Antioxidant Consumption and Risk of Coronary Heart Disease: Emphasis on Vitamin C, Vitamin E, and β-Carotene
- 2 February 1999
- journal article
- review article
- Published by Wolters Kluwer Health in Circulation
- Vol. 99 (4) , 591-595
- https://doi.org/10.1161/01.cir.99.4.591
Abstract
Dietary recommendations aimed at reducing the risk of coronary heart disease have focused largely on the intake of nutrients that affect established risk factors, including plasma lipid and lipoprotein levels, blood pressure, and body weight. Recent developments in our understanding of the atherosclerotic process and factors that trigger ischemic events have led to the consideration of dietary constituents that may alter risk through other mechanisms. Prominent among these are antioxidants, which are proposed to inhibit multiple proatherogenic and prothrombotic oxidative events in the artery wall. This report provides a brief overview of evidence concerning a role for dietary antioxidants in disease prevention, with emphasis on studies in human populations, and describes a number of issues that should be resolved before it would be prudent to make recommendations regarding the prophylactic use of antioxidant supplements. Atherosclerosis is a complex process involving the deposition of plasma lipoproteins and the proliferation of cellular elements in the artery wall. This chronic condition advances through a series of stages beginning with fatty streak lesions composed largely of lipid-engorged macrophage foam cells and ultimately progressing to complex plaques consisting of a core of lipid and necrotic cell debris covered by a fibrous cap.1 These plaques provide a barrier to arterial blood flow and may precipitate clinical events, particularly under conditions that favor plaque rupture and thrombus formation. Over the past 2 decades, considerable evidence has been gathered in support of the hypothesis that free-radical–mediated oxidative processes and specific products arising therefrom play a key role in atherogenesis.2 3 At the center of this hypothesis are low-density lipoproteins (LDLs), which undergo multiple changes on oxidation that are thought to be proatherogenic (see Figure⇓). Oxidation of LDL lipids leads to the production of a diverse array of biologically active compounds, including some that influence the …Keywords
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