturated fat, while the amount of healthy fats in the diet were decreased [5]. The 2004 Victorian Population Health Survey reported that although approximately 60% of women met the daily recommendation regarding fruit consumption, only 5–11% met the recommended five or more serves of vegetables per day [6]. The results for men were even more pronounced: only 1.6–4% of male subjects consumed the recommended daily intake of fruit and vegetables.
In our Norwegian study the effect size for the relationship between magnesium intake and depression was small [7], but most mental illnesses are not due to any single factor, and individual risk factors are very rarely powerful. Dietary factors that contribute a small share of the variance in aetiology may translate to an important effect at the population level due to the number of people exposed (i.e. 100%). Given that diet, unlike many other risk factors, is a modifiable environmental exposure, the development of an evidence base for diet as a preventative strategy and intervention target seems worth pursuing.