Health Impacts Of Vitamin E

It is generally accepted that oxidative damage at the cellular level is significant to the onset of chronic disease. Since vitamin E is the primary fat-soluble antioxidant in mammalian systems, a logical assumption is that supplementation of the human diet with vitamin E potentially could be significant in prevention and/or slowing of the onset of various chronic disease states. This assumption taken together with increasing knowledge about the role vitamin E plays and potential roles other antioxidants available in the food supply might play produced an extremely large body of scientific literature on antioxidants and health. Unfortunately, the body of data does not provide for a clear conclusion on vitamin E and its overall worth when consumed at levels above the recommended dietary allowance (RDA). Diverse opinions about supplemental use of vitamin E remain. The fact remains that the Panel on Dietary Antioxidants and Related Compounds (1), when establishing the DRIs for vitamin E in 2000, concluded that clinical scientific evidence does not support supplemental usage of vitamin E. The literature appearing in nutrition and medical journals evaluating the impact of vitamin E supplementation in various diseases is, indeed, staggering in its quality and amount. In this section, some current views and experimental evidence on the value to human health of vitamin E at supplemental intake levels is presented.

2.3.1. Vitamin E and Aging

Aging is a normal process characterized by morphological and functional changes, most of which are degenerative, that occur as a living system grows older. The role of free radicals in the aging process and the ability of vitamin E to delay the overall process have been topics of intense investigation for decades. Harman, in a series of papers that began in 1956, presented and discussed the free radical theory on aging (62-68). This theory is based on the premise that aging is due to the accumulation of deteriorative changes resulting from free radical reactions at the cellular level that occur throughout the lifespan. Harman suggested that the functional life span could be increased by minimizing free radical events by keeping body weight low, by ingesting diets adequate in nutrients but containing minimal amounts of constituents that enhance free radical damage (copper, polyunsaturated fatty acids, etc.), and maintaining a diet high in antioxidants, including vitamin E (67).

Many theories on aging have been advanced and debated, and the free radical theory of aging continues to be prominent in such debates. Packer and Landvik (69) in 1989 stated, "Research has shown that free radical damage accumulates during the aging process, and evidence is increasing that lipid peroxidation may be an important factor in making aging the long and healthy process that it should be. Animal and human studies have demonstrated protective effects of vitamin E and other antioxidants on free radical reactions and peroxidative changes in the aging process." Likewise, Pryor (70) emphasized the potential of vitamin E and the need for continuing research with the following conclusion: "Although the current literature (up to 1989) gives good hope for a beneficial effect for vitamin E on the variety of pathologies, the data are not yet complete." Taking into account the conclusion of the DRI committee not to recommend supplementation, we are still at the stage of searching for scientific documentation that unequivocally proves the long-term benefits of increased intake of vitamin E. A general consensus is that a balanced diet, providing a goodly amount of many different antioxidants, is desirable for optimal health and, possibly, provides for increased longevity with increased maintenance of good functionality. However, the direct benefits of supplemental vitamin E to fighting specific disease states, as discussed in the following sections, are not clear and, in many instances, evidence of benefit seems to be less conclusive.

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