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Several large-scale, double-blind, placebo-controlled trials have shown convincingly that neither β-carotene1–3⇓⇓ nor vitamin E, alone3–5⇓⇓ or in combination with other antioxidant vitamins,6 reduces the risk of fatal or nonfatal infarction (or other hard clinical end points) in an unselected population of people with established coronary heart disease (CHD) or at high risk of CHD. Two end point trials, much smaller trials that used vitamin E, have reported positive results,7,8⇓ and one trial, which used ultrasound, showed that a combination of vitamins E and C slowed the progression of carotid artery lesions.9However, these are far outweighed by the negative results in the other, much larger trials. Certainly there is no basis for recommending vitamin E supplementation to patients with CHD, especially because it may blunt the effectiveness of hypolipidemic therapy with statins and niacin.6 A surprisingly large fraction of cardiologists (≈40%) have been recommending such regimens10 despite warnings that this use was premature.11At first glance, it might seem that these negative results close the book and that additional clinical trials of any antioxidants would be pointless. Closer examination, we believe, will show that such a conclusion would be premature and inappropriate.12 The hypothesis that oxidative modification of LDL plays a significant role in atherogenesis in humans is not necessarily disproved by the failure of these particular clinical trials any more than a negative trial of an ineffectual antibiotic in Pneumococcal pneumonia would prove that pneumonia is not a bacterial disease. The oxidative modification hypothesis is not that vitamin E will ameliorate the human disease but that oxidative modification of LDL and/or other oxidative events play a significant role in human atherogenesis as it does in animal models of atherogenesis. A corollary of the hypothesis is …

Is the Oxidative Modification Hypothesis Relevant to Human Atherosclerosis?