Observational Epidemiology

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While molecular mechanisms exist to explain potential benefits of antioxidants, clinical outcomes are needed to evaluate the benefit in humans. Observational studies can use information about diet and vitamin intake to identify potential protective effects of antioxidants. Results from cross-sectional, case-control, and cohort studies suggest that antioxidant consumption reduces the risk of developing heart disease and stroke19 with the strongest data in favor of vitamin E.20

Several large cohort studies have evaluated the relationship between vitamin E intake and incidence of CHD. The largest of these is the Nurses' Health Study (NHS), a cohort study of more than 87,000 U.S. female nurses aged 34-59 years with no history of CVD.21 Dietary antioxidant intake and use of antioxidant vitamin supplements were ascertained through a semiquantitative food frequency questionnaire administered at baseline in 1980 with information on antioxidant supplements updated biennially. After 8 years, women in the highest quintile of vitamin E intake had a 34% lower risk of CHD (nonfatal MI and fatal CHD) compared with those in the lowest quintile (P for trend < 0.001). It was vitamin E supplementation - not dietary intake - that was associated with lower risk. Participants who took at least 100 IU of vitamin E supplements per day for more than 2 years experienced reductions of 40% or more in the risk of CHD, alter adjustment for age and cardiac risk factors.

These results were consistent with the Health Professionals Follow-up Study (HPFS), an observational study of nearly 40,000 US male health professionals aged 40-75 years who did not have CHD, diabetes, or hypercholesterolemia.22 After adjustment for cardiac risk factors, the relative risk (RR) of CHD for those in the highest vs. lowest quintile of vitamin E intake was 0.60 (95% confidence interval (CI) 0.44-0.81; P for trend = 0.01). Further analysis revealed that the protective association was strongest for vitamin E consumed in supplements. Men who took at least 100 IU per day for at least 2 years had a multivariate RR of 0.63 (95% CI, 0.47-0.84) for CHD compared with men who did not take vitamin E supplements. A weak association was found for dietary vitamin E intake alone; among men who did not take vitamin supplements, the RR comparing the extreme quartiles was 0.79 (95% CI, 0.54-1.15, P for trend = 0.11).

The Iowa Women's Health Study evaluated the association between antioxidant vitamin intake and CHD mortality over 7 years among 34,486 postmenopausal women with no history of CVD.23 In contrast to the NHS and HPFS findings, vitamin E intake from food but not from supplements was strongly associated with a lower risk of CHD mortality. Women in the highest quintile of dietary vitamin E intake, without any supplementation, had a RR of 0.38 compared with those in the lowest quintile (P for trend = 0.004). Controlling for other dietary factors associated with vitamin E intake, such as intake of linoleic acid, folate, and fiber did not affect the results. Similarly, a Finnish study also found a significant inverse association between dietary intake of vitamin E and CHD mortality among 2,385 women 30-69 years of age over a 14-year period.23

The relationship between vitamin E and CVD has also been examined in two elderly cohorts. The Established Populations for Epidemiologic Studies of the Elderly program, a 10-year study of 11,178 U.S. men and women aged 67-105 years, found a decreased risk of CHD mortality (RR = 0.53; 95% CI, 0.34-0.84) and overall mortality (RR = 0.66; 95% CI, 0.53-0.83) among those taking vitamin E supplements.24 However, no association between dietary vitamin E intake (using the semiquantitative food frequency questionnaire) and MI was observed in the Rotterdam Study which followed 4,802 Dutch men and women aged 55-95 years with no history of MI over 4 years.25

In contrast to studies of vitamin E intake, studies of vitamin E blood levels, conducted as nested case-control studies within large cohorts, have generally yielded null results. For example, a study of 734 men in the Multiple Risk Factor Intervention Trial found no association between serum vitamin E levels and risk of nonfatal MI or CHD death over a 20-year follow-up period.26

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