Vitamin E functions as a powerful antioxidant to protect human cells and fatty tissues from free radical damage. Free radicals are extremely dangerous and reactive oxygen compounds that are constantly being produced from a variety of natural sources such as radiation, air pollution, and the breakdown of proteins in the body. Left unchecked, free radicals course throughout the body, rupturing cell membranes, causing massive damage to skin and connective tissues, and damage cellular DNA which gives rise to various cancers and degenerative diseases. Free radical damage also accumulates in the brain, leading to age-related memory impairment.
Vitamin E, in combination with other antioxidants, works to quench free radicals and prevent oxidation of polyunsaturated fatty acids that make up cell membranes. By neutralizing free radicals and stabilizing fatty cell membranes, vitamin E helps to prevent cancer, arthritis, immune disorders such as lupus, and premature aging. Working with vitamin A and beta carotene, vitamin E protects the lungs from air pollution. Vitamin E also protects the cells lining blood vessels walls from free radical damage, thus preventing atherosclerosis and cardiovascular disease. By protecting red blood cells from damage, vitamin E also prevents a special form of anemia called hemolytic anemia.
Vitamin E also plays an important role in the production of prostaglandins, vital hormone-like substances that regulate blood pressure, reproduction, and muscle contractions. By acting as a antithrombin agent vitamin E can help prevent heart attacks by controlling the formation of potentially fatal blood clots. Vitamin E is also used in the treatment of fibrocystic breasts and premenstrual syndrome, promotes healing while reducing scarring, and prevents the formation of cataracts in the eyes. Recently, researchers reported that men taking vitamin E supplements experience 34% few cases of prostate cancer, and 16% fewer cases of colorectal cancer.
A deficiency of Vitamin E can cause hemolytic anemia in infants, wherein red blood cells are destroyed. Adults rarely experience symptoms of vitamin E deficiency unless afflicted with fat malabsorption syndromes such as cystic fibrosis, sprue and celiac disease. Symptoms are easily treated with alleviated with vitamin E supplementation.
The male sex gland, the testis, is responsible for the production of sperm and the secretion of testosterone. Testosterone, the hormone responsible for sexual desire, is dependent on vitamin E to produce sperm and to provide strong masculine features. The female sex glands, the ovaries, produce estrogen and progesterone. For these hormones to function properly, they require adequate amounts of both vitamin E and niacin. Two recent studies of vitamin E and its ability to significantly reduce the risk of heart failure clearly show that, at higher levels than can be obtained from vitamin-rich foods, vitamin E supplementation was found to reduce the risk of coronary heart disease by as much as 33% to 50%. The impact of the antioxidant vitamin E on women and men was examined in a pair of studies presented at the annual scientific meeting of the American Heart Association in New Orleans.1
Over 87,000 female nurses between the ages of 34 and 59, who were free of coronary heart disease when the study began in 1980, were followed for 8 years. Of the 17% who took vitamin E supplements at the rate of 100 international units (IU) per day, clear benefit accrued in proportion to how long the regimen continued. In assessing the risks, those who took vitamin E for less than 2 years had a 36% reduction in coronary heart disease, and those who took it for more than 2 years had nearly a 50% reduction in cardiovascular disease.
In the study involving male healthcare workers (more than 45,000 were followed from a disease-free baseline established in 1986), vitamin E supplementation in excess of 100 IU for more than 2 years resulted in a 26% reduction in CHD. Meir Stampfer, MD, an investigator in both studies, was amazed by the results, even though he knew that there was a sound scientific basis for the antioxidant hypothesis. This mechanism holds that the "bad" LDL cholesterol is oxidized when not protected, which makes it rancid and thus susceptible to promoting the buildup of fatty lesions on the walls of arteries. Called atherosclerosis, this accumulation is responsible for diminished blood flow and, if allowed to continue, eventual heart attack. Vitamin E is thought to help prevent the oxidation that initiates this disease. 1. Weeks J Lewis Hl.. New studies suggest vitamin E reduces heart disease risk in men and women (abstracts 1847 1848).Amercan Heart Association News Release. November 17, 1992.
Recent studies suggest that as an active blood lipid antioxidant, vitamin E can go a long way toward reducing the risk of atherosclerosis. Atherosclerotic plaque, which congests arteries and contributes to heart attacks and strokes, is thought to be caused by LDL cholesterol altered through the process of free-radical auto-oxidation. The immune system's macrophages gobble up the oxidized LDLs and expand to form unrecognizable "foam" cells which adhere to artery walls and initiate atherosclerotic plaque. One recent study conducted at the University of Texas demonstrated considerably reduced oxidative damage (over 50%) in the blood of men given 800 IU of vitamin E per day for 12 weeks. 1
An Austrian study of shorter duration found a similar effect when levels of vitamin E up to 1,200 IU were given.2 Additionally, the same study showed that the total level of antioxidants, rather than vitamin E alone, had a higher correspondence with the inhibitory effects. Other studies since published have continued to establish the free-radical auto-oxidation of LDL and heart-disease relationship.3,4
1. Jialal 1, Crundy SM. Effect of dietary supplementation with alpha-tocopherol on the oxidative modification of low density lipoprotein. J Lipid Res. 1992;33:899-906.
2. Dieber-Rotheneder M, Puhl H, Waeg G, Striegl G, Esterbauer H. Effect of oral supplementation with D-alpha-tocopherol on the vitamin E content of human low density lipoproteins and resistance to oxidation. J Lipid Res. 1991;32:1325-1332.
3. Steinberg D. Antioxidants in the prevention of human atherosclerosis. Summary of the proceedings of a National Heart, Lung, and Blood Institute Workshop: September 5-6, 1991, Bethesda, Maryland. Circulation. 1992;85:2337-2344
4. Regnstrom J, Nilsson J, Tornvall P, Landou C, Hamsten A. Susceptibility to low-density lipoprotein oxidation and coronary atherosclerosis in man. Lancet. 1992;339:1183-1186.)
It had been thought that several host defense responses and metabolic reactions that occur during infection also occur after exercise. These reactions, known as the "acute phase response," contribute to the breakdown and clearance of damaged tissue after exercise. When the subjects were monitored and examined for 12 days, the deleterious effects of exercise related changes were reduced in those taking vitamin E and the age-related differences were eliminated by increasing the response mechanisms of the older group.
(1. Cannon JG, Orencole S et al. ATn J Physiol Dec 1990, 259 (6 Pt 2),pR1214-9.
2. Cannon JG, Meydani SN, et a!. Am J Physl Jun 1991, i60 (6 Pt 2), pR1235-40)
The Daily Recommended Intake for vitamin E is 30 iu or international units, though commonly, daily doses range from 200 to 1200 iu.
Foods high in vitamin E include wheat germ, whole grains, cold-pressed vegetable oils, nuts and seeds, dark green leafy vegetables, eggs, sweet potatoes, brussels sprouts and whole wheat. Vitamin E supplements are available in both dry form and oil capsules. Vitamin E is also available in the natural or D-alpha-tocopherol form, and as a synthetic or DL-alpha-tocopherol form.
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