Zitat:
In our meta-analysis, we identified a dose-dependent
relationship between vitamin E supplementation and allcause
mortality. Specifically, all-cause mortality progressively
increased for dosages approximately greater than 150
IU/d (anm.: 150IU entspr. ~120mg). This dosage is substantially
lower than the tolerable upper intake level for vitamin E, which is currently designated at 1000 mg of any form of supplementary
alpha-tocopherol per day (corresponding to 1100 IU of synthetic vitamin
E per day or 1500 IU of natural vitamin E per day)
(1). The increase in all-cause mortality has obvious public
health importance and represents a qualitative departure
from previous findings.
weiter:
Zitat:
In fact, some researchers warned against the longterm
administration of mega-dosages of vitamin E because
it could be associated with many adverse effects (57). In
vitro studies have shown that vitamin E may have prooxidant
effects at high doses (58, 59). In in vitro models,
the pro-oxidant effect of vitamin E on low-density lipoproteins
is related to the production of the alpha-tocopheroxyl
radical, which can be inhibited by co-antioxidants such as
vitamin C (60). However, the trials that combined highdosage
vitamin E with vitamin C (48, 49, 51) showed
increased mortality in the vitamin E groups, with the exception
of the small Polyp Prevention Study (PPS) (46).
High dosages of vitamin E may displace other fat-soluble
antioxidants (for example, alpha-tocopherol) (61), disrupting
the natural balance of antioxidant systems and increasing
vulnerability to oxidative damage. Vitamin E may also inhibit
human cytosolic glutathione S-transferases, which
help detoxify drugs and endogenous toxins (62).
Vitamin E also has anticoagulant properties, possibly
by interfering with vitamin K–dependent clotting mechanisms
(63). In fact, the Alpha-Tocopherol, Beta Carotene
(ATBC) Cancer Prevention Study (38) showed a statistically
significant increased risk for hemorrhagic stroke
among participants assigned to vitamin E.
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