Colloidal silver is particularly dangerous in selenium deficiency and negatively impacts the thyroid for the following reason.
Selenium — the key to converting T4 → T3. In the thyroid gland, deiodinase enzymes (D1, D2, D3) operate, in which selenium is embedded in the active center. These enzymes convert relatively "inactive" thyroxine (T4) into active triiodothyronine (T3).
In the case of selenium deficiency, this process is slowed down, and T3 levels become low, even if T4 is normal.
Silver competes with selenium in enzymes. When colloidal silver enters the body, ionized forms of silver can bind to sulfhydryl groups of proteins and active centers of enzymes, including selenium-containing ones.
If selenium is already deficient, silver effectively blocks the remaining active centers — deiodinase enzymes stop working even more. This is a direct path to hypothyroidism.
Silver and accumulation in thyroid tissues. The thyroid gland actively accumulates trace elements (primarily iodine and selenium). In selenium deficiency, instead of selenium, silver may be "incorporated" into proteins (due to chemical similarity and replacement of active centers). In the long term, this creates structural damage to the enzymes and proteins of thyroid tissue.
Amplification of autoimmune processes. Silver, trapped in thyroid proteins, alters their structure, making them "foreign" to the immune system. This increases the risk of autoimmune attacks (like Hashimoto's), especially if there is a concurrent deficiency of antioxidants (selenium, zinc, vitamin D, glutathione).
Vicious circle: less selenium → worse detox → more silver. The thyroid loses its ability to detoxify active forms of oxygen because glutathione peroxidases (selenoproteins) work less effectively. Silver remains in the tissue even longer, further worsening the situation.
As a result: in selenium-deficient regions, the intake of colloidal silver is essentially accelerated damage to thyroid enzymes, and many processes become irreversible.
