Vitamin E deficiency is a very rare problem that results in damage to nerves. When vitamin E deficiency does occur, it strikes people with diseases that prevent the absorption of dietary fats and fat-soluble nutrients.
Vitamin E seems to have only one function in the body: the prevention of the natural and continual process of deterioration of all body tissues. This deterioration is provoked by a number of causes, one being toxic oxygen. During the body's metabolism of atmospheric oxygen, toxic oxygen is produced continuously in the body by the formation of by-products. These toxic by-products include hydrogen peroxide, superoxide, and hypochlorite.
Hypochlorite is a natural product, produced by cells of the immune system. It is also the active component of bleach. Once formed, toxic oxygen can damage various parts of the body, such as the membranes which form the boundaries of every cell. Vitamin E serves the body in protecting membranes from toxic oxygen damage (oxidation). In contrast, vitamin C serves to protect the aqueous – or watery – regions of the cells from oxidation. The membranes that are most sensitive are the membranes of nerves and therefore the main symptom of vitamin E deficiency is damage to the nervous system.
Vitamin E deficiency should not be a concern for most people, since the vitamin is found in a wide variety of foods. Attention has been given to the theory that vitamin E serves to protect against cancer and atherosclerosis. The evidence that normal levels of vitamin E protect against atherosclerosis is fairly convincing. However, there seems to be little or no proof that vitamin E intake above and beyond the RDA can prevent cancer or atherosclerosis.
When vitamin E deficiency occurs, it strikes people with diseases that prevent the absorption of dietary fats and fat-soluble nutrients. These diseases include cystic fibrosis, pancreatitis, and cholestasis (bile-flow obstruction). Bile salts, produced in the liver, are required for the absorption of fats. Cholestasis causes a decrease in the formation of bile salts and the consequent failure of the body to absorb dietary fats. For this reason, this disease may result in vitamin E deficiency.
Premature infants may be at risk for vitamin E deficiency because they may be born with low tissue levels of the vitamin, and because they have a poorly developed capacity for absorbing dietary fats. Infants suffering from fat-malabsorption diseases can develop symptoms of vitamin E deficiency by age two. In adults, the onset of a fat-malabsorption disease can provoke vitamin E deficiency after a longer period, such as ten years.
Vitamin E deficiency in humans results in ataxia (poor muscle coordination with shaky movements), decreased sensation to vibration, lack of reflexes, and paralysis of eye muscles. One particularly severe symptom of vitamin E deficiency is the inability to walk.
Signs and symptoms include dry skin, easy bruising, decreased clotting time, eczema, elevated indirect bilirubin, psoriasis, elevated heavy metals, PMS, cystic fibrosis, sickle cell anemia, beta thalassemia, cataracts, fibrocystic disease, benign prostatic hypertrophy, poor wound healing, hot flashes, growing pains and Osgood-Schlatter disease.
Vitamin E status is measured by assessment of the content of alpha-tocopherol in the blood plasma, using a method called high-pressure liquid chromatography. Blood plasma levels of alpha-tocopherol that are 5.0mg/l or above indicate normal vitamin E status; levels below 5.0mg/l indicate vitamin E deficiency.
One study showed that people with a low physical activity level had a lower reserve of vitamin E than those more highly active. Vitamin E concentration was inversely related to abdominal circumference. The inverse relationship between tocopherol levels and levels of body fat may explain why this is a risk factor for coronary heart disease, due to vitamin E's role as an antioxidant and protective agent in cardiovascular disease. [Journal of Internal Medicine, 1993;234: pp.53-60]
Vitamin E deficiency that occurs with cholestatic liver disease or other malabsorption syndromes can be treated with weekly injections of 100mg alpha-tocopherol that may continue for six months. Vitamin E deficiency in premature infants may require treatment for only a few weeks. The prognosis for correcting the neurological symptoms of vitamin E deficiency is fair to excellent.
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