15.4: Vitamin E

For decades after its discovery, vitamin E presented an awkward and baffling problem to nutrition researchers. It’s been called a vitamin in search of a disease. The reason is simple: Even after the long years it took to discover, isolate, and synthesize vitamin E, decades passed before it could be shown that a deficient intake leads to any specific symptom or disease in humans.

There’s a special irony in this problem. For even though scientists have labored to find specific health effects of vitamin E deficiency, the vitamin has been heralded by the public as a virtual cure-all. Such belief has little reality. It seems to stem from two misinterpretations: First, the general misinterpretation so often at the root of megadose supplementation theory—that if a little will clear up a deficiency symptom, a lot will bring superior protection against whatever problems the deficiency caused. Second, the mistaken extension of theories based on animal deficiency to humans.

On the basis of such misinterpretations, the public doses itself with E to achieve better athletic or sexual performance, to prevent or cure heart disease or stroke, to negate the effects of smoggy air, and to stave off ailments from muscular dystrophy to cancer. But science is still unaware of any major human disease which is caused by a lack of vitamin E. Nor is it known that vitamin E supplements prevent or relieve any illness or confer any special health benefit, although studies continue to explore this possibility. Let’s contrast some popular ideas about this vitamin with some scientific realities of what it is and does.

Science Identifies Vitamin E

In 1922 it was reported that an unidentified fat-soluble substance from several common foods was important for rat reproduction. When female rats were fed diets deficient in this substance, the ovum could be fertilized, but pregnancy couldn’t proceed. But when they were fed wheat germ or lettuce within 7 days of conception, pregnancy went forward normally. (It may seem curious that so unfat a food as lettuce could provide a fat-soluble vitamin. But there are small amounts of oils in most vegetables, and only very small amounts of vitamin E are required.)

It’s evidently because of its relationship to fertility that vitamin E has won its mythical link to sexuality. Some later research showed a relationship between reproduction capacity and E deficiency for male rats as well. But for neither male nor female was there evidence of change in sexual activity—only in its result. Vitamin E deficiency didn’t discourage rat romance—only the birth rate.

Fourteen years were to pass from the time of these animal studies, before vitamin E was isolated in 1936. It was isolated from the oil of wheat germ, and was named tocopherol, meaning to bear young.

In the ensuing years, there’s been continuing confusion about vitamin E’s human function. In the 1940s, for example, Time magazine reported claims that large doses of vitamin E protected against cardiovascular disease. Later experimental evidence consistently refuted the idea. But popular impressions die hard—and vitamin E remains a darling of supplement takers and supplement sellers.

What is Vitamin E?

Vitamin E is a tocopherol, as noted above. There are alpha, beta, gamma, and delta forms of tocopherol, of which alpha-tocopherol is the most potent. The RDA for vitamin E is given as milligrams (mg) alpha-tocopherol. The vitamin E in supplements is given in International Units (IU) instead.

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To convert the IU of vitamin E supplements to the RDA’s mg units, multiply IU of “dl-alpha-” tocopherol, tocopherol acetate, or tocopheryl succinate by 0.45; multiply IU of “d-alpha-” forms by 0.67, e.g., 300 IU dl-alpha-tocopherol = 135 mg (300 X 0.45). 300 IU of d-alpha-tocopherol = 200 mg (300 X 0.67). Adult RDA for vitamin E is 15 mg.

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Vitamin E Chemistry

The chemistry of vitamin E centers on its notable antioxidant effect. The natural presence of the vitamin in many foods protects against rancidity—the oxidation of fats. This is particularly the case with vegetable oils expressed from seeds of cotton, sesame, wheat, corn, and the like, and with oils of nuts, especially almonds. These oils are polyunsaturated (their fatty acids have many double bonds in their structure), and vitamin E guards against their oxidation (see Fig. 15-5). Indeed a fairly good rule of thumb is that vitamin E is likely to be found where there’s highly unsaturated fat.

This is true, not only of our food, but of our body as well. Vitamin E is found in our cell membranes, where it confers antioxidant protection to the unsaturated fat found there (see Fig. 15-5). When there’s vitamin E deficiency, the polyunsaturated fats are more easily oxidized, leading to cell damage.

Symptoms of Vitamin E deficiency haven’t been seen in healthy populations, even in those whose diets have little vitamin E. Deficiencies have only been seen in unusual circumstances. It can occur, for example, in cases of cystic fibrosis because of the fat malabsorption associated with the disease. Vitamin E supplements are routinely given to such at-risk groups.

Vitamin E and False Hopes

Vitamin E may well have raised more false hopes than any other micronutrient—hopes spurred both by dramatic animal experiments and by biochemical theory.

In animal experiments, vitamin E has offered promise for human difficulties ever since it solved rat infertility. Vitamin E deficiency hasn’t been shown to cause infertility for humans, nor have supplements of vitamin E been found to cure it

In a similar way, it was seen early that vitamin E deficiencies in chicks and rabbits led to degeneration of the liver, and to muscular dystrophy. But vitamin E has not been proven to play such roles in human illness. A continuing belief that vitamin E can relieve human muscular dystrophy remains a cruel deception.

In calves, and in some other animals, a shortage of vitamin E can cause heart and blood-vessel damage, raising the hope that extra vitamin E might provide humans with extra protection against such ills. But not so, according to human studies.

In rabbits, low vitamin E intake can limit growth. Evidence that vitamin E may be involved in forming nucleic acids and in the respiration of cells has hinted that vitamin E may play some role in growth and aging. But in human tests, extra vitamin E has failed either to spur growth or to prolong cell life.

Figure 15-5: Vitamin E helps protect the unsaturated fatty acids in our bodies and in our diets.

Inappropriate conclusions are still being drawn from vitamin E research. The animal studies tying vitamin E to cell growth and reproduction triggered claims for the healing of wounds and burns and the prevention of skin aging. Testimonials as to the effectiveness of vitamin E in burn healing may derive from the fact that putting fats on burns to soothe is common practice, and vitamin E ointments come in oily bases. The oil, not vitamin E, is probably what comforts.

There’s certainly much to be learned still about vitamin E. But there’s yet no reason to be concerned about the adequacy of the RDAs.

Many of the human studies of vitamin E supplements are in high-risk groups—people with diabetes, Alzheimer’s disease, heart disease, etc. In these groups, risk is more acceptable if there’s a clear benefit to their disease. The situation is far different for healthy people. When smokers, who have a higher risk of cancer and heart attacks, were given 50 mg vitamin E in one randomized study, they had 5% fewer deaths from heart attacks, but 50% more deaths from hemorrhagic stroke as compared to those not given vitamin E (and no difference in lung cancer).3 In this light, it’s not wise for even a disease-free smoker—much less a disease-free non-smoker—to take vitamin E supplements.

Vitamin E in Foods

Vitamin E is found naturally in the fatty parts of food. Vegetable oils are a particularly rich source because vitamin E is found along with polyunsaturated fats to protect them from oxidation/rancidity (see Fig. 15-5). The oils have different amounts of vitamin E, because all the tocopherols (alpha, beta, gamma, delta) protect the oil from oxidation, but only the alpha form fulfills our RDA for vitamin E.

Salad dressing is a major source of vegetable oil. Removing the oil, as in fat-free dressing, removes its vitamin E as well. But vitamin E is being added to more foods. There’s even vitamin-E-fortified orange juice.

Vitamin E Toxicity

The UL for vitamin E is specifically for supplements because the popularity of massive and long-term, self-prescribed doses of vitamin E are still cause for concern. Excesses of vitamin E are relatively non-toxic, but can present problems in some cases. Large doses can, for example, interfere with vitamin K activity and thereby hamper blood-clotting. This can further increase the risk of bleeding in people who are taking medications to lessen blood-clotting, e.g., aspirin, Coumadin.