Vitamin E and neurologic deficits

Over the past decade it has become apparent that vitamin E is an essential nutrient for maintaining the structural and functional integrity of the developing human nervous system, skeletal muscle, and the retina. The clinical and histologic resemblance of the human neuromuscular disorder associated with chronic fat and vitamin E malabsorption to that observed in experimental vitamin E-deficient animal models is striking. Because of chronic malabsorption of vitamin E, children with CF, chronic cholestasis, abetalipoproteinemia, and short bowel syndrome are at risk for the development of neurologic deficits caused by vitamin E deficiency. Correction of the vitamin E deficiency state prevents, reverses, or, at least, stabilizes the neurologic dysfunction in susceptible individuals. Advances in stable isotope technology permit study of the hepatic discrimination among the various stereoisomers and forms of vitamin E. Investigations into the cause of the primary form of vitamin E deficiency, the isolated vitamin E deficiency syndrome, promise to delineate the normal physiologic processes involved in absorption, transport, and tissue delivery of vitamin E. Studies in progress are addressing the optimal route and form of vitamin E therapy to be used in each predisposing condition. One major task remaining is to better define the mechanism by which vitamin E deficiency leads to neurologic injury.