Vitamin E

Vitamin E's primary role appears to be as an antioxidant. In this role, vitamin E protects fatty acids (oils) against oxidation and rancidity. This role grows in importance when you realize that all the cells and sub cellular membranes of the body contain a sizeable portion of fatty acids which require such protection against oxidation. These fatty acids (usually polyunsaturated) serve vital roles in the cells, and scientists believe oxidation of them causes not only many diseases but some of the symptoms of aging as well.

Many enzyme systems are impaired during a vitamin E deficiency. However, no exact function for vitamin E in a particular enzyme reaction has been found. Some scientists believe the effect on enzyme systems may be due to oxidation (or peroxidation) of the tissue components of the enzyme system.

Vitamin E's protective effects on the cell have been demonstrated in several studies with red blood cells. One study involved a group of people given 600 IU of vitamin E per day for ten days, then tested for the ability of their red blood cells to resist oxidative "aging" when exposed to light and excess oxygen. Whereas red blood cells from non supplemented people were completely "budded" (this refers to oxidative damage), those from the supplemented group were only about eight percent budded.

As red blood cells age, they become less "filterable." One study with rats found that vitamin E-supplemented animals had red blood cells which were remarkably resistant to the aging effect of lead poisoning. Red blood cells from E-supplemented rats which were also poisoned with lead were still more filterable than red blood cells from animals fed no lead but who received a diet deficient in vitamin E. Normal aging of the red blood cells from the supplemented animals also failed to produce any significant difference in their filterability.

A study of cystic fibrosis patients with vitamin E deficiencies found that their red blood cells had greatly increased susceptibility to abnormal oxidative destruction. Although they all had biochemical signs of increased destruction of red blood cells, none yet had the symptoms of anemia. Supplements of from 100 to 200 IU of vitamin E quickly increased the survival time of their red blood cells to normal. The researchers concluded that vitamin E was essential for the maintenance of normal red blood cell structure and function.

In rats, vitamin E deficiency produces degeneration of the gonads, leading to loss of sperm motility in males and fetal death and resorption in the females. With this degeneration of the sex glands also comes an impairment of their function, the secretion of sex hormones. Vitamin E deficiency during development can result in a delay of puberty.

Deficiency of vitamin E can also result in diminished function of the pituitary-thyroid system. A hyperthyroid state tends to increase vitamin E requirements, since more fatty acids are concentrated in the muscles, particularly the heart muscle, and any increase in fatty acids requires more vitamin E to protect against oxidation.

Degeneration and dystrophy of the skeletal, striated and cardiac muscles also occur in a vitamin E deficiency. Degeneration of the endocrine glands, peripheral vascular system, and nervous system have also been reported. In some animals, nervous system lesions take the form of softening of the brain.

The only widely recognized effect of a deficiency of vitamin E in humans is the decreased survival time of red blood cells. This was demonstrated, however, with only a partial deficiency. The subjects still received five IU of vitamin E per day. Also, there was not rigorous biochemical testing of the effects on other cell systems, some of which may have been more severely affected. Degeneration of the brain and spinal cord have also been reported in vitamin E-deficient children.

There is more than one form of vitamin E, or tocopherol. Actually, there are at least four tocopherols which have been isolated, the alpha, beta, gamma, and delta tocopherols. Of the four, the alpha fraction is the most active, and in vitamin E supplements the level of vitamin E activity (international units, IU) is measured according to how much alpha tocopherol is present. Synthetic vitamin E is synthetic alpha tocopherol. In vitamin supplements, the natural form of vitamin E will be labeled d-alpha tocopherol, and the synthetic dl-alpha tocopherol. The natural form of vitamin E is more potent; however, this difference in potency is accounted for in calculating vitamin E "activity" in IU. So a supplement of 100 IU of d-alpha will be as potent as 100 IU of dl-alpha tocopherol. One researcher did find that the natural form and the water-soluble form of vitamin E were more effective in raising blood levels than the synthetic form. But this was measured in persons with lupus erythematosus. No such comparison is available for healthy persons. Studies have shown, however, that once adjusted for differences in potency, the same dose of either natural or synthetic vitamin E produces the same blood and tissue levels of tocopherol. For most of the studies and therapeutic uses described, the standard form of vitamin E is the synthetic form.

Cooking does not normally destroy significant amounts of vitamin E. Frying, however, especially in deep fat, can cause most of the vitamin E to be oxidized. Storage for long periods can destroy vitamin E, too.

Vitamin E supplements are available in doses ranging from a few IU to more than 1000 IU.

Where is it found ?

The richest natural sources of vitamin E are the oils in the seeds of cereal grains. Wheat germ oil is foremost among these, followed by soybean oil, cottonseed oil, sunflower seed oil, and corn oil. Nuts, eggs, fish, and organ meats contribute considerably smaller quantities. Because fruits and vegetables are not consumed in the quantities necessary to provide enough vitamin E, they are not considered significant sources.

Who is likely to be deficient ?

Severe vitamin E deficiencies are rare.

How much to take

The RDA for vitamin E was lowered from a maximum of thirty IU to fifteen IU. It now stands at fifteen IU for men and ten IU for women. The primary reason for the drop seems to be that dieticians were complaining that it was difficult, if not impossible, to compose diets which supplied thirty IU of vitamin E. That's not surprising when you understand that refining of flour removes just about all of the vitamin E. White flour products devoid of vitamin E (since the vitamin is not replaced by fortification) make up a sizeable portion of the calories in the average diet. Several authorities on vitamin E, including the researcher who performed the only human deficiency study, have stated that the new RDA is too low to maintain adequate vitamin E status.

Side effects

Vitamin E toxicity is very rare; supplements are widely considered to be safe.
A diet high in unsaturated fat increases vitamin E requirements. Vitamin E and selenium work together to protect fat-soluble parts of the body.

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