This text is
based on p 67 of Hemilä
(2006)
These documents have up to date links to documents that are available
via
the net.
Harri Hemilä
Department of Public Health
University of Helsinki,
Helsinki, Finland
harri.hemila@helsinki.fi
Overt vitamin E deficiency symptoms have never been described in normal
individuals consuming diets low in vitamin E because it is found in
such a great variety of foods, and is stored in the body for such long
periods (FNB 2000). Thus there is no known minimum intake level that
prevents vitamin E deficiency in the same sense as 10 mg/day of vitamin
C prevents scurvy.
The most recent US recommendation of vitamin E intake uses ‘hydrogen
peroxide-induced hemolysis’ as the outcome on which the adequacy of
vitamin E is assessed, based on the argument that "In the absence of
other scientifically sound data, hydrogen peroxide-induced hemolysis is
the best marker at the present time" (FNB 2000 p 232).
The plasma
concentration of 12 μmol/l α-tocopherol was chosen as the minimal
level, since this concentration is associated with normal in vitro
hydrogen peroxide-induced hemolysis. "Based on NHANES III data, more
than 95% of the population surveyed would have plasma concentrations
greater than 12 μmol/l, thus indicating that the American public is not
vitamin E deficient by this criterion" (FNB 2000 p 233).
Since a study
with subjects who had been on a controlled vitamin E diet for over 6
years found 12 μmol/l to correspond to a dietary vitamin E intake level
of 12 mg/day (pp 232-6),
the RDA level was set at 15 mg/day to provide
an arbitrary margin of safety.
However, this kind of argument does not seem reasonable. ‘Hydrogen
peroxide-induced hemolysis’ is a surrogate marker and there is no
evidence cited that the percentage of hemolysis would meaningfully
correlate with any clinically relevant outcome (FNB 2000). The
correlation between dietary vitamin E intake and plasma α-tocopherol
concentration is also very weak or nonexistent in freely living people.
One study "reported that plasma α-tocopherol concentrations were not
associated with dietary intake, whereas some others report that
associations seen were largely due to vitamin E supplement intake …
[and] … plasma α-tocopherol concentrations in NHANES III did not
correlate with the 24-hour dietary recall data" (FNB 2000 p 210).
Thus,
there is no evidence that among freely living people vitamin E intake
might meaningfully correlate with plasma α-tocopherol level and,
moreover, there is no evidence that the percentage of hemolysis might
correlate with any clinically relevant outcome.
In any case, the current vitamin E recommendation for both men and
women was set at 15 mg/day (FNB 2000 p 237).
Consequently, in the USA,
90% of men and 99% of women aged 19-30 years have a vitamin E intake
lower than 15 mg/day (FNB 2000 pp 422-3).
However, there is no evidence
cited that this 90-99% of young adults with an intake lower than the
RDA level might suffer any harmful effect on health because of their
‘low’ intake (FNB 2000). Thus the level of vitamin E recommendation is
arbitrary to an extreme degree.
In the previous RDA recommendation, the recommended vitamin E intake
was based on the following argument: "The allowance … is therefore
based primarily on customary intakes from U.S. food sources. … the
subcommittee has established an arbitrary but practical allowance for
male adults of 10 mg of alpha-tocopherol equivalents per day. Because
women are generally smaller, their allowance is 8 mg/day" (FNB 1989a p
103). At these older RDA levels, only 25% of US men and 50% of
women
aged 19-30 years would get less than the recommended level (FNB 2000 pp
422-3).
