Vitamin E deficiency
|Vitamin E deficiency|
|Classification and external resources|
Vitamin E deficiency causes neurological problems due to poor nerve conduction and changes in membrane structure and function.
Signs of vitamin E deficiency include:
- Neuromuscular problems - such as spinocerebellar ataxia and myopathies.
- Neurological problems - may include dysarthria, absence of deep tendon reflexes, loss of vibratory sensation and proprioception, and positive Babinski sign.
- Anemia - due to oxidative damage to red blood cells 
- Retinopathy 
- Impairment of the immune response 
- Premature, very low birth weight infants - birth weights less than 1500 grams, or 3.5 pounds. A neonatologist, a pediatrician specializing in the care of newborns, typically evaluates the nutritional needs of premature infants.
- Rare disorders of fat metabolism - There is a rare genetic condition termed isolated vitamin E deficiency or ataxia with isolated with vitamin E deficiency, caused by mutations in the gene for the tocopherol transfer protein. These individuals have an extremely poor capacity to absorb vitamin E and develop neurological complications that are reversed by high doses of vitamin E.
- Fat malabsorption - Some dietary fat is needed for the absorption of vitamin E from the gastrointestinal tract. Anyone diagnosed with cystic fibrosis, individuals who have had part or all of their stomach removed, and individuals with malabsorptive problems such as Crohn's disease, liver disease or pancreatic insufficiency may not absorb fat (people who cannot absorb fat often pass greasy stools or have chronic diarrhea and bloating). Abetalipoproteinemia is a rare inherited disorder of fat metabolism that results in poor absorption of dietary fat and vitamin E. The vitamin E deficiency associated with this disease causes problems such as poor transmission of nerve impulses, muscle weakness, and degeneration of the retina that can cause blindness.
- Visual changes - Photoreceptor outer segment membranes have a very high concentration of Polyunsaturated fatty acids (PUFA's) and are potentially very susceptible to oxidative damage (the retina consumes 5-10 times more oxygen per milligram than any other tissue tested). Vitamin E is present in the outer segment and is the only well-recognized chain-breaking, lipid-soluble antioxidant in vivo. After 12 months of experimental vitamin E deficiency in rats, visual function was absent or grossly abnormal. There was a 90% loss of DHA from the retina - probably caused by peroxidative degradation - and changes in retinal membrane fluidity. 
The treatment is some form of Vitamin E supplementation.
Aggressive vitamin E replacement therapy has been shown to either prevent, halt or improve visual abnormalities.
- Brigelius-Flohé R, Traber MG (July 1999). "Vitamin E: function and metabolism". FASEB J. 13 (10): 1145–55. PMID 10385606.
- Office of Dietary Supplements. "Vitamin E Professional Fact Sheet". National Institutes of Health. Retrieved 14 August 2010.
- Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press, 2000.
- Kowdley KV, Mason JB, Meydani SN, Cornwall S, Grand RJ (June 1992). "Vitamin E deficiency and impaired cellular immunity related to intestinal fat malabsorption". Gastroenterology 102 (6): 2139–42. PMID 1587435.
- Traber MG, Sies H (1996). "Vitamin E in humans: demand and delivery". Annu. Rev. Nutr. 16: 321–47. doi:10.1146/annurev.nu.16.070196.001541. PMID 8839930.
- Manor D, Morley S (2007). "The alpha-tocopherol transfer protein". Vitam. Horm. 76: 45–65. doi:10.1016/S0083-6729(07)76003-X. PMID 17628171.
- Muller DP, Lloyd JK, Wolff OH (1983). "Vitamin E and neurological function: abetalipoproteinaemia and other disorders of fat absorption". Ciba Found. Symp. 101: 106–21. PMID 6557902.