We use essential cookies (authentication, your saved goals/stack) by default. With your permission we’ll also enable privacy-respecting analytics (Vercel Web Analytics, anonymous load-time metrics) and error-replay diagnostics (Sentry — DOM snapshots only when an error fires) so we can fix bugs faster. Learn more about cookies
Rosuvastatin (Crestor) — HMG-CoA reductase inhibitor (statin)
A prescription oral statin (Crestor) that inhibits HMG-CoA reductase, the rate-limiting enzyme of cholesterol synthesis — one of the most potent statins, lowering LDL-C ~45–55%. In JUPITER (~17,800 people with elevated hsCRP), rosuvastatin cut major cardiovascular events and all-cause mortality; IVUS trials (ASTEROID, SATURN) show coronary plaque regression. Risks: myalgia, rare rhabdomyolysis, a small new-onset-diabetes signal, and transient liver-enzyme rise. Prescription drug, not a supplement.
Prescription medication — not a dietary supplement
Rosuvastatin (Crestor) is a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Most Rosuvastatin (Crestor) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from high-quality meta-analyses and randomised trials published 2006–2026 with a typical study size of 1,039 participants.
Based on 218 studies · 23 meta-analyses · 192 RCTs · 111,472 total participants
Confidence
High confidenceBy outcome
Rosuvastatin has some of the strongest human cardiovascular evidence of any lipid-lowering drug: a well-defined HMG-CoA-reductase mechanism, potent ~45–55% LDL lowering, the JUPITER primary-prevention trial showing reduced major cardiovascular events and all-cause mortality, IVUS-documented coronary plaque regression, and the CTT meta-analysis establishing a dose-response LDL→event relationship. The score is tempered by real trade-offs — myalgia, rare rhabdomyolysis, a small new-onset-diabetes signal, and transient liver-enzyme elevations.
253 rigorous studies
227 randomized trials · 23 meta-analyses · 15 systematic reviews
Our evidence rating for Rosuvastatin (Crestor) is accountable to this entire body of rigorous research indexed in PubMed — not a hand-picked subset.
PubMed · as of Jul 2026
107 trials ongoing or recruiting · 604 completed on ClinicalTrials.gov
120 of the completed trials have posted results
Registered trials show research momentum for Rosuvastatin (Crestor), not proof of effect — a registration is a plan, and posted results are sponsor-reported, not peer-reviewed. They are never counted toward the evidence rating above.
Browse these trials on ClinicalTrials.govClinicalTrials.gov · as of Aug 2026
Rosuvastatin is an oral HMG-CoA reductase inhibitor (statin) that blocks the rate-limiting enzyme of hepatic cholesterol synthesis.
Depleting intracellular cholesterol up-regulates hepatic LDL receptors, which clear LDL-C from the blood — the same class mechanism shared by all statins, but rosuvastatin is among the most potent, lowering LDL-C roughly 45–55% at standard doses.
It is a first-line drug for LDL lowering and atherosclerotic cardiovascular disease (ASCVD) prevention.
Its landmark outcome trial, JUPITER (NEJM 2008, ~17,800 apparently healthy people with normal LDL but elevated high-sensitivity CRP), showed rosuvastatin 20 mg reduced major cardiovascular events by ~44% AND all-cause mortality by ~20% — a rare mortality signal in a primary-prevention statin trial.
Imaging trials reinforce the mechanism: METEOR (JAMA 2007) slowed carotid intima-media thickness progression in low-risk subclinical atherosclerosis, while ASTEROID (JAMA 2006) and SATURN (NEJM 2011) used serial intravascular ultrasound to demonstrate regression of coronary atheroma under high-intensity rosuvastatin.
The broader statin evidence base is anchored by the Cholesterol Treatment Trialists' (CTT) meta-analysis of ~170,000 participants, which established that each ~1 mmol/L LDL reduction cuts major vascular events by just over a fifth — a dose-response that underpins the 'lower LDL is better' principle and rosuvastatin's role as a backbone of aggressive ApoB lowering in physician longevity stacks.
The honest trade-offs are real: muscle symptoms (myalgia, very rarely rhabdomyolysis), a small but consistent increase in new-onset type 2 diabetes (statins ~9% relative increase in a collaborative meta-analysis), and occasional transient transaminase elevations.
Rosuvastatin is renally cleared in part, requires dose reduction in severe renal impairment and in some Asian populations, and has notable interactions (cyclosporine, gemfibrozil, certain antivirals).
It is a prescription drug presented here for informational purposes only, not as a recommendation; the score reflects genuinely strong human LDL, plaque, and cardiovascular-outcome evidence weighed against its tolerability and metabolic trade-offs.
Competitively inhibits HMG-CoA reductase, the rate-limiting enzyme of hepatic cholesterol synthesis, lowering intracellular cholesterol.
Falling intracellular cholesterol up-regulates hepatic LDL receptors, which clear circulating LDL-C and ApoB particles from the blood.
Sustained LDL lowering plus anti-inflammatory (CRP-lowering) effects stabilize and can regress atherosclerotic plaque on imaging.
How Rosuvastatin (Crestor) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Use a reduced dose (typically max 10 mg/day) and monitor — rosuvastatin is partly renally cleared.
Higher plasma exposure reported; a lower starting dose is recommended.
Contraindicated — statins are avoided in pregnancy and lactation.
Markedly raises rosuvastatin blood levels and myopathy risk — combination contraindicated.
Increases rosuvastatin exposure and myopathy/rhabdomyolysis risk; avoid or limit the dose.
Some HIV/HCV antivirals raise rosuvastatin levels; dose limits apply.
May increase INR; monitor anticoagulation when starting or changing dose.
Reduce rosuvastatin absorption; separate dosing by at least 2 hours.
Tip: Usually mild; report persistent or severe pain. Check CK if symptoms are significant; consider dose reduction or a statin holiday under a clinician.
Tip: Small, usually transient transaminase rise; periodic liver-function monitoring.
Tip: Small absolute increase, outweighed by cardiovascular benefit in higher-risk patients; monitor glucose/HbA1c.
Tip: Rare but serious; risk rises with high doses and interacting drugs. Seek care for severe muscle pain, weakness, or dark urine.
Rosuvastatin (Crestor) has an evidence score of 4.5/10 — emerging evidence based on 206 indexed studies, including 2 meta-analyses. A prescription oral statin (Crestor) that inhibits HMG-CoA reductase, the rate-limiting enzyme of cholesterol synthesis — one of the most potent statins, lowering LDL-C ~45–55%. In JUPITER (~17,800 people with elevated hsCRP), rosuvastatin cut major cardiovascular events and all-cause mortality; IVUS trials (ASTEROID, SATURN) show coronary plaque regression. Risks: myalgia, rare rhabdomyolysis, a small new-onset-diabetes signal, and transient liver-enzyme rise. Prescription drug, not a supplement. Representative study: PMID 21067804.
The commonly studied dose of Rosuvastatin (Crestor) is 5–20 mg once daily (up to 40 mg in selected high-risk patients), titrated to LDL/ApoB targets — under a clinician. A prescription drug; not a self-directed supplement regimen.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Timing is flexible for Rosuvastatin (Crestor) — consistent daily use matters more than the time of day. Rosuvastatin's long ~19-hour half-life lets it be taken at any time of day, unlike short-acting statins that are dosed in the evening.
Rosuvastatin (Crestor) is generally safe at recommended doses, with a few precautions worth noting. The most commonly reported side effects are myalgia (muscle aches), elevated liver enzymes, new-onset type 2 diabetes. Use caution if any of these apply to you: Active liver disease or unexplained persistent transaminase elevations; Pregnancy and breastfeeding; Known hypersensitivity to rosuvastatin.
Pioglitazone (Actos)
Mostly mechanism / observationalAn oral thiazolidinedione (Actos) diabetes drug that improves insulin sensitivity via PPAR-gamma. It drew geroscience interest after reducing recurrent stroke/MI in insulin-resistant non-diabetics (IRIS) and improving NASH liver histology — but weight gain, fluid retention / heart-failure risk, fracture risk, and a debated bladder-cancer signal keep enthusiasm in check. Prescription drug, not a supplement.
CoQ10
Likely helpsA lipid-soluble antioxidant central to mitochondrial energy production, with the strongest trial support for fertility/IVF outcomes and heart failure.
Red Yeast Rice
Likely helpsFermented rice containing natural statins that effectively lower LDL cholesterol — the original statin.
Berberine
Likely helpsActivates AMPK to regulate blood sugar, improve insulin sensitivity, and support lipid metabolism — comparable to metformin in some trials.
Explore: Best supplements for Vitality & Longevity
Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 218 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Tap node to isolate • Pinch to zoom • Tap edge for research