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vitamin E

Monday 23 March 2009

A group of eight closely related fat-soluble compounds-four tocopherols and four tocotrienols-all exhibit vitamin E biologic activity, but α-tocopherol is the most active and the most widely available. Vitamin E is abundant in so many foods-vegetables, grains, nuts and their oils, dairy products, fish, and meat-that a diet sufficient to sustain life is unlikely to be insufficient in vitamin E.

The absorption of tocopherols, as of all fat-soluble vitamins, requires normal biliary tract and pancreatic function. After absorption, vitamin E is transported in the blood in the form of chylomicrons, which rapidly equilibrate with the plasma lipoproteins, mainly LDLs. Unlike vitamin A, which is stored predominantly in the liver, vitamin E accumulates throughout the body, mostly in fat depots but also in liver and muscle.

Vitamin E is one of a group of antioxidants that serve to scavenge free radicals formed in redox reactions throughout the body (Chapter 1). It plays a role in termination of free radical-generated lipid peroxidation chain reactions, particularly in cellular and subcellular membranes that are rich in polyunsaturated lipids. These chain-terminating nutrients are complemented by selenium, which is converted to selenocysteine and is essential for the activities of glutathione peroxidase and thioredoxin reductase.

These antioxidants metabolize peroxides before they can initiate membrane damage, thus maintaining intracellular redox status.8 For reasons that are not clear, the nervous system is a particular target of vitamin E deficiency.

Although the basis for this affinity is not entirely clear, it is speculated that neurons with long axons are particularly vulnerable because of their large membrane surface area. Mature red cells may also be vulnerable to vitamin E deficiency because they are at risk for oxidative injury imposed by the generation of superoxide radicals during oxygenation of hemoglobin.


Hypovitaminosis E resulting from a deficient diet is uncommon in the Western world and occurs almost exclusively in association with:
- (1) fat malabsorption that accompanies cholestasis, cystic fibrosis, and primary small intestinal disease;
- (2) infant low birth weight with immature liver and gastrointestinal tract;
- (3) abetalipoproteinemia, a rare autosomal recessive disorder in which transport of vitamin E is abnormal because the apoprotein B component of chylomicrons, LDLs, and very-low-density lipoproteins (VLDLs) is not synthesized;
- (4) rare autosomal recessive syndrome of impaired vitamin E metabolism.

The neurologic manifestations of vitamin E deficiency are depressed or, more often, absent tendon reflexes; ataxia; dysarthria; loss of position and vibration sense; and loss of pain sensation. Muscle weakness is also common.

In addition, there may be impaired vision and disorders of eye movement, sometimes progressing to total ophthalmoplegia. Anemia is not a feature of the deficiency state in adults but is often found in premature infants and is probably multifactorial in origin.

In closing, attention should be drawn to the ongoing interest in the possible protective effects of vitamin E and other antioxidants against atherosclerosis and cancer, the two most common causes of death in the United States. In the case of atherosclerosis, it is suggested that vitamin E may inhibit atheroma formation by reducing the oxidation of LDL.

However, there is no conclusive evidence to support an atheroprotective effect of supplemental vitamin E. In the context of cancer, antioxidants are postulated to scavenge free radicals, thereby preventing DNA damage and mutagenesis. There is limited epidemiologic evidence supporting a protective effect of supplemental vitamin E and lycopene-rich foods against prostate cancer.


The anatomic changes found in the nervous system depend on the duration and severity of the deficiency state. Most consistent is degeneration of the axons in the posterior columns of the spinal cord, with focal accumulation of lipopigment and loss of nerve cells in the dorsal root ganglia, attributed to a dying-back type of axonopathy.

Myelin degeneration in sensory axons of peripheral nerves may also be present, and in more marked cases, degenerative changes in the spinocerebellar tracts may occur as well. In occasional cases, features of both primary and denervation muscle disease have been observed in skeletal muscle.

Vitamin E-deficient erythrocytes are more susceptible to oxidative stress and have a shorter half-life in the circulating blood.