iThyroid.com

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JJ: The following study indicates that silver might a key supplement that could suppress TED.  TED (thyroid eye disease) is characterized by excessive growth of the fibroblasts at the back of the eye.  This study shows that "silver ions greatly inhibited fibroblast proliferation." 

Silver fits in with the cadmium hypothesis.  Silver is just to the left of cadmium in the Periodic Table and excessive amounts of cadmium might suppress silver, just as excessive amounts of zinc (just above cadmium) suppress copper (just above silver).  Since we've seen that copper is a suppressive mineral in the functions of the thyroid and the immune system, it is not unreasonable to suspect that silver is also involved in suppressive functions such as suppressing fibroblast growth.  This is an extremely good reason for those suffering from TED to take a colloidal silver supplement (follow directions on the bottle).

Certain concentrations of the antiseptic AgNO3, a potent broad-spectrum antimicrobial agent, exert cytotoxic effects on fibroblasts and endothelial cells which are directly related to the wound-healing process. In vitro assessment of human fibroblast cytotoxicity has proved to be a useful method for characterizing cell toxicity mechanisms of topically-applied antiseptics. In the present study human dermal fibroblasts were exposed to AgNO3 at concentrations of 4.12-82.4 microM for 8 and 24 h. Silver ions greatly inhibited fibroblast proliferation and prolonged AgNO3 exposure produced Ag-dependent cell loss. In the sequence of events occurring during our in vitro experimental model, the inhibitory action on DNA synthesis was the primary event in AgNO3 cytotoxicity, associated with significant loss of cell protein.silver nitrate cytotoxicity in human dermal fibroblasts.doc

Female SJL (H-2s) mice developed serum IgG anti-nucleolar antibodies (ANoA) after 5 weeks treatment with 0.05% or 0.01% silver nitrate (AgNO3) in drinking water. Five more weeks of treatment increased the ANoA titre to 3410 +/- 853 and 640 +/- 175 (reciprocal mean +/- s.e.m.), respectively. Controls receiving ordinary tap water and mice given 0.002% AgNO3 showed no antinucleolar antibodies. The high-titre ANoA targeted a 34-kD nucleolar protein identified as fibrillarin, the major autoantigen in murine mercury-induced autoimmunity and in a fraction of patients with systemic scleroderma. Serum autoantibodies to chromatin or histones, kidney, spleen, stomach, thyroid, or skin antigens (except the nucleolus) were not found in any of the mice. There was no consistent significant increase of serum IgG1, IgG2a, IgG2b, or IgG3 concentrations after AgNO3 treatment compared with controls. Mice treated with 0.05% AgNO3 for 10 weeks showed a slight decrease in serum IgG1, IgG2b and IgG3 concentrations. These mice also showed a small but statistically significant increase in renal, mesangial IgM deposits, which was not accompanied by any increase in C3c deposits, whereas mice given lower doses of silver nitrate showed no significant increase in mesangial immunoglobulin immune deposits. Systemic vessel wall immune deposits were not found in any of the mice. In mice given 0.05% silver nitrate, the kidney showed the highest concentration of silver (12.2 +/- 0.09 micrograms Ag/g wet weight; mean +/- s.e.m.), followed by the spleen (8.7 +/- 1.3), and the liver (3.9 +/- 0.4). Treatment with 0.01% silver nitrate caused a different distribution of silver, with the highest concentration in the spleen (2.1 +/- 0.16 micrograms Ag/g), followed by the kidney (0.63 +/- 0.037), and the liver (< 0.29 micrograms Ag/g; mean). Silver seems to be a more specific inducer of antinucleolar/anti-fibrillarin autoantibodies than mercury and gold, lacks the general immune stimulating potential of mercury, and has only a weak tendency to induce renal immune deposits. These observations suggest that the autoimmune sequelae induced in mice by metals is dependent, not only upon the genetic haplotype of the murine strain, but also on the metal under investigation. silver induces anti-fibrillarin autoantibodies.doc

Menkes disease is a genetic disorder of copper metabolism. Copper uptake and retention assays on fibroblast or amniotic fluid cell cultures have been used for pre- and postnatal diagnosis. These copper loading tests are complicated by the use of 64Cu, which is not commonly available and has a very short (12.8 hours) physical half life. Besides copper, silver is also a substrate for the bacterial homologue of the Menkes transport protein. We report here that loading tests using radioactive silver (110mAg), instead of copper, can be used for the diagnosis of Menkes disease. 110mAg is commercially available and has a convenient physical half life of 250 days, which makes it suitable for use in diagnostic laboratories. Our studies support the hypothesis that reduction of divalent to monovalent copper is an essential step preceding transport.silver loading of fibroblasts in Menkes disease.doc

The following study indicates abnormalities of vitamin B12, folic acid, and thyroidal function were found in workers at a silver-reclaiming factory. While the study looks at cyanide intoxication, there is the possibility that excess silver interferes with these functions. 

JAMA 1985 Jan 18;253(3):367-71

Cyanide intoxication among silver-reclaiming workers.

Blanc P, Hogan M, Mallin K, Hryhorczuk D, Hessl S, Bernard B

Thirty-six former workers in a silver-reclaiming facility who had been exposed over a long-term to excessive levels of cyanide were studied to determine acute and residual toxic reactions. The study involved physical examinations, laboratory studies, and a questionnaire to determine levels of exposure, symptoms during employment, and current symptoms. Questionnaire data showed that during the time of active employment there was a high prevalence of symptoms that are consistent with acute cyanide toxic reactions. A significant positive trend for prevalence of cyanide-related symptoms measured against levels of exposure was demonstrated, supporting a dose-response effect. Some symptoms occurring seven or more months after exposure had ceased also exhibited a dose-response trend. Mild abnormalities of vitamin B12, folate, and thyroid function were detected and suggest long-term cyanide effects.

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