An inexpensive nutrient that, at gram doses, changes blood fats more broadly than almost anything sold without a prescription, including the inherited particle few treatments touch. Those changes are firmly established; fewer heart attacks or longer life are not. Added to intensive cholesterol treatment it adds nothing, while bringing new diabetes, liver strain and flushing. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Apolipoprotein B | < 80 mg/dL; < 60 mg/dL if high cardiovascular risk | Counts every artery-clogging particle; the primary efficacy target |
| Lipoprotein(a) | < 75 nmol/L (< 30 mg/dL) | The particle niacin lowers that few other agents touch |
| LDL cholesterol | < 70 mg/dL if high risk; < 100 mg/dL otherwise | Standard efficacy check, though apolipoprotein B is more informative |
| HDL cholesterol | 50–80 mg/dL | Tracks the effect niacin produces most strongly |
| Triglycerides | < 80 mg/dL | Falls early on niacin; a sensitive marker of the fat-release effect |
| Fasting glucose | 75–86 mg/dL | The earliest signal of niacin's glucose harm |
| HbA1c | 4.8–5.3% | Confirms whether a glucose drift is real rather than day-to-day noise |
| Fasting insulin | 2–5 µIU/mL | Detects rising insulin resistance before glucose moves |
| Alanine aminotransferase | 10–26 U/L (men); 8–22 U/L (women) | The stop signal for hepatotoxicity |
| Serum urate | 3.5–6.0 mg/dL | Niacin competes with urate for kidney excretion, precipitating gout |
| High-sensitivity C-reactive protein | < 1.0 mg/L | Tracks the inflammatory effect, which only appears if baseline exceeds 3 mg/L |
| Homocysteine | < 9 µmol/L | Screens for strain on methyl-group supply from clearing surplus niacin |
Cadence: Full baseline set before starting; then liver enzymes, fasting glucose and lipids at 6–8 weeks after reaching the target dose, again at 6 months, then every 6–12 months while treatment continues. Any dose increase resets the 6–8 week clock. Serum urate at baseline and annually, or sooner if joint symptoms appear.