Van Woudenbergh et al. (1) report that consumption of lean but not of fatty fish was associated prospectively with a significant increase in risk of new-onset type 2 diabetes, not accounted for by differences in eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) consumption. They further report that this risk was abolished by adjustment for intakes of selenium, cholesterol, and vitamin D. In an earlier cross-sectional study from Holland, we showed that vitamin D status in a cohort of elderly men from the Zutphen subgroup of the Seven Nations Study was inversely associated with glycemia, but that vitamin D status was not accounted for by fish consumption (2).
We have more recently found, in a cross-sectional study of almost 1,000 British Bangladeshi adults eating an average of 4.4 meals containing fish (mainly imported fresh-water fish) per week, that lower levels of glycemia are predicted independently by increases in the intake of fish rich in vitamin D by multiple regression analysis (after adjustment for age, body build, sex, smoking, season, and betel chewing), whereas increases in glycemia were independently predicted by increases in overall fish consumption (standardized β coefficient = −0.17, P < 0.0001, and standardized β coefficient = 0.1, P = 0.002, respectively) (N.M. and colleagues, unpublished data). Can the authors, therefore, tell us where the 88% of vitamin D intake from sources other than oily fish came from?
Acknowledgments
No potential conflicts of interest relevant to this article were reported.
