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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #144132
Title: VITAMIN E AND PREVENTION OF HEART DISEASE IN HIGH-RISK PATIENTS

Author
item MEYDANI, MOHSEN - HNRCA

Submitted to: Nutrition Reviews
Publication Type: Review Article
Publication Acceptance Date: 1/1/2000
Publication Date: 9/1/2000
Citation: Meydani, M. 2000. Vitamin e and prevention of heart disease in high-risk patients. Nutrition Reviews. 58(9):278-81.

Interpretive Summary:

Technical Abstract: Over the past two decades, the health benefits of vitamin E have been examined in numerous studies, many of which have demonstrated a clear reduction in the relative risk of cardiovascular disease (CVD) with vitamin E. The LDL oxidation hypothesis has been the main reason to stimulate investigation of vitamin E and other antioxidants for prevention of CVD. The LDL oxidation hypothesis is a generally accepted hypothesis for the development of atherosclerosis, an age-related process and a major cause of morbidity and mortality from CVD in Western countries. Oxidation of LDL particles in the arterial wall may initiate a complex cascade of events that lead to the development of fatty streaks, atherosclerotic plaques, and eventually stenosis of the arteries or rupture of plaque and heart attack. LDL particles contain polyunsaturated fatty acids (PUFA), which are susceptible to oxidation. Vitamin E, mainly alpha-tocopherol, is the major fat-soluble antioxidant present in the LDL particle. On average, between 5 and 9 vitamin E molecules are carried by each LDL particle and protect LDL from oxidative damage. In vivo, free radicals generated by endothelial cells of the arterial wall are believed to oxidize LDL particles, making them chemotactic to attract monocytes, and being recognized by scavenger receptors, and taken up by macrophages, forming lipid laden foam cells in the fatty streaks lesions. In vitro studies have indicated that increasing the vitamin E content of LDL particles by increasing vitamin E intake increases LDL resistance to oxidation and decreases its uptake by macrophages. Therefore, it is believed that vitamin E¿s protection of LDL from oxidation in vitro might be a plausible mechanism for the in vivo effect of vitamin E in reducing risk of CVD as reported in several observational studies.