Canada. Thus, current dietary patterns appear to provide sufficient vitamin E to prevent deficiency symptoms such as peripheral neuropathy. However, since vitamin E intakes are underestimated, particularly with respect to estimates of intake associated with fats (see later section “ Underreporting in Dietary Surveys ”), an AI could not be reliably determined from the available data on intakes.
Data on human experimental vitamin E deficiency are very limited but do provide some guidance in estimating a requirement. The values recommended here are based largely on studies of induced vitamin E deficiency in humans and the correlation with hydrogen peroxide-induced erythrocyte lysis and plasma α-tocopherol concentrations.
Only one study has been carried out in apparently healthy human adults who were depleted of vitamin E over 6 years and then repleted (Horwitt, 1960, 1962; Horwitt et al., 1956). In response to vitamin E deficiency, increased erythrocyte fragility (as assessed by an in vitro test of hydrogen peroxide-induced hemolysis) was observed, which was reversed by vitamin E supplementation.
The hydrogen peroxide-induced hemolysis test has drawbacks in that it is critically dependent upon the concentration of hydrogen peroxide used, the erythrocyte content of catalase and antioxidants, and the precise incubation conditions. Nonetheless, it is one of the few tests in which the marker (erythrocyte lysis) has been correlated with a health deficit (decreased erythrocyte survival) that has been shown to be corrected by supplemental vitamin E. Therefore, the data from this study were used to estimate intakes for α-tocopherol requirements.
It is recognized that there are great uncertainties in the data utilized to set the α-tocopherol requirements. However, in the absence of other scientifically sound data, hydrogen peroxide-induced hemolysis is the best marker at the present time. It should be emphasized that research is urgently needed to explore the use of other biomarkers to assess vitamin E requirements.
The requirements for vitamin E intakes are therefore based primarily on studies in which plasma α-tocopherol concentrations and corresponding hydrogen peroxide-induced erythrocyte lysis were determined (Horwitt, 1960, 1962, 1974; Horwitt et al., 1956, 1963, 1972). Vitamin E depletion in 19 normal, adult men was studied by feeding them a 2,200-kcal diet containing 3 mg (7 µmol)/day (range