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Copyright: © 2012 Zingg JM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. A possible preventive effect of supplementation with vitamin E (α-tocopherol) against atherosclerosis and other diseases such as cancer and neurodegeneration has been addressed in many studies (reviewed in [1-3]). Whereas in most animal studies vitamin E supplementation reduces cardiovascular disease (CVD), human randomized clinical trials and epidemiologic studies have reported both positive and negative outcomes (reviewed in [2]). Meta-analyses of the clinical studies even suggested an increased all-cause mortality with high doses of vitamin E supplementation [4,5], although other more recent studies did not confirm this [6,7]. Similar to that, a significant increase in prostate cancer risk was observed in the recent follow-up study of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) [8], whereas a preventive effect of vitamin E was observed in a study on nonalcoholic steatohepatitis (NASH) in adults without diabetes [9]. Intriguingly, based on the molecular properties of vitamin E as free radical scavenger, some of these results were not expected, suggesting that the current molecular models of vitamin E action may need to be revised.

Vitamin E and Disease Risk: Research Focus Turns on Genetic Polymorphisms and Molecular Mechanisms