Pouwer and de Jonge (1) raise two interesting points regarding our findings on depressive symptoms, insulin resistance, and diabetes risk (2). First, they suggest that insulin resistance may increase the risk for depression. This may be a plausible hypothesis, but it is an unlikely explanation for our findings. Participants were excluded from our analyses if they had overt diabetes (fasting blood glucose of ≥126 mg/dl or a self-reported history of diabetes) at the baseline examination. Moreover, although 126 (4.7%) participants in our study could be considered to have pre-diabetes, characterized by fasting blood glucose values between 110 and 125 mg/dl and typically considered an insulin-resistant state, the majority of our participants had normal glucose values and were not insulin resistant. For our analyses, we calculated insulin resistance by the revised homeostasis model assessment of insulin resistance (HOMA-IR) (3), which provides a continuum of values; thus, we did not define “cases” of insulin resistance. We did find that depressive symptoms were predictive of incident cases of diabetes over 3 years of follow up. In response to the hypothesis suggested by Pouwer and de Jonge, we reanalyzed our data and found that HOMA-IR values at baseline were not predictive of depression (P = 0.87) over the 3 years of the study among women who were not initially depressed.
Second, Pouwer and de Jonge (1) argue that intake and metabolism of ω-3 fatty acids may be important in the risk for depression and type 2 diabetes. This is an intriguing hypothesis; dietary factors may indeed influence risk for depression and, in turn, insulin resistance and diabetes risk. Data on consumption of ω-3 fatty acids in the SWAN population are available from a food frequency questionnaire completed at baseline. Therefore, we repeated our analyses of diabetes and insulin resistance, with adjustments for age, race, education, study site, and dietary consumption of ω-3 fatty acids. These analyses showed that ω-3 fatty acid consumption was not related to HOMA-IR (P = 0.42) or risk of diabetes (P = 0.65) in our population, and including this factor as a covariate did not affect the observed relationships between depression and either outcome. Nonetheless, dietary interventions may be useful for reducing depression or insulin resistance. Our data do not address that issue.
