trigonometry1972@gmail.co
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 Posted: Thu Nov 20, 2008 11:29 am Post subject: The SELECT study was even more bogus than even I had realize |
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Some have complained for some years that the SELECT study was
planning to use and then was using the least effective form of vitamin
E
in the form of d.l alpha tocopherol. Well it seems they
also used the less effective form of selenium for PC prevention.
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Med Hypotheses. 2006;67(2):318-22. Epub 2006 Mar 30.
Cancer chemoprevention: selenium as a prooxidant, not an antioxidant.
Drake EN.
Rocky Mountain Selenium, Inc.,
2101 Ridge Road, Estes Park, Rocky Mountain, CO
80517, USA.
endrake@airbits.com
Although the average daily dietary selenium (Se) intake in the United
States is
consistently above the adult RDA of 55 microg Se/day, supranutritional
supplements of 200 microg Se/day have been shown to provide
chemopreventive
benefits against several cancers, particularly prostate cancer. The
hypothesis
herein contends that selenium compounds with the greatest
anticarcinogenic
potency are likely to be sodium selenite with Se in the +4 oxidation
state and
methylseleninic acid. These compounds exert their cancer
chemopreventive effects
by directly oxidizing critical thiol-containing cellular substrates,
and are more
effective than the more frequently preferred (used) supplements of
selenomethionine and Se-methylselenocysteine that lack oxidation
capability.
Selenate (+6 Se) the immediate precursor of selenite (+4 Se) can be
metabolically
reduced, and although less potent than the +4 Se compounds cited
above, appears
to be a more effective anticarcinogen than organic forms of dietary
selenium.
Apoptosis, an important, Se-induced anticarcinogenic mechanism, is
accomplished
by the direct oxidation of vicinal sulfhydryl groups in cysteine
clusters within
the catalytic domains of cellular enzymes (e.g., protein kinase C),
and by the
production of CH3Se-, which reacts with O2 to generate superoxide and
other
reactive oxygen species (ROS). Activated oncogenes "prime" cells for
Se-induced
prooxidative apoptosis thereby providing the needed margin for
"killing" cancer
cells while leaving normal, healthy cells unharmed. Selenoethers, such
as
selenomethionine and Se-methylselenocysteine are not oxidizing agents,
and first,
must be converted to methylselenol (CH3Se-) that can be directly
oxidized to
methylseleninic acid. The addition of methioninase, to
selenomethionine, or
beta-lyase to Se-methylselenocysteine, rapidly produces significant
amounts of
methylselenol, which may be oxidized to methylseleninic acid or may
react with O2
to produce superoxide and ROS, resulting in anticarcinogenic
activities
comparable to selenite or methylseleninic acid. The relatively large
amounts of
selenomethionine or Se-methylselenocysteine needed to produce
apoptosis in cancer
cells compared with selenite or methylseleninic acid are a probable
consequence
of low tissue levels of the required enzymes. Even though many studies
have
consistently shown that selenomethionine is an ineffective
anticarcinogen at
doses corresponding to those currently allowed by the FDA, it has been
chosen as
the Se intervention agent in the 32,500-man (phase III), NCI-funded
SELECT trial,
which tests the effectiveness of dietary supplements of dietary
supplements of Se
and tocopherol, individually or in combination, in the prevention of
prostate
cancer. In 2013, when the data are in, the value of using Se
supplements for
cancer chemoprevention is likely to be underestimated.
PMID: 16574336 |
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