Marshall writes, over three posts : "Argyria is caused by the same mechanism that is used when developing photographs. It is the same thing. If you start with a salt of silver, and expose it to light, some of it will reduce to silver metal. Then if you have a developer (caffine is a good developer) in an alkaline solution (blood is normally alkaline), additional silver will plate out from the compound onto the metallic particles, making them grow. That is the photographic process, and that is how one gets argyria.
Now, the process requires silver salts. There are no substitutes. Colloidal silver contains no silver salts. Basically silver salts are what are in unexposed film. Silver colloid is what is in a developed photograph. If you put a developed photo into the sun what does it do. It fades, it doesn't turn darker. That is because a developed photo has no silver salts to add to the silver particles since it is already nothing but reduced silver particles. Thus colloidal silver cannot cause argyria. Theoretically I guess one could take CS with sufficient ppm and in sufficient quantity to cause aggregation, but one would likely become sick from too much water first, as the amounts would be truely phenominal..." "...If I recall the silveroz product claims that it is ionic silver, not colloidal silver. I questioned a year or so ago whether or not silver oz could lead to argyria on this very list, but at that time no one reported such problems. I do not believe the silver oz product is the same as what we consider colloidal silver..." "...Does anyone know if chelation acts on CS in your blood? I believe that chelation only works on single atoms, but could be wrong. If it worked on clusters then it should get rid of argyria, right...?" Marshall and all. As far as I can ascertain, it is impossible to absorb metals (minerals) in anything other than ionic form, ie single atomic ions, as opposed to aggrigates, colloids or groups of metals. Colloids and metallic clusters are ionised by the gastric juices so that they may be complexed by metal transporters across the intestinal wall. If this is true, it would tend to make most of the statements above redundant. In the development of Argyria, I believe it is the total silver load which is important not the source, as the silver, once absorbed, is likely to be indistinguishable from one source to another. If silver is found in surface tissue in large amounts, as a result of the overwhelming of the natural chelating mechanisms, then it will be complexed by chlorine, sulphur or selenium etc. and may be photo-reduced to form dark pigments. I believe it is wrong to state that silver colloids cannot cause Argyria, other than to say that the total silver load required is unlikely to be achieved in the normal course of events. There is no reason to think that silver will not be chelated as any other monovalent ion. Different chelating agents have preferences for different valencies (divalent, trivalent etc.), and it would be wise, in my opinion, to forego silver intake during the course of the therapy so that the therapy can be directed towards to removing toxic minerals, unhindered. Here is a representative abstract regarding mineral absorption : "The regulation of mineral absorption in the gastrointestinal tract. Proc Nutr Soc 1999 Feb;58(1):147-53 (ISSN: 0029-6651) Powell JJ; Jugdaohsingh R; Thompson RP [Find other articles with these Authors] Gastrointestinal Laboratory, Rayne Institute, St Thomas' Hospital, London, UK. jonpo...@ucdavis.edu. The absorption of metal ions in the mammalian single-stomached gut is fortunately highly selective, and both luminal and tissue regulation occur. Initially, assimilation of metal ions in an available form is facilitated by the intestinal secretions, chiefly soluble mucus (mucin) that retards hydrolysis of ions such as Cu, Fe and Zn. Metal ions then bind and traverse the mucosally-adherent mucus layer with an efficiency M+ > M2+ > M3+. At the mucosa Fe3+ is probably uniquely reduced to Fe2+, and all divalent cations (including Fe2+) are transported by a membrane protein (such as divalent cation transporter 1) into the cell. This minimizes absorption of toxic trivalent metals (e.g. Al3+). Intracellular metal-binding molecules (such as mobilferrin) may be present at the intracellular side of the apical membrane, anchored to a transmembrane protein such as an integrin complex. This mobilferrin would receive the metal ion from divalent cation transporter 1 and, with part of the integrin molecule, transport the metal to the cytosol for safe sequestration in a larger complex such as ferritin or 'paraferritin'. beta 2-Microglobulin and HFE (previously termed human leucocyte antigen H) may be involved in stabilizing metal mobilferrin-integrin to form this latter complex. Finally, a systemic metal-binding protein such as transferrin may enter the antiluminal (basolateral) side of the cell for binding of the sequestered metal ion and delivery to the circulation. Regulatory proteins, such as HFE, may determine the degree of ion transport from intestinal cells to the circulation. Gradients in pH and perhaps pCa or even pNa could allow the switching of ions between the different transporters throughout this mechanism. " Regards Ivan. -- The silver-list is a moderated forum for discussion of colloidal silver. To join or quit silver-list or silver-digest send an e-mail message to: silver-list-requ...@eskimo.com -or- silver-digest-requ...@eskimo.com with the word subscribe or unsubscribe in the SUBJECT line. To post, address your message to: silver-list@eskimo.com Silver-list archive: http://escribe.com/health/thesilverlist/index.html List maintainer: Mike Devour <mdev...@eskimo.com>
