ABSTRACT
Because antioxidants can delay or prevent LDL oxidation, it was suggested that diets low in antioxidant vitamins C and or E might predispose to CHD [reviewed in (9,10)]. Observational epidemiologic studies from both sides of the Atlantic support this view. For instance, in the Nurses’ Health Study and the Health Professionals Study, subjects who regularly consumed large amounts of vitamin E (> 300 IU/d) developed less CHD (11,12). Although these studies did not support a similar, independent benefit of dietary vitamin C, another study from the United States did (13). A similar study from Finland demonstrated an increased risk of CHD in men with plasma levels suggestive of vitamin C deficiency (14). A recent case-control study showed that the risk of a first heart attack was not increased in Edinburgh men with similarly low levels of vitamin C (15). The most consistent support comes from studies in which plasma or adipose levels of β-carotene were measured (16-18). High levels of this antioxidant are associated with a decreased risk of CHD, particularly in smokers. Low plasma vitamin E levels were associated with an increased risk of angina and myocardial infarction in Edinburgh men (18), but not in Finland or other European countries (16-17). All of these observational studies could suffer from confounding by lifestyle or social class (19,20). Large intervention studies, which do not have this weakness, do not support the view that antioxidant vitamin supplements are effective in primary or secondary prevention of CHD (4,17,21-23).
