assessing human requirements for the amounts needed to maintain body pools. Almost no data exist on pool sizes or tissue concentrations of vitamin E, especially the various forms of vitamin E. Studies using isotope-labeled vitamin E may provide kinetic data that can be used to determine daily α-tocopherol requirements in the future.
Overt vitamin E deficiency is so rare in humans that signs of deficiency (e.g., neurological abnormalities) and comparisons of deficiency signs with dietary intakes are simply not available to serve as a basis for estimating requirements.
Several studies have reported the determinants of plasma α-tocopherol, as measured by high-performance liquid chromatography methods, and provided mathematical models that attempted to correlate usual vitamin E intakes with normal plasma concentrations (Ascherio et al., 1992; Gascón-Vila et al., 1997; Kardinaal et al., 1995; Stryker et al., 1988). Kardinaal et al. (1995) reported that plasma α-tocopherol concentrations were not associated with dietary intake, whereas others (Ascherio et al., 1992; Stryker et al., 1988) report that associations seen were largely due to vitamin E supplement intake. Recently, Ford and Sowell (1999) reported that plasma α-tocopherol concentrations in the Third National Health and Nutrition Examination Survey (NHANES III) did not correlate with the 24-hour dietary recall data. In any case, the correlation between intake and normal vitamin E plasma concentrations (greater than 16 µmol/L [688 µg/dL]) is not strong and could not be used as the basis for estimating the α-tocopherol requirement. However, in vitamin E-depleted subjects a linear increase in plasma α-tocopherol concentration was found with increasing vitamin E intake up to 17 mg (39.5 µmol)/day (Horwitt, 1960).
Studies in children with cystic fibrosis and in vitamin E-depleted adults provide evidence for the relationship between vitamin E status, plasma α-tocopherol concentrations, and erythrocyte susceptibility to hydrogen peroxide-induced lysis (Farrell et al., 1977; Horwitt, 1960). The children become vitamin E deficient because the impaired secretion of pancreatic digestive enzymes causes steatorrhea and vitamin E malabsorption, even when pancreatic