We read with interest the article by Everson-Rose et al. (1), which indicated that depressive symptoms were associated with a greater risk of diabetes at 3-year follow-up. The authors discussed several mechanisms by which depression may contribute to subsequent insulin resistance and type 2 diabetes, in particular, excess cortisol and central adiposity, altered immune function, and behavioral factors such as compliance and physical activity.
In this letter, we would like to suggest two additional explanations for the findings of Everson-Rose et al. First, patients with and without significant depressive symptoms clearly differed at baseline in the homeostasis model assessment of insulin resistance, a difference that remained fairly constant over time instead of accelerating for the depressed group. Therefore, the reverse hypothesis suggesting that insulin resistance results in a higher risk for depression seems more likely.
Second, there may be shared factors that increase the risk for both type 2 diabetes and depression. Notably, an impaired fatty acid metabolism is related to depression and to features of the metabolic syndrome (2). Low consumption of ω-3 fatty acids is associated with hypertriglyceridemia, cardiovascular disease, insulin resistance, and type 2 diabetes (3–5). Moreover, lowered ω-3 levels have been reported in erythrocytes of patients with depression (6). ω-3 fatty acids also have anti-inflammatory effects, and three recent placebo-controlled trials have found ω-3 acid, in particular eicosapentaenoic acid, to be effective in reducing depression (7).
We conclude that in this intriguing field of research, careful attention should be given to accurate controlling for confounders. Specifically, the assessment of fatty acid intake and metabolism should be included in future studies on the associations between depression and features of the metabolic syndrome.
