RE: Colloidal Silver and Selenium

July 22, 2009

Jay,

I hesitate to respond to you regarding CS and selenium. I seem to upset some when I post information that does not agree with commonly accepted beliefs. But I do not want to see misinformation about important colloidal silver issues propagated. Selenium is one of those issues.

Just FYI, I use CS daily and in larger doses than most, I think. Like you I want to avoid argyria no matter how remote the possibility of getting it. I have been researching this subject and as yet I have not found a plausible cure for argyria. I am continuing to research this subject but I do think that there are things that a knowledgeable person can do to minimize the potential for getting argyria and things that a person can do to actively reduce silver accumulation. Prevention as opposed to reversal. Right now I use bentonite clay regularly, zeolite periodically (cycling) and I am researching several forms of EDTA.

Optimal selenium supplementation for cancer and optimal selenium supplementation for CS are not the same. You mention a cure for argyria that calls out selenium. Actually, I know of two separate and apparently independent cures that call out selenium as the primary anti argyria agent and know of a third formula that is not posted anywhere on the internet. The problem with all of them is that selenium will not work for reversing argyria and in fact the current scientific data shows that excessive amounts of selenium combined with high levels of silver can aggravate argyria. I believe that those cures are old and based on old and outdated studies. I cannot believe that anyone would intentionally misrepresent or misinterpret scientific studies.

First, you should supplement with selenium when using CS for extended periods. Selenium is critical for proper liver functioning and deficient selenium levels will cause liver necrosis. And that liver necrosis will also shut down the biliary excretion path eliminating the excretion pathway for 99% of ingested silver. If the body has no way to get rid of the silver it will deposit the excess silver in the tissues. Vitamin E helps protect the liver and can to some extent protect the liver from low selenium levels but it cannot compensate for very low levels of selenium. So be sure to supplement with Vitamin E too.

One problem is that silver binds easily with most forms of selenium. High levels of silver can bind up so much selenium that a selenium deficiency can result without supplementation.

It is this binding of silver by selenium that is the basis for the belief that selenium will help remove silver from the tissues and carry it out of the body. Thereby reversing argyria. However, this is not correct. In actuality, selenium binding with the silver reduces silver excretion and causes more silver to be deposited in the tissues. Thereby increasing the risk of argyria. However there is one form of selenium that does not bind with silver and cause this effect. That form of silver is selenomethionine. If you are using a lot of CS, you should take selenomethionine supplementation. However this form of selenium is not a form that is effective against cancer to my knowledge.

There was one study that showed increased levels of silver in the feces when selenium was taken orally but there was no increased levels of silver excreted when the selenium was given intravenously. Apparently, the orally administered selenium was binding with silver in the digestive tract and preventing the silver or selenium from ever entering the bloodstream. This indicates that you should not take silver and selenium at the same time but separated in time. By several hours in my opinion.

As you can see, I believe that it is important to understand how selenium and silver interact in the body to be able to supplement optimally with selenium.

I didn't provide study references in my last post, although I could have, but I will this time.

Here are some of the studies and books supporting what I have said with some passages quoted from the studies.

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:

Silver is excreted in the bile by using glutathione (GSH) as a carrier molecule.

Selenite, a form of selenium, inhibits the excretion of silver while silver does not influence the excretion of selenium into bile.

Selenite causes the retention of silver in the blood, kidney and brain.

The effects above are caused by silver-selenium complexes that are nearly water insoluble and probably unavailable for biliary excretion.

Therefore, selenium reduces the excretion of silver and causes retention in the blood and tissues.(my comment)

Selenium in nutrition

(http://books.google.com/books?id=UIvn2gR2P60C & pg=PA54 & lpg=PA54 & dq=silver+selenium & source=bl & ots=CHufuaFTtL & sig=CUX8XoF4FDgxdEq9sJhsti0ZmEw & hl=en & ei=uUNJStGJMYyW9gS-n-GTDQ & sa=X & oi=book_result & ct=result & resnum=4)

“Selenium has been shown to reduce the toxicity of cadmium, inorganic and methyl mercury, thallium and silver. Selenium apparently decreases the rate of excretion of these toxic substances and changes the distribution of these elements in the body (Parizek et al., 1974).”

Modification of a Selenium Toxicity in Chicks by Dietary Silver and Copper

(http://jn.nutrition.org/cgi/content/abstract/105/6/769)

“The results of these experiments suggest that silver modifies selenium toxicity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.”

Interactions of Selenium and Antioxidants with Mercury, Cadmium and Silver

(http://toxsci.oxfordjournals.org/cgi/pdf_extract/1/5/368)

“Selenium causes the accumulation of metals in tissue, whereas vitamin E does not have this effect t(Black el al., 1980, Welsh, 1979).”

Toxicological Profile for Silver

http://www.atsdr.cdc.gov/toxprofiles/tp146-c2.pdf

“Under conditions of exposure to high doses of selenium, the sulfur can be replaced by selenium (Berry and Galle 1982). 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 above, 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 document in the following document.

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.”

Remember that silver is excreted in the bile by using glutathione (GSH) as a carrier molecule. And the study above determined that selenomethionine provides for synthesis of glutathione without combining with silver.

There are more studies/articles but I think these cover it well enough.

- Steve

oleander soup oleander soup On Behalf Of JayMonday, July 20, 2009 5:01 PMoleander soup Subject: Re: Colloidal Silver

Thanks Melly,I know about that. I am working on slowly building a supply of vitamins, supplements and other items to do scientific research on myself. First, though I have to see about filing for bankruptcy. I remember getting a post from someone in this group that went into detail about a "cure" for argyria. I tried to do a search, but couldn't find what I was looking for. Not all selenium is the same. I think it is difficult to get the right one. I just did a search for selenium on the group and the most recent is March 16, 2009. I just got a post a week or so ago that mention selenium. Something is wrong with .All the best to you and everyone,Jay

July 23, 2009

I was wrong when I said that selenomethionine may not be affective against cancer. See:

Selenomethionine inhibits growth and suppresses cyclooxygenase-2 (COX-2) protein expression in human colon cancer cell lines.

http://www.ncbi.nlm.nih.gov/pubmed/12432249

Currently, selenium (in the form of high selenium containing yeast or selenomethionine) is being evaluated for anticancer effects against both human colon polyp recurrence and human prostate cancer, respectively. Chemical speciation analysis of the high selenium containing yeast indicates that selenomethionine (SeMet) is a major constituent of selenized yeast. We tested the hypothesis that SeMet might affect colon cancer cell growth by mechanisms involving cyclooxygenases (COX). The growth of all four-colon cancer cell lines tested was inhibited by selenomethionine. Furthermore, selenomethionine decreased COX-2 protein and PGE2 levels in HCA-7 cells. Selenomethionine suppressed COX-2 RNA levels in HCA-7 cells which could account for decreased COX-2 protein levels. Finally, the addition of PGE2 protected cells from the antiproliferative effects of selenomethionine in a concentration dependent manner. Selenomethionine might regulate COX-2 at the transcriptional level. These data suggests that Se-Met-induced cell growth inhibition may be, in part, mediated by COX-2 dependent mechanisms. The results of this study support the use of selenium agents in colon cancer chemoprevention trials.

- Steve