Statins block the liver enzyme that makes cholesterol, stripping artery-damaging particles from the blood. They reduce heart attacks, strokes and death from any cause. The case is strong with existing plaque, high particle counts, high inflammation or inherited high cholesterol; the gain over a few years is small when arteries are demonstrably clean. Costs are real, mostly modest and measurable. (Full Review)
| Marker | Target | Why |
|---|---|---|
| ApoB | <80 mg/dL; <60 with plaque | Particle count; the primary target |
| LDL cholesterol | <70 mg/dL; <55 with plaque | Guideline metric; basis of dose selection |
| Lp(a) | <30 mg/dL (<75 nmol/L) | Inherited risk statins raise, not lower |
| hsCRP | <1.0 mg/L | Residual inflammatory risk |
| HbA1c | 5.0–5.4% | Metabolic drift carrying the diabetes risk |
| Fasting glucose | 75–90 mg/dL | Earlier signal of insulin resistance than HbA1c |
| ALT and AST | <25 U/L men, <20 U/L women | Dose-dependent liver enzyme elevation |
| Creatine kinase | <200 U/L, stable against baseline | Separates muscle injury from nocebo |
| eGFR and creatinine | eGFR >90 mL/min/1.73 m² | Clearance affects exposure and dose |
| Thyroid-stimulating hormone | 0.5–2.0 mIU/L | Untreated hypothyroidism causes myalgia |
| Vitamin D (25-hydroxy) | 40–60 ng/mL | Deficiency causes muscle aching |
| Coenzyme Q10 | No target; track change from baseline | Proposed basis of muscle and fatigue complaints |
Cadence: Full baseline panel before the first dose. Lipids with ApoB at 6–8 weeks and after any dose change; full panel with HbA1c and liver enzymes at 6 months, then annually once stable. Creatine kinase on symptoms, not on schedule.