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