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
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 2006–2011 with a typical study size of 1,039 participants.
Based on 6 studies · 2 meta-analyses · 3 RCTs · 111,472 total participants
Confidence
HighBy outcome
Rosuvastatin (Crestor) has an evidence score of 4.5/10 — strong evidence based on 6 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.
Nicotinamide Riboside
Mostly mechanism / observationalA vitamin B3 precursor that reliably raises cellular NAD+ levels and is well tolerated — but human trials have so far shown mostly null or mixed results on the functional outcomes (muscle, metabolism, blood pressure, cognition) that elevation is meant to drive.
Alirocumab (Praluent)
Notable regimens that report including Rosuvastatin (Crestor) — documented, not endorsed.
Last reviewed June 2026 · evidence from 6 studies · how we score
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.
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.
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.
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.
Tap node to isolate • Pinch to zoom • Tap edge for research
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.
Loading: No loading dose; started at 5–10 mg once daily and titrated to lipid targets.
Can be taken without food
| Form | Type |
|---|---|
| 💊Oral tablet (rosuvastatin 5–20 mg) | Recommended |
| 💊Higher-dose tablet (40 mg) for selected high-risk patients | Alternative |
| 💊Fixed-dose combinations with ezetimibe | Alternative |
Started low and titrated to LDL/ApoB targets; often combined with ezetimibe when additional LDL lowering is needed.
Minimum: 4 weeks
Optimal: 52 weeks
Cycling: Not required
Note: Once daily at any time of day thanks to the long half-life; separate from antacids and bile-acid sequestrants by a few hours.
Dose-response data unavailable. The current published research for Rosuvastatin (Crestor) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
Lowers LDL-C ~45–55% at standard doses — among the strongest of any statin.
In JUPITER, reduced major cardiovascular events ~44% and all-cause mortality ~20% in primary prevention with elevated hsCRP.
Serial-IVUS trials (ASTEROID, SATURN) show coronary atheroma regression; METEOR slowed carotid intima-media thickening.
Myalgia (muscle aches) is the most common complaint; rhabdomyolysis is rare but serious, especially with interacting drugs.
Statins as a class slightly raise new-onset type 2 diabetes risk (~9% relative); a trade-off against large cardiovascular benefit.
Small, usually transient transaminase elevations; clinically significant liver injury is rare.
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.
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.
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.
A fully human monoclonal-antibody PCSK9 inhibitor (Praluent), injected under the skin every 2 weeks, that lowers LDL cholesterol by ~50–60%. In the ODYSSEY OUTCOMES trial of ~18,900 post-heart-attack patients it reduced major cardiovascular events and showed a possible all-cause mortality signal. Generally well tolerated; injection-site reactions and high cost/access are the main trade-offs. Prescription drug, not a supplement.
May increase INR; monitor anticoagulation when starting or changing dose.
Reduce rosuvastatin absorption; separate dosing by at least 2 hours.