Vitamin E deficiency

Vitamin E deficiency

In experimental animals vitamin E deficiency results in a number of different conditions.

●      Deficient female animals suffer the death and reab-sorption of the fetuses. This provided the basis of the original biological assay of vitamin E.

●      In male animals deficiency results in testicular atrophy and degeneration of the germinal epithe-lium of the seminiferous tubules.

●      Both skeletal and cardiac muscle are affected in deficient animals. This necrotizing myopathy is sometimes called nutritional muscular dystrophy – an unfortunate term, since there is no evidence that human muscular dystrophy is related to vitamin E deficiency.

●      The integrity of blood vessel walls is affected, with leakage of blood plasma into subcutaneous tissues and accumulation under the skin of a green fluid: exudative diathesis.

●      The nervous system is affected, with the develop-ment of central nervous system necrosis and axonal dystrophy. This is exacerbated by feeding diets rich in PUFAs.

Dietary deficiency of vitamin E in human beings is unknown, although patients with severe fat malab-sorption, cystic fibrosis, some forms of chronic liver disease or (very rare) congenital lack of plasma β-lipoprotein suffer deficiency because they are unable to absorb the vitamin or transport it around the body.

They suffer from severe damage to nerve and muscle membranes.

Premature infants are at risk of vitamin E defi-ciency, since they are often born with inadequate reserves of the vitamin. The red blood cell membranes of deficient infants are abnormally fragile, as a result of unchecked oxidative radical attack. This may lead to hemolytic anemia if they are not given supple-ments of the vitamin.

Experimental animals that are depleted of vitamin E become sterile. However, there is no evidence that vitamin E nutritional status is in any way associated with human fertility, and there is certainly no evi-dence that vitamin E supplements increase sexual potency, prowess, or vigor.