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B. Greg Brown, MD, PhD; John Crowley, PhD

JAMA. 2005;293:1387-1390.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

During the past 15 years, epidemiological,^1-2 basic biological,^3-5 and experimental studies on atherosclerosis have supported the hypothesis that antioxidants protect against atherosclerosis^6-8 by limiting low-density lipoprotein oxidation in the arterial wall. This mechanism inhibits the pathological accumulation of cholesteryl ester in plaque via the macrophage scavenger receptor, a process that can cause plaque rupture and cardiovascular events.^9-10 Similarly, biological mechanisms have been identified in carcinogenesis that may be blocked by antioxidants.^11-14 In the past decade, a number of prospective, randomized, placebo-controlled, 3- to 6-year clinical trials have been published, testing the effect of vitamin E and other antioxidant vitamins or their combinations on clinical manifestations of cardiovascular disease and cancer.^15-21 These trials have surprisingly yet consistently shown that commonly used antioxidant vitamin regimens (vitamins E, C, beta carotene, or a combination) do not significantly reduce overall cardiovascular events or cancer.

Why not? . . . [Full Text of this Article]

Author Affiliations: Department of Medicine, Cardiology Division, University of Washington School of Medicine, Seattle (Dr Brown); Department of Cancer Research and Biostatistics, Fred Hutchinson Cancer Research Center; and Department of Biostatistics, University of Washington School of Public Health and Community Medicine, Seattle (Dr Crowley).

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