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Vitamin E and atherosclerosis
1Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.
Insights
Vitamin E may protect against heart disease by preventing LDL oxidation and inflammation. This review integrates current knowledge on atherosclerosis and vitamin E
Area of Science:
- Cardiovascular Science
- Nutritional Science
- Biochemistry
Background:
- Atherosclerosis is a chronic inflammatory disease driven by endothelial injury and LDL oxidation.
- Oxidized LDL triggers inflammatory responses, leading to plaque formation and lumen narrowing.
- Vitamin E's role in preventing heart disease has been debated but is gaining support.
Purpose of the Study:
- To review the biological functions of vitamin E in the context of atherogenesis.
- To integrate current knowledge on atherosclerosis with vitamin E's protective mechanisms.
- To provide evidence supporting vitamin E's efficacy in preventing heart disease.
Main Methods:
- Review of existing epidemiologic studies and clinical trials.
- Integration of current knowledge on atherogenesis and vitamin E's biological functions.
- Analysis of vitamin E's effects on LDL oxidation, inflammation, and vascular cell functions.
Main Results:
- Vitamin E retards LDL oxidation and inhibits smooth muscle cell proliferation.
- It inhibits platelet aggregation and the expression of adhesion molecules.
- Vitamin E potentiates prostacyclin release and attenuates leukotriene synthesis.
Conclusions:
- Vitamin E demonstrates protective effects against atherosclerosis development.
- Its biological functions align with mechanisms that prevent cardiovascular disease.
- Evidence supports vitamin E as a potential therapeutic agent for heart disease.
Abstract:
Vitamin E was advocated as an effective treatment for heart disease by Dr. Even Shute of London, Ontario more than 50 years ago. His pioneering claims, which were unacceptable to the medical community at large, have been confirmed by recent findings from epidemiologic studies and clinical trials. This review integrates our current knowledge of atherogenesis with the biological functions of vitamin E. The response-to-injury hypothesis explains atherosclerosis as a chronic inflammatory response to injury of the endothelium, which leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components. Inflammatory and other stimuli trigger an overproduction of free radicals, which promote peroxidation of lipids in LDL trapped in the subendothelial space. Products of LDL oxidation are bioactive, and they induce endothelial expression and secretion of cytokines, growth factors and several cell surface adhesion molecules. The last-mentioned are capable of recruiting circulating monocytes and T lymphocytes into the intima where monocytes are differentiated into macrophages, the precursor of foam cells. In response to the growth factors and cytokines, smooth muscle cells proliferate in the intima, resulting in the narrowing of the lumen. Oxidized LDL can also inhibit endothelial production of prostacyclin and nitric oxide, two potent autacoids that are vasodilators and inhibitors of platelet aggregation. Evidence is presented that vitamin E is protective against the development of atherosclerosis. Vitamin E enrichment has been shown to retard LDL oxidation, inhibit the proliferation of smooth muscle cells, inhibit platelet adhesion and aggregation, inhibit the expression and function of adhesion molecules, attenuate the synthesis of leukotrienes and potentiate the release of prostacyclin through up-regulating the expression of cytosolic phospholipase A2 and cyclooxygenase. Collectively, these biological functions of vitamin E may account for its protection against the development of atherosclerosis.