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The oxidation of LDL by oxygen free radicals results in the unregulated uptake of modified LDL by macrophages in arterial walls, accelerating the atherosclerotic process. Antioxidant nutrients, which can directly scavenge free radicals, include alpha-tocopherol (vitamin E isomer) and ascorbic acid (vitamin C), which have shown antioxidant activity both in vitro and in vivo, as well as beta-carotene (a provitamin A carotenoid) which has displayed anti-oxidant activity in vitro5 These mechanisms suggested that increased dietary intake or supplementation of these nutrients would be protective against atheroslerotic vascular disorders. This was supported by evidence from observational studies for vitamin E and beta-carotene, but results of clinical trials employing supplements have been disappointing.

Observational cohort data suggest a protective role for carotenoids. In a meta-analysis, the pooled relative risk reduction for cardiovascular death in those who ate diets rich in beta-carotene was 31% (95% CI 41-20), when dietary and blood carotene levels were measured to compare high and low consumers. The randomized trials, in contrast, reported a moderate adverse effect of beta-carotene supplementation, with a relative increase in the risk of cardiovascular death of 12% in a meta-analysis of four trials.53 Cancer risk was also increased.

Several large cohort studies showed significant reductions in the incidence of cardiac events in men and women taking high-dose vitamin E supplements.52 However, the HOPE trial, a definitive clinical trial relating vitamin E supplementation to cardiovascular outcomes, revealed no effect of vitamin E supplementation (at 400 IU/day, for a mean follow up of 4-5 years) on MI, stroke or death from cardiovascular causes in men or women.54 Other trials also failed to demonstrate a cardioprotective effect of vitamin E supplements.55

The conflict between diet-based observational studies and clinical trials employing supplements may arise because of one or more explanatory factors: confounding, interactions/ synergistic activity (among antioxidants - with other nutrients), isomers with differing activity in food compared to supplements, other associated protective elements in natural foods (for example, flavonoids, phytoestrogens) and/or temporal dissociation of antioxidant blood levels from fat intake in meals when administered as once a day pills. While the failure of pill supplementation does not necessarily exclude protective effects of dietary antioxidants, current evidence does not support supplementation of any of these antioxidant vitamins for prevention of CHD. However, intake of their primary food resources, especially fruit and vegetables, may be encouraged.

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