A single molecule from grape seed that quiets worn-out cells at low intake and kills them at higher intake. Animal and laboratory evidence is broad; no human result exists, and how much reaches human tissue is unmeasured. Plausible harms are modest: stomach upset, headache, allergic reaction in grape-sensitive people, blocked plant-source iron absorption, added blood-thinning and blood-pressure lowering. (Full Review)
| Marker | Target | Why |
|---|---|---|
| High-sensitivity C-reactive protein | <0.5 mg/L | Tracks the inflammatory load the compound targets |
| Interleukin-6 | No established target; track change from own baseline | Core component of the inflammatory secretion pattern of senescent cells |
| Seated and standing blood pressure | <120/80 mmHg seated, <20 mmHg systolic drop on standing | Detects additive blood-pressure lowering on existing therapy |
| Platelet count | 175–250 × 10⁹/L | Bleeding margin for the platelet-inhibition risk |
| International normalised ratio | Within the prescribed anticoagulation target | Catches destabilised anticoagulation, the most consequential interaction |
| Alanine aminotransferase | 10–26 U/L women, 10–30 U/L men | Hepatic reserve against strain from concentrated botanical extracts |
| Ferritin | 50–100 ng/mL | Iron status before and during tannin exposure |
| Estimated glomerular filtration rate | >90 mL/min/1.73 m² | Baseline renal function, the organ with the largest fibrosis dataset |
| Grip strength | No established target; track change from own baseline | Human analogue of the rodent functional endpoint |
Cadence: At 4 weeks, at 12 weeks, then every 6 months while use continues. Clotting-time check brought forward to within 1–2 weeks of the first dose on anticoagulants; blood pressure logged at home twice daily for the first 4 weeks.