An update: vitamin E supplementation and heart disease

Abstract

In vitro studies and experiments in animal models provide a large and compelling body of evidence that oxidation of low-density lipoprotein (LDL) and/or related oxidative mechanisms play a critical role in the initiation and progression of atherogenesis. A corollary to the theory that reactive oxygen and nitrogen species ("free radicals") are the key molecules in this process is that antioxidants that can protect LDL from peroxidation should decrease the risk of developing atherosclerosis, attenuate its progression, or even reverse established disease. However, recently, clinical trials employing the principal lipid-soluble dietary antioxidant, vitamin E, have provided mixed results indicating either benefit, no effect, or an adverse impact on patients with cardiovascular disease (CVD). Consideration of the design and outcome of these studies together with new reports about the action of antioxidants suggests approaches for new studies as well as a basis for current advice to patients.