Vitamin E was discovered in 1922, but not until 1983 that vitamin E was demonstrated to be dietary essential for human beings.
Vitamin E deficiency was first describe in children with fat malabsorption syndromes, principally abetalipoproteinemia, cystic fibrosis, and cholestatic liver disease.
They have been reports of vitamin E deficiency symptoms in person with protein calories malnutrition.
The frequency of human vitamin E deficiency is very rare, deficiency is usually associated with disease of fat malababsorption such as cystic fibrosis.
In individual at risk, it is clear that vitamin E supplements should be recommended to prevent deficiency symptoms.
Without vitamin E, the red blood cells break open and spill their contents, probably due to oxidation of the polyunsaturated fatty acids in their membranes.
The classic sign of vitamins E deficiency, known as erythrocyte hemolysis, is seen in premature infants, born before the transfer of vitamin E from the mother to the infant that takes place in the last week of pregnancy.
The primary human vitamin E deficiency symptoms is a peripheral neuropathy characterized by the degeneration of the large caliber axons in the sensory neurons.
Other vitamin E deficiency symptoms observed in humans include spinocerebellar ataxia, skeletal myopathy, and pigmented retinopathy.
Prolonged vitamin E deficiency also can causes neuromuscular dysfunction involving the spinal cord and retina of the eye.
Vitamin E Deficiency in Human