Chrysin is a plant compound that destroys cancer cells in the lab but is barely absorbed when swallowed, so its lab promise has not translated to people. No human cancer benefit is proven. The most plausible role is local action in the gut, and its main real-world concern is interfering with other medications. (Full Review)
| Marker | Target | Why |
|---|---|---|
| ALT / AST | ALT ~10–26 U/L; AST ~10–26 U/L | Chrysin and interacting drugs are processed by the liver |
| Estradiol (if hormone-sensitive context) | Varies by sex and menopausal status | Chrysin inhibits aromatase in the lab; relevant only with high-absorption forms |
| Comprehensive metabolic panel (incl. kidney markers) | eGFR >90 mL/min/1.73m²; normal electrolytes | Conjugates are renally excreted; gauges clearance capacity |
| Therapeutic drug levels (if on interacting medication) | Drug-specific target range | Chrysin may raise levels of conjugation-dependent drugs |
Cadence: Baseline, then roughly 4–8 weeks, then periodically (every 6–12 months) where interacting co-medications apply