Can Vitamin E Prevent Heart Disease?
To E or not to E?
Some of the most interesting nutrition research in recent years has produced preliminary evidence that large doses of vitamin E may reduce the occurrence of heart attacks. As a result, vitamin E has received a great deal of media attention, prompting consumers to spend $300 million a year on vitamin E supplements. A few health and nutrition experts are ready to jump on the bandwagon and recommend supplementation, but others are asking whether the evidence really warrants such a move.
Judging by sales, vitamin E is one of the most sought-after dietary supplement among Americans. The nutrient is popular, it seems, even among professionals.
And no wonder. The claims for the nutrient’s benefits are prevalent and appealing. “Health-food” literature and the media would have us believe that taking vitamin E will prevent arthritis, cataracts, stroke, diabetes, cancer, and heart disease. In addition, it’s supposed to boost the immune system, ease symptoms of premenstrual syndrome, delay symptoms of Alzheimer’s disease, and protect the body from aging.
Vitamin E Basics
Vitamin E was discovered in the 1920s when rats fed a basic diet became unable to reproduce viable offspring but were cured when given tocopherol, a substance that had been isolated from vegetable oils. In fact, the term “tocopherol” comes from Greek words meaning “to bear offspring.” Vitamin E became the name given to a group of eight fat-soluble compounds–four tocopherols (designated alpha, beta, gamma, and delta) and four tocotrienols (designated with the same Greek letters). It was not until 1966 that vitamin E was considered essential for humans.
All of these compounds have different degrees of biological activity. The most active form of the vitamin is the “d” isomer of alpha-tocopherol, which is found in many supplements. Recent research has indicated that other forms, such as gamma-tocopherol, may also be important to the body. Though gamma-tocopherol has only one-tenth the biological activity of alpha-tocopherol, it is more widely distributed in foods. It’s found in foods such as sunflower seeds, almonds, and wheat germ.
Vitamin E requires the presence of fats and bile in the gut to be absorbed. The degree to which vitamin E is absorbed by the body is dependent on the total absorption of dietary fat. Absorption can be as high as 70%. However, when taken in doses well above the Recommended Dietary Allowance (RDA), the absorption rate of vitamin E drops to less than 10%. Vitamin E travels through the body by way of chylomicrons and other lipoproteins, and it is distributed to almost all tissues in the body. It is most concentrated in tissues containing an abundance of fatty acids, such as cell membranes.
The primary function of vitamin E appears to be to act as an antioxidant. When incorporated into the lipid portion of cell membranes and carrier molecules, it protects these structures from toxic compounds, heavy metals, drugs, radiation, and free radicals. It also appears to protect cholesterol from oxidative damage.
The recommended intake for vitamin E is expressed in alpha-tocopherol equivalents ([Alpha]-TE). One [Alpha]-TE is equal to 1 mg of alpha-tocopherol. Vitamin supplement labels usually express vitamin E content in IUs (international units). One IU is equal to 1 mg of synthetic vitamin E or about 0.74 mg of natural [Alpha]-tocopherol. The current RDA for vitamin E is 10 mg for men (15 IU) and 8 mg (12 IU) for women. The RDA can be met with a tablespoon of corn oil.
Since many people medicate themselves with large amounts of vitamin E, it is fortunate that its toxicity is relatively low. However, the known toxicity of the other fat-soluble vitamins suggests that caution should be taken with long-term megadoses of vitamin E. High intakes of vitamin E can interfere with intestinal absorption of vitamins A and K. And at dosages exceeding 1,000 mg per day, vitamin E has been shown to enhance the effects of Coumadin therapy and to be antagonistic to the blood-clotting action of vitamin K.
Vitamin E and Head Disease
The oxidation of lipoproteins appears to play an important role in the development of atherosclerosis, the disease process that leads to heart attacks as well as strokes. Considerable evidence exists that antioxidant vitamins from both the diet and from supplements may prevent lipoprotein oxidation and its biological effects in the body. The strongest evidence seems to be for vitamin E.
Support for the role of antioxidant vitamins in heart disease prevention has come from observational studies, particularly two cohort studies that were published in 1993. In the first study, the Nurses’ Health Study, the researchers concluded that among over 85,000 middle-aged women in the study, there was a 40% reduced risk of coronary artery disease for those who took vitamin E supplements compared to those who did not (N Engl J Med 1993;328: 1444-9). The second study, the Health Professionals Follow-up Study, involved over 39,000 males and provided evidence of a significant association between a high intake of vitamin E from supplements and a lower risk of heart disease (N Engl J Med 1993; 328:1450-1456).
Though these observational studies have pointed to the possibility of beneficial effects of vitamin E, they cannot establish cause and effect. And there has been very little direct evidence of benefit from randomized trials, which can establish a causal connection. Recently published results from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study did not support the results of the observational studies. This randomized trial tested the effects of daily doses of 50 IU of vitamin E, 20 mg of beta carotene, both, or placebo on over 29,000 male smokers for five to eight years. The researchers found that with vitamin E supplementation, there was an increase in the risk of hemorrhagic stroke. And with beta-carotene supplementation, there was an increase in mortality from lung cancer and ischemic heart disease. This trial raised the possibility that antioxidant supplements may have harmful as well as beneficial effects (N Engl J Med 1994; 330:1029-1035).
Two more recently published observational studies produced conflicting results. In a seven-year study of over 34,000 postmenopausal women, researchers found that the intake of vitamin E from food was inversely associated with the risk of death from heart disease and concluded that postmenopausal women could lower their risk of heart disease without using supplements (N Engl J Med 1996; 334:1156-1162). However, in the Rotterdam Study, researchers did not find an association between dietary vitamin E and heart disease in an elderly population (Am J Clin Nutr 1999;69:261-266).
Last March at the Conference on Cardiovascular Disease Epidemiology and Prevention, Dr. Lori Mosca of the University of Michigan presented a study suggesting that vitamin E supplements provide little benefit to health and may cause harm in women after menopause. The study found that women who obtained vitamin E from their diet experienced significant reductions in LDL oxidation while the women who obtained vitamin E from supplements experienced increased LDL oxidation. Dr. Mosca believes that it may be the gamma-tocopherol in food that is protective instead of alpha-tocopherol found in supplements.
The results of secondary prevention trials (and those with known heart disease) have been more supportive of potential benefits of antioxidant vitamins. The Cambridge Heart Antioxidant Study (CHAOS) examined the effects of 400 to 800 IU of alpha-tocopherol on subsequent cardiovascular events. The risk of heart attack and other cardiovascular events was reduced in the group receiving vitamin E supplements (Lancet 1996;346: 781-786). A secondary analysis of the ATBC study also found that the risk of a second heart attack was reduced in those taking vitamin E supplements (Lancet 1997;349:1714-1720).
According to a recent Science Advisory from the American Heart Association (AHA), there are not enough data on the long-term safety and efficacy of vitamin E supplementation to justify any population-wide recommendations for supplementation for the primary prevention of heart disease. The advisory also states that the role of vitamin E in secondary prevention is encouraging and leaves open the possibility of future recommendations regarding vitamin E supplementation in those with heart disease if further studies confirm the findings (Circulation 1999; 99:591-595).
It is still unknown whether there are serious negative effects associated with taking vitamin E supplements. It is also unknown whether some other unidentified component in foods may actually be responsible for a reduced risk of heart disease. The Food and Drug Administration (FDA) is examining the scientific data to determine whether there is adequate evidence to support a health claim for antioxidants and disease prevention. A decision is expected next year.
Over time, a clearer picture should emerge, but for now, the AHA advises that based on current knowledge about vitamin E (and other antioxidant vitamins), “the most prudent and scientifically supportable recommendation for the general population is to consume a balanced diet with emphasis on antioxidant-rich fruits and vegetables and whole grains.”
Beth Fontenot is a freelance nutrition writer and the Nutrition Coordinator on the faculty of the Louisiana State University Medical Center-Shreveport Family Practice Residency Program at Lake Charles Memorial Hospital in Lake Charles, LA.
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