Copyright 2001 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2001
To the Editor: Dr Meagher and colleagues1 found that vitamin E supplementation had no effect on measures of lipid peroxidation in healthy individuals, and thus questioned the rationale for this intervention. However, Stephens et al,2 whom they cite, comment, "We believe that the inhibition of oxidation is likely to exert its main effects by modification of plaque enlargement or rupture" and also that "the extent of the risk reduction suggests that the benefit [of vitamin E] may be due to more than one mechanism, such as the alpha-tocopherol mediated reductions in platelet adhesion and aggregation. . . ."3 The end points suggested by Stephens et al2 are difficult to measure in healthy individuals as they would require a safe and reliable method for assessing plaque sizes. Plaque rupture can occur in the aorta without producing symptoms; it is only when plaque rupture occurs in critical arteries, such as the epicardial coronary arteries, that clinical events may occur. There may be an inverse correlation between dietary vitamin E intake and rates of coronary vascular disease.4
Richardson PD. Vitamin E Supplementation in Healthy Persons. JAMA. 2001;285(19):2449–2450. doi:10.1001/jama.285.19.2449
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