Vitamin E is thought to function primarily as a chain-breaking
antioxidant that prevents the propagation of lipid peroxidation.
Overt deficiency is very rare, seen only in individuals unable to
absorb the vitamin or with inherited abnormalities that prevent
the maintenance of normal blood concentrations. Thus, current
dietary patterns appear to provide sufficient vitamin E to prevent
deficiency symptoms such as peripheral neuropathy. Estimates of
vitamin E intake are underreported, due in part to underreporting
of amounts of dietary fat consumed and lack of specificity of sources
in the diet. Data on human experimental vitamin E deficiency are
very limited but provide some guidance as to the appropriate Recommended
Dietary Allowance (RDA). The values recommended
here
are based largely on induced vitamin E deficiency in humans
and
the correlation between hydrogen peroxide-induced erythrocyte
lysis and plasma α-tocopherol
concentrations. The RDA for
both
men and women is 15 mg (35
µmol)/day
of α-tocopherol.
Vitamin
E activity of α-tocopherol
as defined in this report is
limited
to that available from the naturally occuring form (RRR-)
and
the other three synthetic 2R-stereoisomer
forms (RSR-,
RRS-,
and
RSS-)
of α-tocopherol
for purposes of establishing the human
requirement
for vitamin E. Other naturally occurring forms of
vitamin
E (β-,
γ-, and δ-tocopherols and the tocotrienols) do not
contribute toward meeting the vitamin E requirement because
(although absorbed) they are not converted to α-tocopherol by
humans and are recognized poorly by the α-tocopherol transfer
protein (α-TTP) in the liver. Therefore, the RDA is based only on
the α-tocopherol form of vitamin E which represents a change