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sheldon Views: 39,181
Published: 14 years ago
 
This is a reply to # 67,345

use vitamin E capsules only from bottles labeled 100% natural!


Unless the bottle of vitamin E is labeled (100%) natural do not use it !!!
It can be 90% synthetic with much less healing benefits even if labeled natural.

the alpha-tocopherol transfer protein and vitamin e
adequacy
maret g. traber, ph.d.
associate professor of nutrition
lpi principal investigator

scott w. leonard
lpi research assistant


summary: a protein synthesized in the liver
preferentially selects the natural form of vitamin e
for distribution to the tissues. a special mouse
strain without this protein and highly susceptible to
atherosclerosis developed lesions larger and more
complex than those in mice susceptible to
atherosclerosis that have the protein. measurements of
lipid oxidation in the mice suggest that vitamin e
inhibits atherosclerosis through its antioxidant
properties. taken together, these studies indicate
that long-term optimal intake of vitamin e in humans
may protect against heart disease.

millions of americans use vitamin e supplements. most
vitamin e supplements contain synthetic
alpha-tocopherol, but unlike other vitamins, synthetic
vitamin e is not identical to natural.
alpha-tocopherol (alpha-tocopherol) is present in
nature in only one form, rrr-alpha-tocopherol. the
chemical synthesis of alpha-tocopherol results in
eight different forms, only one of which is
rrr-alpha-tocopherol. chemically synthesized vitamin e
is known as all rac-alpha-tocopherol. these forms
differ in that they can be “right” or “left” (r or s)
at three different places in the alpha-tocopherol
molecule. the most important place is what’s known as
the 2-position—half of the synthetic is 2r and half is
2s (see diagram).

to add to the confusion, vitamin e supplements are
labeled d-alpha for natural and dl-alpha for
synthetic. to study how the body uses natural or
synthetic vitamin e, we used chemically labeled forms
containing deuterium as tracers. deuterium is a
stable, non-radioactive isotope of hydrogen that is
used as a chemical tracer to study chemical reactions
and the movement and deposition of chemicals in the
body. when we fed equal amounts of deuterium-labeled
natural and synthetic vitamin e to humans, both plasma
and tissues subsequently contained twice as much
natural as synthetic vitamin e. this difference is
thought to arise from differences of the affinity of
the hepatic alpha-tocopherol transfer protein
(alpha-ttp) for the various forms, with a preference
for the 2r-alpha-tocopherol forms.

in humans, all vitamin e forms are absorbed in the
intestine. the majority of the absorbed vitamin e is
delivered to the liver, where the naturally occurring
form of vitamin e, rrr-alpha-tocopherol, is
preferentially secreted into the circulation for
delivery to tissues. importantly, humans with ataxia
from vitamin e deficiency have defects in the
alpha-ttp. these people become vitamin e deficient
because they are unable to secrete alpha-tocopherol
into the circulation. however, because the amounts and
activities of alpha-ttp have not been measured in the
patients’livers, the functions of alpha-ttp have
remained incompletely understood. moreover, the
mechanisms for the regulation of vitamin e in tissues
are not known. this led us todevelop a genetic model
of vitamin e deficiency byeliminating the alpha-ttp
gene in mice in order to characterize the function of
the protein coded for by the gene. the alpha-ttp-null
mice lack the alpha-ttp found in normal mice.

we used the alpha-ttp-null mice to test whether
alpha-ttp is responsible for maintaining plasma
alpha-tocopherol concentrations. we also wanted to
determine if alpha-ttp influences the observed
preference for natural rrr-alpha-tocopherol. even
though a human genetic mutation has produced a very
small population of people who lack the alpha-ttp,
alpha-ttp-null mice were used for these experiments
because we were able to perform well-controlled
experiments that cannot be performed with humans. we
hypothesized that alpha-ttp preferentially selects the
2r-alpha-tocopherol forms of vitamin e for secretion
into plasma and delivery to tissues. we analyzed 17
different tissues to evaluate whether alpha-tocopherol
can accumulate despite the deficiency of hepatic
alpha-ttp. mice were fed diets that contained
deuterium-labeled natural and synthetic vitamin e in a
one-to-one ratio. after the mice consumed the diet for
3 months, 85% of the vitamin e in their tissues was
found to be labeled. in the mice deficient in
alpha-ttp, the levels of vitamin e in plasma and
tissues were extremely low compared to normal mice. in
tissues from the normal mice, the ratio of natural to
synthetic vitamin e was 2 to 1, but in the
alpha-ttp-null mice there were equal, small amounts of
natural and synthetic vitamin e in tissues. these data
suggest that alpha-tocopherol concentrations are
highly dependent upon the function of alpha-ttp and
that this protein preferentially selects only the
2r-alpha-tocopherol forms from all
rac-alpha-tocopherol for secretion into plasma. in the
normal mice with alpha-ttp, the enrichment of tissues
with natural vitamin e appears to be due to uptake of
alpha-tocopherol from the plasma, which contained
twice as much natural as synthetic vitamin e.

in another study we recently published in the
proceedings of the national academy of sciences, we
used the alpha-ttp-null mice to study the relationship
between vitamin e and atherosclerosis. many experts
believe that a high plasma vitamin e concentration
protects against atherosclerosis, but the results from
clinical intervention studies published thus far have
been equivocal. in our study, alpha-ttp-null mice were
bred with a mouse strain that is very susceptible to
atherosclerosis. these “double-null” mice were then
used to test the hypothesis that a decrease in plasma
vitamin e caused by alpha-ttp deficiency would promote
atherosclerosis.

the mice were fed a chow diet that was low fat and
generally adequate for mice for 30 weeks. as expected,
we found that alpha-ttp-null mice had plasma and
tissue alpha-tocopherol concentrations only about 15%
of the levels in normal control mice. we then measured
the area of the atherosclerotic lesions. the lesion
areas in the double-null mice were about 36% larger
than in the controls that were susceptible to
atherosclerosis but not deficient in alpha-ttp. the
aortic lesions in the double-null mice consistently
had more complex lesions with necrotic cores,
cholesterol crystals, and a fibrous cap. plasma
cholesterol, vitamin c, and urate levels were similar
in the double-null mice and controls.

to study the relationship between atherosclerotic
lesion development and lipid oxidation, we analyzed
aortic levels of total f2-isoprostanes, which are
substances used as a sensitive measure of lipid
oxidation. total f2-isoprostanes were found to be
2-fold higher in the double-null mice compared to
controls, suggesting that vitamin e inhibits
atherosclerosis through its antioxidant properties.
it now appears that vitamin e can help prevent
atherosclerosis and that its deficiency will
accelerate but not cause atherosclerosis. our second
mouse study was important in understanding the role of
vitamin e in heart disease because there is no clear
evidence demonstrating how vitamin e may actually be
beneficial in preventing or decreasing cardiovascular
disease. it is known that vitamin e protects fats from
oxidizing, but now we also have an in vivo model
showing that not only is there increased fat oxidation
when animals are vitamin e deficient but also that
vitamin e is necessary to protect against
atherosclerotic lesion formation. since similar
mechanisms are likely to occur in humans, it seems
reasonable to suppose that vitamin e will help counter
oxidative stress and protect us from atherosclerosis.

calculation of the amount of alpha-tocopherol in
vitamin e supplements:
for rrr-alpha-tocopherol (natural or
d-alpha-tocopherol) multiply the iu x 0.67
example:
100 iu of natural vitamin e = 67 mg of natural vitamin
e
for all-rac-alpha-tocopherol (synthetic or
dl-alpha-tocopherol) multiply the iu x 0.45
example:
100 iu of synthetic vitamin e = 45 mg of natural
vitamin e






 

 
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