Vitamin E
Two large longitudinal studies in the United States examined the association between "tamin E intake and risk of CHD. In a group of 39, 910 male health professionals, those who took vitamin E supplements in doses of at least lOOIU per day for over 2 yr had a 37% lower ::elative risk of CHD compared to men who did not take vitamin E supplements, after TIijustment for age, coronary risk factors, and intake of vitamin C and B-carotene. In the -,urses' Health Study of 87,245 female nurses, women who took vitamin E supplements for more than 2 yr had a 41 % lower relative risk of major coronary disease. This effect persisted after adjustment for age, smoking, obesity, exercise, blood pressure, plasma cholesterol, and e of postmenopausal estrogen replacement, aspirin, vitamin C, and p-carotene.
It must be noted that this effect was limited to vitamin E supplement use.
High vitamin E intakes from dietary sources were not associated with a significant decrease in risk, although even the highest dietary vitamin E intakes were far lower than intakes among supplement users. Support from case-control studies based on biological samples is sparse, although Gey and coworkers found that plasma levels of vitamin E in men aged 40 49 yr correlated strongly and inversely with the age-specific mortality from CHD in 16 European regions. A population case-control study also evaluated the relation between undiagnosed angina pectoris and plasma antioxidant levels in men aged 35 - 54 yr. Plasma levels of vitamin C, vitamin E, and carotene manifested a significant inverse correlation with undiagnosed angina.
The inverse association between vitamin E levels and angina remained signifi-cant after adjustment for smoking habits, age, blood pressure, relative weight, and blood lipid levels. However, these results have been offset by several negative studies. There was no association between plasma vitamin E and prevalence of CHD in a cross-sectional survey of 1132 Finnish men. Similarly, most nested case-control studies found no relationship between plasma vitamin E levels and subsequent coronary mortality or risk of MI. The reason for these disparate results is unknown, but may include changes in diet following disease diagnosis, poor classification of controls, and lack of variation in plasma levels within populations not using supplements.
