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Vitamin E is a term used for molecules that exhibit the biological activity of alpha-tocopherol.

Function

Vitamin E is an antioxidant that prevents free radical damage in biological membranes. It is a potent scavenger of peroxyl radicals and protects polyunsaturated fatty acids within phospholipids in membranes and in plasma lipoproteins. Vitamin E has an effect on several enzyme activities and membrane properties. It is involved in the regulation of vascular smooth muscle cell proliferation and protein kinase C activity.

Absorption and excretion

Vitamin E absorption into the intestinal lumen requires bile and pancreatic secretions. Vitamin E is incorporated into chylomicrons and secreted from the intestine to the lymph. The chylomicrons are taken up by lipoproteins, such as high-density lip oproteins (HDL), and travel to the liver. Vitamin E is secreted by the liver in very low-density lipoproteins (VLDL). VLDL form low-density lipoproteins (LDL) and the vitamin E is transferred to HDL. Most of the vitamin E in the body is stored in adipose tissue. Vitamin E is excreted in the bile, urine, feces, and through the skin. Vitamin C and other hydrogen donors regenerate oxidized vitamin E in the body, restoring the antioxidant activity of vitamin E.

Clinical conditions

Vitamin E deficiency is very rare and almost never occurs due to a dietary deficiency. A genetic defect in hepatic alpha-tocopherol transfer protein causes a vitamin E deficiency characterized by peripheral neuropathy. Vitamin E supplements o f 800-1200 milligrams (mg) per day can prevent neurological problems in people with this defect. Vitamin E deficiency can also be caused by a genetic defect in lipoprotein synthesis. People with this defect have an impaired ability to absorb dietary fat. Symptoms include steatorrhea, retarded growth, retinitis pigmentosa, and neurological disorders with ataxia. Vitamin E deficiency can also result from fat malabsorption. Fat malabsorption can be caused by a resection of the small bowel, Crohn's disease, celiac disease, and chronic pancreatitis. Children with cystic fibrosis can become vitamin E deficient due to impaired secretion of pancreatic digestive enzymes. Vitamin E supplementation is less effective for patients with fat malabsorption due to the role of fat in absorption of vitamin E.

Recommended intake

The Daily Reference Intake (DRI) of vitamin E set by the Food and Nutrition Board of the National Academy of Sciences is expressed as mg of alpha-tocopherol or alpha-tocopherol equivalents. Current recommendations include: 6-11 mg for child ren, 15 mg for adults and pregnant women, and 19 mg for lactating women. For infants there is an adequate intake (rather than a recommended intake) of 4-6 mg per day.

Food Sources

Vegetable oils are the best sources of vitamin E. Unprocessed cereal grains and nuts are good sources. Meats containing animal fat also contain vitamin E.

Supplementation

Supplemental vitamin E may be beneficial for the following indications: retinopathy in premature infants, anemia in infants, cardiovascular disorders, immune function, and cataracts. The National Academy of Sciences has set a tolerable upper inta ke level of 1000 mg for adults but such a limit has not been determined for infants. Supplemental vitamin E is available in two forms. The natural form is designated as d-alpha-tocopherol; the synthetic form is dl-alpha-tocopherol. Natura l vitamin E is more beneficial than the synthetic version.

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