A five-plant oral blend, one daily dose, meant to prompt cells to build their own protective enzymes. The laboratory case is coherent; benefit in people has not followed. Trials found almost nothing, and nothing shows it changes how a person feels, functions or how long they live. Safety looks unremarkable at the marketed dose; the evidence is thin. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Alanine aminotransferase | 10–20 U/L (men), 8–17 U/L (women) | Most sensitive marker of liver cell injury |
| Aspartate aminotransferase | 10–20 U/L | Pairs with ALT to separate liver from muscle origin |
| Alkaline phosphatase | 50–90 U/L | Detects the cholestatic pattern seen in ashwagandha liver injury |
| Gamma-glutamyl transferase | Under 20 U/L | Confirms that a raised ALP is of liver origin |
| Total bilirubin | 0.3–1.0 mg/dL | Detects the jaundice that defined every reported ashwagandha case |
| Serum uric acid | 3.5–5.5 mg/dL (men), 3.0–5.0 mg/dL (women) | The one blend-specific signal reported, and directly actionable in gout |
| High-sensitivity C-reactive protein | Under 0.5 mg/L | The inflammatory outcome the blend is marketed to improve |
| Thyroid-stimulating hormone | 0.5–2.0 mIU/L | Ashwagandha shifts thyroid hormone modestly |
| Free thyroxine | 1.0–1.5 ng/dL | The specific hormone shown to rise with ashwagandha |
| Ferritin | 50–150 ng/mL (men), 30–120 ng/mL (women) | Curcumin and catechins chelate iron and can deepen a deficiency |
Cadence: Baseline set before the first dose; liver panel and uric acid repeated at 8–12 weeks; full panel at 6 months; every 6–12 months thereafter while use continues