Thanks, Steve. I just checked and it is selenomethionine. I take 200 mcg
at dinnertime. So I will keep my level around 4 oz/day unless I get sick
and need to increase it short term.
I appreciate the assistance.
PT
----- Original Message -----
From: "Norton, Steve" <[email protected]>
To: <[email protected]>
Sent: Friday, August 27, 2010 10:12 AM
Subject: Re:CS>My first post - selenium
At 4 oz a day, you are at the max daily amount I would take for 10 ppm
CS. Personally, at that amount I would use the selenomethionine form of
selenium. Do you know that the selenium you are taking is not
selenomethionine?
Taking the selenium at a different time helps in that it prevents the
selenium from complexing with the silver in the digestive tract. If they
did complex in the digestive tract, the selenium/silver complex would
just pass on out in the feces. But the amount of CS you are taking (at
10 ppm) is around the maximum amount the liver can excrete in a day. (I
know about the Altman study that indicates that most of the silver in
EIS is excreted by the kidney. But the info is misleading if you do not
really understand EIS in vivo and how different forms of silver are
excreted by the body. But it is somewhat complex and I do not want to
get into that here.) So the chances of selenium and silver complexing is
significant and I would use selenomethionine to avoid it. Just FYI, I
personally only supplement with selenomethionine. Many forms of selenium
complexes with silver but selenomethionine is the only form I have study
data on that indicates it does not complex with silver.
Below I provide some info on selenium and silver.
- Steve N
Hepatobiliary transport and organ distribution of silver in the rat as
influenced by selenite.
http://www.ncbi.nlm.nih.gov/pubmed/7292506
"Bile from rats injected with 110mAgNO3 (1 micromol/kg) were
fractionated on Sephadex G-15 revealing binding of silver to one high
molecular weight substance and one low molecular weight substance
eluting corresponding to the void volume and glutathione (GSH)
respectively. Fractionation of AgNO3 and GSH mixed in vitro gave rise to
a polynuclear complex and a 1 : 1 complex of Ag+-GSH which both eluted
corresponding to silver in bile. Depletion of GSH in the liver by
diethylmaleate (3.9 mmol/kg) caused a parallel decrease in the biliary
excretion of both silver and reduced GSH. These findings support the
hypothesis that silver is excreted into bile by a GSH-dependent
mechanism most likely using GSH as a carrier molecule. Selenite (1
micromol/kg) inhibited the biliary excretion of silver while AgNO3 (1
mumol/kg) did not influence the excretion of selenium into bile.
Pretreatment with selenite (1 micromol/kg) also caused a retention of
silver (AgNO3, 1 micromol/kg) in the blood, kidney and brain. The liver
content of silver was decreased and the organ to plasma ratio of silver
was unchanged for erythrocytes, but decreased for the brain, kidney and
liver, respectively. The effects caused by selenite are attributed to
the formation of Ag2Se complexes which are nearly water insoluble and
probably unavailable for biliary excretion. Selenium metabolites
(GSSeSG, GSSeH) which are excreted into bile are probably not available
for complexing with Ag+."
[I will try and simplify the text above:
1. Silver (in solution) is excreted in the bile by using
glutathione (GSH) as a carrier molecule.
2. Selenite, a form of selenium, inhibits the excretion of silver
while silver does not influence the excretion of selenium into bile.
3. Selenite causes the retention of silver in the blood, kidney and
brain.
4. The effects above are caused by silver-selenium complexes that
are nearly water insoluble and probably unavailable for biliary
excretion.
5. Ergo, selenium reduces the excretion of silver and causes
retention in the blood and tissues.]
Toxicological Profile for Silver
http://www.atsdr.cdc.gov/toxprofiles/tp146-c2.pdf
"The deposition of silver in the kidney was increased under conditions
of high selenium exposure. This may be important in the development of
argyria in people exposed to silver who ingest foods that contain large
amounts of selenium."
"It should be noted that selenium plays a dual role in the toxicity of
silver. On the one hand, it increases the silver deposition rate in body
tissues, which suggests that humans exposed to both high selenium and
high silver may be more likely to develop argyria. On the other hand, a
Selenium deficient diet combined with high silver intake can cause liver
necrosis."
As I mentioned, the selenomethionine form of selenium does not cause an
accumulation of silver in the tissues and still provides the necessary
support of the liver. That is documented in the following study:
Agricultural and Biological Chemistry, Vol.47
Bioavailability of Selenite, Selenomethionine and Selenocystine in Rats
with Silver Loading
To view study select the full text abstract at:
http://www.journalarchive.jst.go.jp/english/jnlabstract_en.php?cdjournal
=bbb1961&cdvol=47&noissue=4&startpage=807
"Nevertheless, selenomethionine was the most effective for synthesis of
glutathione perioxidase in the rat liver with silver. This is presumably
because selenomethionine would be hard to combine with accumulating
silver in the liver unless metabolized."
Silver in solution is excreted in the bile by using glutathione (GSH) as
a carrier molecule. And the study determined that selenomethionine
provides for synthesis of glutathione without combining with silver.
Small silver particulate is excreted by the kidney.
There are more studies/articles but I think these cover it well enough.
-----Original Message-----
From: needling around [mailto:[email protected]]
Sent: Thursday, August 26, 2010 6:46 PM
To: [email protected]
Subject: EXTERNAL:Re: Re:CS>My first post
Hi Steve,
Is there a dosage level of CS that requires the change to
selenomethionine
instead of selenium? I take selenium once a day in the evening and am
wondering if I need to change the formulation. I take approximately 2
oz CS
am and pm. If the CS is taken hours away from the selenium does that
help?
Thank you.
PT
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