ABSTRACT
At the time of writing this abstract, a total of >400 articles on the topic “selenium AND diabetes” were published and available via PubMed, including 86 reviews. When studying this literature, a major bottom line emerges claiming that high Se intake causes type 2 diabetes mellitus (Rayman & Stranges, 2013; Rocourt & Cheng, 2013). This conclusion is mainly based on US American Association Studies, which by definition do not provide causal links. The most recent respective cross-sectional analysis reports that serum Se concentrations are on average higher in diabetic participants compared to non-diabetic participants by 7.3 μg/L (Laclaustra et al., 2009). Interestingly, the average serum Se concentrations of these subjects were around 140 μg/l, and thus outside the range in which the expression of selenoproteins are affected by Se intake (Combs et al., 2011). It is thus more than doubtful that the reported diabetes rates are related to selenoproteins. Moreover, these findings are of marginal importance for the majority of humans have Se concentrations below 100 μg/L. Well-controlled Se supplementation trials were conducted in the US to study causal relations. Analysis of the NPC data 7.7 years after initiation of the study (where by an extra 200 μg Se per day was provided to the participants for an average of 4.5 years) indicated that among the women participating, there were 9 new cases of self-reported diabetes in the Se group and 8 respective cases in the control group, i.e., no difference (Stranges et al., 2007). Similarly, the SELECT study did not observe a statistically increased risk for diabetes upon Se supplementation (Lippman et al., 2009). Despite these inconclusive data, a common fear of diabetes induction has spread even in populations in which a selenium supplement would reduce a number of health risks thereby hindering a meaningful supplementation of selenium-poor subjects.
