A southern African herb sold as a natural testosterone booster. Its appeal rests entirely on a few rat studies; the testosterone effect is unverified in people. The same doses that raised hormones stressed the liver and kidneys and worsened blood fats, and the herb can interfere with many medications. Large unknowns paired with real warning signs. (Full Review)
| Marker | Target | Why |
|---|---|---|
| ALT (alanine aminotransferase) | ~10–26 U/L | Detects liver-cell injury, the main animal signal |
| AST (aspartate aminotransferase) | ~10–26 U/L | Complements ALT for liver injury |
| GGT (gamma-glutamyl transferase) | <25 U/L (men) | Sensitive marker of liver/bile stress and oxidative load |
| Total bilirubin | 0.3–1.0 mg/dL | Rose in treated rats; reflects liver clearance |
| Creatinine / eGFR | eGFR >90 mL/min/1.73 m² | Tracks the renal tubular toxicity seen in animals |
| Total testosterone | ~500–900 ng/dL (men) | Primary intended target of the intervention |
| Free testosterone | Upper third of reference range | The bioactive fraction driving any effect |
| Estradiol | ~20–30 pg/mL (men) | Rat data suggested estrogen reduction |
| LH (luteinizing hormone) | 1.5–9 IU/L | Tests the proposed HPG-axis mechanism |
| Lipid panel (HDL, triglycerides) | HDL >50 mg/dL; TG <100 mg/dL | Captures the pro-atherogenic shift seen in rats |
Cadence: Liver/kidney panel and lipids at baseline and again at ~4–8 weeks; hormone markers (total/free testosterone, estradiol, LH) at baseline and after 6–8 weeks, then every 3–6 months only if continued.