Two inexpensive, long-used oral medications — one for erectile difficulty, one for cholesterol — each block a different step in how tumor cells obtain cholesterol. The most reliable benefits lie outside cancer. Against cancer the record is thin, drawn from health records rather than treatment trials. The combination itself is untested; risks are well characterized and mostly modest. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Alanine aminotransferase (ALT) | 10–26 U/L (men), 8–22 U/L (women) | Detects statin liver toxicity and distinguishes it from liver metastases |
| Creatine kinase (CK) | Below 200 U/L and stable against the individual's own baseline | Separates benign muscle ache from muscle injury and impending rhabdomyolysis |
| LDL cholesterol | 1.4–1.8 mmol/L (55–70 mg/dL) on treatment | Confirms the statin is actually suppressing cholesterol synthesis at the dose used |
| HbA1c | 4.8–5.4% (29–36 mmol/mol) | Catches the modest statin-attributable drift toward type 2 diabetes |
| Estimated glomerular filtration rate (eGFR) | Above 90 mL/min/1.73 m² | Kidney injury is the pathway by which rhabdomyolysis becomes life-threatening |
| Seated and standing blood pressure | Seated 110–125/70–80 mmHg with a standing drop under 10 mmHg systolic | Quantifies the vasodilatory burden of the PDE5 inhibitor and its additive effects |
| Thyroid-stimulating hormone (TSH) | 0.5–2.0 mIU/L | Undiagnosed hypothyroidism multiplies statin muscle risk and mimics its symptoms |
Cadence: 6 weeks after starting each agent, again at 3 months, then every 6 months once stable, with creatine kinase and liver enzymes repeated at any point that muscle symptoms, dark urine or jaundice appear.