Vitamin E is a potent antioxidant with proven anti-cancer activity that also has proven protective effects against cardiovascular disease. In its natural food state, Vitamin E is actually a family of seven different tocopherols, but the form used for most supplements and medical studies is the alpha-tocopherol form. Vitamin E was originally isolated from wheat germ oil. Its fat-soluble properties allow Vitamin E to function as a potent antioxidant in both the fat-soluble and the water-soluble parts of the cell membrane. Vitamin E helps maintain cell wall integrity and preserve energy metabolism of the cell by inhibiting lipid peroxidation of cell membranes. Vitamin E is also and immune-enhancer and protects against pollution-derived lung damage.
The anticancer activity of Vitamin E is thought to be via its antioxidant action and immune enhancement properties. Vitamin E works synergistically with other potent cellular antioxidants including selenium, Vitamin C, zinc and others. For example, Vitamin E enhances the cancer preventive effect of selenium on chemical-induced breast caccer in rats, acts with zinc as a stabilizer of cell membranes, requires selenium for adequate absorption from the gastrointestinal tract, is destroyed more readily by free radicals in the presence of copper or iron unless adequate Vitamin C is present, and is required to maintain normal levels of Vitamin A in the liver and plasma.
Vitamin E has been shown to prevent the free-radical oxidation (damage) of cholesterol, considered to be an early step in the development of coronary artery disease. Some clinical trials have found that Vitamin E supplements can reduce the risk of coronary artery disease and heart attacks while others have not. Because heart disease takes many years to develop, long-term intake of Vitamin E may play a role in its prevention.
In a study of 307 women ranging from 30 to 69 years of age, those with either low intake or low blood levels of Vitamin E were far more likely to have atherosclerotic plaques at the carotid bifurcation and, conversely, those with the highest intake or blood levels of the Vitamin E were least likely to have early signs of atherosclerosis. The women with the lowest blood levels of Vitamin E were twice as likely to have signs of early cardiovascular disease.
Vitamin E has been shown to be one of the strongest protectors against the environmental pollutants, ozone and nitric oxide. Nitrites are major sources of free radical damage to cells. Nitrites, like many chemicals, are not carcinogenic until they are converted to an active form in the body. In some cases Vitamin E can prevent the conversion of inactive forms of such cancer causing substances to active forms.
Vitamin E also prevents the action of tumor promoting and tumor initiating agents which are present in the environment and diet.
Vitamin E influences the effectiveness of many drugs currently used in cancer treatment. In vitro studies, Vitamin E acetate in combination with vincristine, 5-fluorouracil, adriamycin, or chlorozotacin produces a synergistic effect, whereas Vitamin E in combination with bleomycin, I-(2-cholrethyl)-3-cyclohexyl-1-triazeno-imidazole-4-carboxamie (DTIC), mutamycin or (cis-diamine) dichloro-platinum II (cis-platinum II) produces an additive effect in inhibiting growth of neuroblastoma cells.
In glioma cell cultures, Vitamin E acetate in combination with vincristine or CCNU produces a synergistic effect, whereas Vitamin E in combination with bleomycin, 5-fluorouracil, adriamycin, DTIC, mutamycin and cis-platinum produces an additive effect on the inhibition of growth.
These studies suggest that the effectiveness of the interaction of Vitamin E with cancer chemotherapeutic drugs depends upon tumor form and type of drug. Vitamin E also enhances the effect of some naturally occurring substances such as prostaglandins and sodium butyrate on neuroblastoma cells in vitro. The relevance of the above results in humans is not known at this time.
Vitamin E appears to protect against radiation damage and to also protect against radiation-induced cancers in vitro. Vitamin E protects cells from the toxicity of certain heavy metals, including mercury-induced brain damage. Vitamin E also protects against lung damage generated by cigarette smoke.
Vitamin E appears to protect against various cancers through several actions: Vitamin E kills tumor cells directly, enhances the effect of tumor therapeutic agents (drug, radiation and heat), reduces the toxic effect of tumor cells, and enhances normal immune functions.
Vitamin E's ability to reduce free radicals may slow aging and reduce risk of cancer risk.
Selected References
Battisti C et al. Vitamin E serum levels and gastric cancer: results from a cohort of patients in Tuscany, Italy. Cancer Lett 151(1):15-8, 2000.
Bostick RM et al. Reduced risk of colon cancer with high intake of vitamin E: the Iowa women's health study. Cancer Res 53:4230-4237, 1993.
Gunawardena K et al. Vitamin E and other antioxidants inhibit human prostate cancer cells through apoptosis. Prostate 44(4):287-95, 2000.
Horvath PM et al. Synergistic effect of vitamin E and selenium in the chemoprevention of mammary carcinogenesis in rats. Cancer Res 43:5335- 5341, 1983.
Knekt P et al. Serum vitamin E, serum selenium, and the risk of gastrointestinal cancer. Int J Cancer 42:846-850, 1988.
Meydani SN et al. Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects. Am J Clin Nutr 52:557-563, 1990.
Wald NJ et al. Serum vitamin E and subsequent risk of cancer. Br J Cancer 56:69-72, 1987.