Abstract

Some, but not all, observational data concerning diet and health suggest an inverse relationship between dietary vitamin C and cardiovascular disease (CVD) morbidity and mortality.1 If such a relationship exists, vitamin C presumably protects against CVD through its antioxidant properties, possibly by preventing lipid peroxidation. Others have suggested that vitamin C might protect against CVD through effects on blood pressure (BP) and arterial stiffness.2–6 Such an effect is suggested by epidemiologic associations noted in some populations,7 but the role of this nutrient in BP regulation remains unclear, owing to design issues and/or confounding variables. For example, a recent analysis of the prospective Western Electric study2 suggests that low antioxidant intake is associated with the rise in BP with age. In that study, intake of both vitamin C and β-carotene were combined to form an “antioxidant score,” so the effect of vitamin C alone was not estimated. Even in studies that isolate vitamin C intake, results are inconclusive: not all studies demonstrate an inverse relationship between vitamin C and BP; key nutrients (eg, sodium) are not accurately measured by most diet survey methods; and more importantly, these observational studies are potentially confounded by intake of other nutrients that affect BP. For example, in the Western Electric study, the investigators did not adjust for intake of potassium, a nutrient with well-known BP-lowering effects,9 which is found in many antioxidant-rich foods. Thus, although a relationship between vitamin C intake and BP is suggested, the epidemiologic data are inconclusive. Randomized controlled trials offer many advantages over prospective observational studies, including minimizing the effects of other confounding variables. Despite these advantages, a total of 7 previous trials examining BP effects of vitamin C have been inconclusive. Two of 4 randomized trials reviewed by Ness et al8 suggest no effect. …

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