Background
Vitamin E, one of the most important lipid-soluble antioxidant nutrients, is found in nut oils, sunflower seeds, whole grains, wheat germ, and spinach. Severe deficiency, as may occur in persons with abetalipoproteinemia or fat malabsorption, profoundly affects the central nervous system and can cause ataxia and a peripheral neuropathy resembling Friedreich ataxia.
Patients receiving large doses of vitamin E may experience a halt in the progression of the disease. Vitamin E overdose is difficult to achieve and, thus, is extremely uncommon.
This vitamin is thought to have a role in preventing atherosclerosis by inhibiting the oxidation of low-density lipoprotein (LDL).
Several epidemiologic studies have indicated that high dietary intake of vitamin E is associated with high serum concentrations of alpha tocopherol, as well as with lower rates of ischemic heart disease.
However, although the Cambridge Heart Antioxidant Study supported this hypothesis, a subsequent report, the prospective Heart Outcomes Prevention Evaluation Study, did not.
Vitamin deficiencies related to cystic fibrosis, chronic cholestatic liver disease, abetalipoproteinemia, short-bowel syndrome, isolated vitamin E deficiency syndrome, and other malabsorption syndromes may lead to varying degrees of neurologic deficits.
One milligram is equivalent to 1.5 international units (IU).