Silver kills microbes on contact, and topical silver dressings have measured healing effects. Oral use has no demonstrated benefit in people; the one controlled human comparison showed no improvement over saltwater. Absorbed silver builds up in skin, eyes, liver and kidney; permanent blue-grey discoloration is well documented after months of daily use. Topical use keeps exposure local; oral does not. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Serum silver | Below 1 µg/L, ideally undetectable | Confirms whether systemic loading is happening at all |
| 24-hour urine silver | Below 2 µg/L | Shows current excretion and recent intake |
| ALT and AST | Both below 25 U/L | Liver is the main site of silver deposition |
| Creatinine and eGFR | eGFR above 90 mL/min/1.73 m² | Kidney is the second deposition site and the route for soluble silver |
| CBC with differential | No new value below the laboratory range in any cell line | Soluble silver exposure has been linked to changes in blood-cell counts |
| Serum selenium | 110–150 µg/L | Silver is trapped as silver selenide, so depletion is plausible with sustained intake |
| TSH | 0.5–2.0 mIU/L | Silver may reduce levothyroxine absorption when taken close together |
| Standardised skin and gum photographs | No established numeric target — track each image against the individual's own baseline | Earliest detectable sign of argyria appears in sun-exposed skin and at the gum line |
Cadence: Baseline, then serum silver and photographs at three months and every six months for as long as use continues; liver enzymes, kidney function, blood count and selenium every six to twelve months.