Vitamin E deficiency occurs only rarely in humans and overt deficiency symptoms
in normal individuals consuming diets low in vitamin E have never been described (IOM,
2000). Vitamin E deficiency occurs only as a result of genetic abnormalities in
α–tocopherol transfer protein, as a result of various fat malabsorption syndromes, or as a
result of protein-ener
gy malnutrition (IOM, 2000).
Deficiency can of course result from insufficient dietary intake of the vitamin.
Several other dietary factors affect the need for vitamin E. Two are most important in
this regard: selenium (Se) and polyunsaturated fatty acids (PUFAs). Se spares the need
for vitamin E and therefore, adequate intake of vitamin E becomes even more important
in individuals taking low Se-diets (Combs, 1992).
The primary human vitamin E deficiency symptom is a peripheral neuropathy
characterized by the degeneration of the large-caliber axons in the sensory neurons.