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Supplement

Does Vitamin E Decrease Heart Attack Risk? Summary and Implications with Respect to Dietary Recommendations¹

Department of Nutrition and Food Management, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331-6512 and Division of Critical Care and Pulmonary Medicine, Department of Internal Medicine, University of California, Davis, School of Medicine, Sacramento, CA 95817

The hypothesis that oxidative stress has a role in atherosclerosis rests on a large body of experimental work carried out in animal models of heart disease. The situation is more complex in humans, in that the results from vitamin E supplementation trials have been conflicting. Nonetheless, there is emerging information that -tocopherol may play a critical role in maintaining the function of key cellular components in the atherosclerotic process through its ability to inhibit the activity of protein kinase C, a key player in many signal transduction pathways. -Tocopherol modulates pathways of platelet aggregation, endothelial cell nitric oxide production, monocyte/macrophage superoxide production and smooth muscle cell proliferation. Regulation of adhesion molecule expression and inflammatory cell cytokine production by -tocopherol has also been reported. More studies are required to relate -tocopherol intakes to optimal tissue responses in humans.

KEY WORDS: • -tocopherol • atherosclerosis • cytokine • adhesion molecule • platelet aggregation • nitric oxide • superoxide