A bacterial compound found in traces in food, sold in far larger amounts. It switches on the machinery that builds and protects the cell's energy producers. Small, mostly manufacturer-funded trials report better memory, lower inflammation and modestly lower cholesterol. The striking survival and tissue findings come from worms and mice. No long-term human data. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Serum creatinine | 0.6–1.0 mg/dL | Detects the one organ toxicity shown in animals |
| eGFR | >90 mL/min/1.73 m² | Confirms the sole clearance route is intact |
| Urinalysis (blood, protein) | Negative for both | Screens for the tubular injury seen in rats |
| hs-CRP | <0.5 mg/L | Primary human-validated inflammatory endpoint |
| LDL cholesterol | <100 mg/dL, or <70 mg/dL with existing arterial disease | Identifies who can respond and tracks the effect |
| Triglycerides | <80 mg/dL | Context for the lipid response; PQQ did not move it |
| ALT | 10–26 U/L (men), 8–22 U/L (women) | Baseline liver safety; hepatic benefits are rodent-only |
| Anti-Müllerian hormone | Age-appropriate; no PQQ-specific target exists — track change from the individual's own baseline | The only human signal of harm |
| Fasting glucose | 75–85 mg/dL | Context for the rodent metabolic claims |
Cadence: Full panel at baseline. Kidney markers and lipid panel repeated at 12 weeks, then every 6–12 months. Cognitive testing at 12 weeks. Anti-Müllerian hormone rechecked at 3 months where it was measured at baseline.