This is a resend as a Plain Text message. The Rich Text version did not appear to post. I think because it is too large. I have revised it slighly from the Rich Text version.
Selenium To understand the importance of selenium, you need first to understand how silver is excreted from body. Tests indicate that the great majority of ingested silver is excreted through the feces (liver) and very little through the urine (kidney). Additionally, the path for the excretion of silver in the feces was in the bile from the gallbladder into the small intestine.This is known as biliary excretion. From "Spacecraft Water Exposure Guidelines for Selected Contaminants: Volume 1" (To save time, unless otherwise noted quotes in the following post will be from this document unless otherwise noted): "When colloidal silver was administered to Wistar rats orally at 1.68 g/kg for 4 d or 0.42 g/kg for 12 d, about 2-5% of the dose was absorbed (Dequidt et al. 1974, as cited in ATSDR 1990). In another study by Scott and Hamilton (1950), it was found that when carrier-free radioactive silver (<1 :g; 1 :Ci) was intragastrically administered to rats, 99% of the dose was eliminated in the feces and 0.18% was eliminated in the urine within 4 d. The total tissue distribution of the radioactivity was about 0.84% of the dose." ..."Scott and Hamilton (1950) studied the distribution of silver after an intramuscular administration of radioactive metallic silver alone as a tracer dose and then coadministered with two doses of nickel nitrate (0.4 mg/kg/d and 4.0 mg/kg/d). They reported that when excretion in the feces was decreased, a corresponding increase was noted in the deposition of silver in the pancreas, gastrointestinal tract, and thyroid. This increase suggested that the liver elimination pathway might be saturated. Several studies indicate that the elimination of silver follows a 2- or 3- exponential profile, one with a short half-life and others with a half-life of several days. In the Newton and Holmes (1966) study cited above, calculation of the amount of silver excreted in the feces by a man who accidentally inhaled an unknown amount of radioactive silver dust indicated that elimination from the body followed a biphasic exponential decay curve.the first phase had a half-life of 1 d, and the second terminal phase had a half-life of 43 d. Matuk (1983) reported similar results after an intraperitoneal injection of radioactive silver. There was an initial rapid loss of radioactivity from plasma, liver, and kidneys, which was followed by a slower rate of loss. The loss was somewhat linear and slower from forebrain and spleen. As shown above, silver is excreted predominantly in the feces and, to a minor extent, in the urine following an oral dose. The rate of excretion is rapid in the first week and then slows, showing biphasic elimination kinetics in humans given silver acetate orally (East et al. 1980). Furchner et al. (1968) also reported that when radioactive silver nitrate was administered orally to mice, rats, dogs, and monkeys, 90-98% of the absorbed dose was eliminated in the feces (within 2-4 d) and only minor amounts were excreted in urine. They also reported interspecies differences in the clearance of silver. A 2-exponential component described the elimination data in mice and monkeys, and a 3-exponential component described the data from rats and dogs. Differences in the transit time through the gut has been offered as possible explanation (the transit time is 8 h in mice and rats and about 24 h in dogs and monkeys) (Furchner et al. 1968). It might also be attributed to the interspecies differences in biliary excretion rate reported by Kalaasen (1979)." Sorry for so long an extraction but it is important to understand the role of the biliary excretion path and the rate of silver excretion. I will repeat a small part of the quote above: "They reported that when excretion in the feces was decreased, a corresponding increase was noted in the deposition of silver in the pancreas, gastrointestinal tract, and thyroid. This increase suggested that the liver elimination pathway might be saturated." One way to increase silver retention is to take o much silver that the biliary excretion path is saturated and cannot process out the silver fast enough. This brings up the question of just how much silver can the body excrete in a day. The following study puts that at about 1 mg of silver per day (or 3.4 oz of 10 ppm CS): "In a study involving biologic monitoring of workers (n = 37) in one of the silver smelting and refining industries in which the exposure is entirely by inhalation, silver was found in the blood (0.011 :g per milliliter [mL]), urine (<0.005 :g/mL), and feces (15 :g/g). Control subjects excreted about 1.5 :g/g in the feces (n = 35). The author suggests that human fecal excretion of silver at exposure levels equal to the Threshold Limit Value (TLV) (0.1 mg per cubic meter [m3]) would be about 1 mg of silver per day (Di- Vincenzo et al. 1985)." If you exceed this limit continuously over a period of time silver will be deposited in the tissues. But not all the silver you take is absorbed into the blood stream. The report contains a lot of animal test data but information on human absorption of ingested silver is scant. The researcher finally made an educated guess, based on animal studies, that 10% of ingested silver is absorbed into the bloodstream. )Your guess is as good as mine as to whether this is correct.) That would indicate that you can take up to 34 oz of 10 ppm CS per day and not saturate the biliary excretion path. Obviously if something physically impedes biliary excretion path silver will be stored in the tissues. This is where gallstones and the gallbladder can be an issue. (I wonder if liver flushes, which actually flush the gallbladder, would be a good thing to do occasionally while on silver.) And now about selenium. Selenium readily binds with silver to form silver selenide. Silver selenide has a very low solubility in water. The quote in the original post shows that silver selenide deposits are found in the skin of argyia persons. But selenium is necessary to a properly functioning liver. A deficiency of selenium, or vitamin-E. causes liver necrosis which will shut down the biliary excretion path. Obviously this must be prevented. The potential for selenium deficiency is increased by silver combining with selenium and forming silver selenide and reducing the bioavailable selenium. Some more excerpts: "Wagner et al. (1975) did not find any growth depression or liver necrosis when Holtzman rats (10 per group) were given silver acetate in drinking water at 7.6 mg/kg/d for 52 d while ingesting a diet that had the recom mended concentrations of selenium and vitamin E. In another study by Diplock et al. (1967), no effects were seen in Holtzman rats given silver at 97 mg/kg/d as silver acetate in water for 50 d when the diet was complete. Liver necrosis was seen only in rats fed a vitamin-E deficient diet." ..." Silver has also been reported to inhibit glutathione (GSH) peroxidase, a seleno-enzyme. Administration of silver acetate at 751 parts per million (ppm) (silver at 484 mg/L or 73 mg/kg/d) in water for 15 wk to young Holtzman rats (fed a diet adequate in vitamin E and selenium) reduced liver GSH peroxidase activity to 5% of controls. In the erythrocytes and the kidneys, the enzyme activities were reduced to 37% of controls (Wagner et al. 1975). The same authors reported that when the rats were exposed to silver in drinking water at 76 mg/L (7.3 mg/kg/d) for 52 d, GSH peroxidase was only at 30% of the levels in control rats fed selenium at 0.5 ppm in the diet. These effects are probably due to the selenium deficiency caused by silver." ..." Diplock et al. (1967) reported that vitamin E and selenium in the diet could significantly influence the toxicity of silver. When weanling Norwegian hooded rats fed a basal vitamin-E deficient diet were provided drinking water containing silver at 970 mg/L (as silver acetate), all rats developed liver necrosis within 2-4 wk and died. In another group, when selenium was added at 1 ppm to the vitamin-E deficient diet, and the drinking water contained silver acetate, only four of nine rats died. In another group that was fed a diet containing vitamin E and was sacrificed after 50 d of silver exposure, no liver necrosis was found. Bunyan et al. (1968) reported similar observations in rats exposed to silver at 650 mg/L (as silver acetate) in drinking water. Liver necrosis was seen when the dietary selenium was reduced. Necrosis was induced at much lower doses of silver (80 mg/L). Vitamin E appeared to reverse that effect. Also, Grasso et al. (1969) reported that when silver (silver acetate) was fed either in the diet (at 130-1,000 ppm, or 4-33 mg/kg/d) or in drinking water (97.5 mg/kg/d) to vitamin-E deficient rats, fatal necrosis was noted. Alexander and Aaseth (1981) reported that depletion of liver GSH by diethyl maleate decreased biliary excretion of silver into the bile. Selenite also inhibited the biliary excretion of silver and increased its retention in the tissues. It was suggested that selenite formed an insoluble complex with silver that retarded biliary excretion. It is not clear if that is in any way related to the effect of selenium-containing diets in reducing the GSH peroxidase (see Wagner et al. 1975, described above)." Some good news is that vitamin-E helps protect the liver and may even help protect against liver necrosis when selenium is low but probably not when selenium is missing. This is why I think that taking high dose vitamin E is good. Also, I did not come across any negative interactions between silver and vitamin E. Please note in the quotes above the following: "Alexander and Aaseth (1981) reported that depletion of liver GSH by diethyl maleate decreased biliary excretion of silver into the bile. Selenite also inhibited the biliary excretion of silver and increased its retention in the tissues." On one hand selenium is necessary to prevent liver necrosis and causing decreased biliary excretion of silver into the bile. On the other hand selenium forms selenite with silver and can inhibit the biliary excretion of silver and increase silver's retention in the tissues. Catch 22! The recipes in the first post are based on the belief that selenium helps remove silver from the body. What I have been able to find says that selenium causes silver to be deposited in the tissues rather than excreted. I admit to having having some problem with an article at silver medicine (http://www.silvermedicine.org/argyria.html) Here is an excerpt from the silver medicine article: "As an example, the EPA RISK studies document clinical evidence demonstrating that a selenium deficiency increases the risk of argyria, and an over-abundance of selenium in the body may increase the silver deposited in non-critical internal tissues ( the silver buildup in the latter case does not enduce a toxic reaction to silver, however, increased levels of silver were measured in some organs ). The body utilizes selenium to help eliminate silver from the body: Silver bonds with selenium. When the body is depleted of selenium, the amount of silver deposited into tissues is drastically increased. This was conclusively demonstrated by a researcher known as Petering in the 1970's." Yes, selenium deficency inhibits the biliary elimination of silver and if you eliminate the selenium deficiency, silver excretion increases signicicantly due to a now properly functioning liver. But what is missed in the recipes, and possibly in the Silver Medicine article, is that increased selenium does not help eliminate silver from the body. The following studies clearly document that selenium eliminates silver from the bloodstream but by causing it to DEPOSIT IN THE TISSUES. This is why I think you should not megadose selenium when taking silver. Studies: Relationship of silver with selenium and mercury in the liver of two species of toothed whales (odontocetes) (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6V6N-3YMFRDK- 2V&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searc hStrId=943300636&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVer sion=0&_userid=10&md5=0b0ab2f770a9f71d8d02f950cb336911) "Like mercury, silver was positively correlated with selenium in both pilot and beluga whales. This suggests a possible role for selenium in the accumulation and storage of silver in both species of whales, and raises questions about the potential for silver at such high concentrations to affect radical-scavenging enzyme systems in these marine mammals." 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)." 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." Selenium in nutrition (http://books.google.com/books?id=UIvn2gR2P60C&pg=PA54&lpg=PA54&dq=silve r+selenium&source=bl&ots=CHufuaFTtL&sig=CUX8XoF4FDgxdEq9sJhsti0ZmEw&hl=e n&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)." The Blue Man - Silver and Selenium (http://www.jeolusa.com/APPLICATIONS/REALab/TheBlueMan/tabid/503/Default .aspx) Silver saved the Blue Man from selenium toxicity. Just a curious FYI. I had been wondering if all types of selenium cause problem interactions with silver. The following study seems to indicate that use of the selenomethionine form of selenium causes significantly less accumulation of silver in the tissues and still provides the necessary support to the liver: Bioavailability of Selenite, Selenomethionine and Selenocystine in Rats with Silver Loading http://www.journalarchive.jst.go.jp/jnlpdf.php?cdjournal=bbb1961&cdvol=4 7&noissue=4&startpage=807&lang=en&from=jnlabstract I will discuss MSM and Vitamin C in another post. - Steve N -- The Silver List is a moderated forum for discussing Colloidal Silver. Instructions for unsubscribing are posted at: http://silverlist.org To post, address your message to: silver-list@eskimo.com Address Off-Topic messages to: silver-off-topic-l...@eskimo.com The Silver List and Off Topic List archives are currently down... List maintainer: Mike Devour <mdev...@eskimo.com>
