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Abstract
Epidemiological and experimental studies suggest that antioxidants like vitamin E (α-tocopherol) may play an important role in prevention of chronic disease. Several observational surveys have linked populations with a large intake of vitamin E with reduced incidence of heart disease. These observations have been strengthened by the demonstration of strong antioxidant activity by vitamin E in cellular, molecular and animal experiments. These results have highlighted a potential role for vitamin E supplementation in the prevention of chronic disease in humans. Interestingly however, large-scale clinical trials of vitamin E and other antioxidants in preventing specific disease processes (e.g., coronary artery disease) have generated conflicting and mixed outcomes. In this review, the role of vitamin E in the prevention of atherosclerosis and carcinogenesis has been carefully examined with particular emphasis on salient human studies (clinical trials) and their limitations. In addition, pertinent biochemical, physiological and metabolic features of vitamin E have also been incorporated. A list of common natural food sources of vitamin E has been provided. Important in vitro and animal studies related to the antiatherosclerotic and anticarcinogenic actions of vitamin E have been discussed in detail. Finally, the direction of future investigations in primary and secondary prevention of chronic diseases by vitamin E supplementation has been outlined.
Key teaching points:
• Vitamin E is a fat soluble vitamin which is absorbed from the human small intestine (enterocyte) after solubilization in bile salt micelles.
• In human diets, γ-tocopherol is the principal form of vitamin E, while α-tocopherol is the primary form in vitamin E supplements. α-tocopherol helps protect cell membranes from the lipid peroxidation by trapping peroxyl radicals and is regenerated by an electron donor like vitamin C.
• Vitamin E is available in abundance in common nuts and seeds such as almonds, peanuts, sunflower seeds, filbert and vegetable oils. Currently, the RDA of vitamin E for an average size person is 15 mg α-tocopherol per day.
• Vitamin E is transported in plasma with lipoproteins in the plasma (i.e., HDL and LDL) and protects against free radical peroxidation of the carrier protein.
• Protective action of vitamin E against atherosclerosis (i.e., coronary and coratid artery disease) is most likely related to its preventive action against lipid peroxidation. The ability of vitamin E to induce apoptosis in tumor cells and modulate oncogenes may be essential for its anticarcinogenic effect.
• While a large body of cellular, animal and epidemiological studies has demonstrated effectiveness of vitamin E in reducing the progression of atherosclerosis and reducing frequency of certain cancers, the results of large scale clinical trials with vitamin E have failed to show its beneficial effect in a consistent manner.
• Long term (>5 years) longitudinal studies are needed in patients with well defined coronary and carotid artery disease with precise endpoints in response to an optimal dose of vitamin E supplement either alone or in combination with other antioxidants to establish its clinical efficacy in prevention of atherosclerosis.
Key teaching points:
• Vitamin E is a fat soluble vitamin which is absorbed from the human small intestine (enterocyte) after solubilization in bile salt micelles.
• In human diets, γ-tocopherol is the principal form of vitamin E, while α-tocopherol is the primary form in vitamin E supplements. α-tocopherol helps protect cell membranes from the lipid peroxidation by trapping peroxyl radicals and is regenerated by an electron donor like vitamin C.
• Vitamin E is available in abundance in common nuts and seeds such as almonds, peanuts, sunflower seeds, filbert and vegetable oils. Currently, the RDA of vitamin E for an average size person is 15 mg α-tocopherol per day.
• Vitamin E is transported in plasma with lipoproteins in the plasma (i.e., HDL and LDL) and protects against free radical peroxidation of the carrier protein.
• Protective action of vitamin E against atherosclerosis (i.e., coronary and coratid artery disease) is most likely related to its preventive action against lipid peroxidation. The ability of vitamin E to induce apoptosis in tumor cells and modulate oncogenes may be essential for its anticarcinogenic effect.
• While a large body of cellular, animal and epidemiological studies has demonstrated effectiveness of vitamin E in reducing the progression of atherosclerosis and reducing frequency of certain cancers, the results of large scale clinical trials with vitamin E have failed to show its beneficial effect in a consistent manner.
• Long term (>5 years) longitudinal studies are needed in patients with well defined coronary and carotid artery disease with precise endpoints in response to an optimal dose of vitamin E supplement either alone or in combination with other antioxidants to establish its clinical efficacy in prevention of atherosclerosis.
The authors would like to acknowledge the contributions of Dr. Jeffery Blumberg, Professor, School of Nutrition Sciences and Policy, Jean Meyer USDA-HNRC on Aging, Tufts University, Boston, Massachusetts. Dr. Blumberg was instrumental in enhancing the quality of this manuscript by his critical suggestions and constructive comments. Moreover, he helped us identify specific areas relevant for future investigations in this field. His encouragement to complete this project is most appreciated.