Crestor®
Rosuvastatin Calcium
Version 2025-04 · Last reviewed April 1, 2025 · Methodology
List Price
$300+ (brand)
With Insurance
$10–30
Supplement Questions
Omega-3 Fatty Acids
Patients on statins frequently ask about omega-3 for triglyceride management and cardiovascular support.
Vitamin D3
Some evidence that vitamin D status affects statin metabolism. Both address cardiovascular risk factors and are frequently taken together.
CoQ10
Statins inhibit the same pathway used to synthesize CoQ10 in the body. Many patients taking Crestor ask whether CoQ10 supplements address statin-related muscle symptoms.
How It Works
Rosuvastatin works identically to atorvastatin — blocking HMG-CoA reductase to reduce liver cholesterol synthesis and force the liver to clear LDL from the blood. It is more hydrophilic (water-soluble), which reduces its uptake into muscle and may translate to slightly lower myopathy risk per dose.
Why the side effects happen
Same mechanism as atorvastatin. Rosuvastatin's higher hydrophilicity means less penetration into muscle and brain, potentially explaining slightly lower rates of myalgia in head-to-head trials. However, the difference is modest and individual variation dominates.
When Will I Feel It?
LDL reduction is faster than most statins — significant drops seen within 2 weeks. Full effect at 4–6 weeks.
LDL begins falling. More rapid onset than many other statins due to higher potency.
Full lipid effect achieved. Standard recheck at 6–8 weeks from starting.
Cardiovascular risk reduction accumulates. JUPITER trial: 44% reduction in major cardiac events in patients with elevated CRP.
Adherence Note
Rosuvastatin does not need to be taken in the evening (unlike simvastatin). Take at the same time daily. Avoid large amounts of grapefruit juice — less interaction than with atorvastatin but still present.
Medical Disclaimer
The information on this page is compiled from publicly available clinical trial data, FDA prescribing information, and peer-reviewed literature. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations. Individual responses to medications vary. Always consult a qualified healthcare provider before starting, stopping, or changing any medication.
Common Side Effects
While taking this medication, you may experience the following common side effects. We've included tips on how to manage them.
Muscle pain (myalgia)
10%Most common reason for stopping statins. CoQ10 100–200mg may help. Report any severe or proximal muscle weakness immediately.
Liver enzyme elevation
3%Baseline LFTs before starting; recheck at 3 months. Usually resolves with dose reduction.
New-onset diabetes
9% relative increaseClass effect. Annual fasting glucose. This is a real, documented risk — especially in pre-diabetic patients.
Cognitive effects / memory fog
4%FDA 2012 safety communication. "Fuzzy thinking" and memory lapses reported; usually reversible on stopping.
Proteinuria at high doses
3% (at 40mg)Annual urine protein test at doses >20mg; benign in most cases but monitor kidney function.
Serious Adverse Effects
- • Rhabdomyolysis — rare but life-threatening muscle breakdown; dark/cola-colored urine with muscle weakness requires emergency care
- • Severe myopathy — proximal muscle weakness (difficulty climbing stairs, rising from chair) should be reported immediately
- • Liver failure — rare; any jaundice, dark urine, or severe abdominal pain requires immediate evaluation
- • Statin-induced immune-mediated necrotizing myopathy (IMNM) — rare but may continue worsening even after stopping statin
Drug Interactions
Major Interactions (Avoid)
Moderate Interactions (Caution)
Food Interactions
When to Contact Your Doctor
This medication requires ongoing medical supervision. The following situations warrant a prompt conversation with your prescribing physician — do not wait for your next scheduled appointment.
Contact soon if you notice
- Rhabdomyolysis — rare but life-threatening muscle breakdown; dark/cola-colored urine with muscle weakness requires emergency care
- Severe myopathy — proximal muscle weakness (difficulty climbing stairs, rising from chair) should be reported immediately
- Liver failure — rare; any jaundice, dark urine, or severe abdominal pain requires immediate evaluation
- Statin-induced immune-mediated necrotizing myopathy (IMNM) — rare but may continue worsening even after stopping statin
- If you have established heart disease: stopping statins abruptly has been associated with rebound inflammation — discuss with cardiologist
Also discuss if you want to
- Review whether this medication is still appropriate for you
- Consider dosage adjustments based on response
- Explore lifestyle or non-drug alternatives
- Understand stopping or tapering options
- Plan monitoring labs and follow-up
In the US, call 911 or go to the nearest emergency room for severe symptoms. Poison Control: 1-800-222-1222.
Special Populations
Safety classifications for specific groups — discuss with your provider before use.
Statins inhibit cholesterol synthesis required for fetal development. Stop before conception or immediately when pregnancy confirmed.
Stop while breastfeeding — infant cholesterol synthesis would be impaired.
Estrogen keeps your liver's LDL receptors active — those are the structures that pull LDL out of your bloodstream. When estrogen drops at menopause, there are fewer receptors and LDL naturally rises. Many women are prescribed a statin for numbers that climbed during the menopause transition. Ask your doctor: is hormone therapy a better first step? It addresses the cause, not just the number.
Only for familial hypercholesterolemia in children 7+. Lifestyle interventions should be maximized first.
Greater myopathy risk due to age-related decline in muscle mass. Start at 5mg; maximum 20mg in elderly with risk factors.
Severe renal impairment (eGFR <30): start at 5mg; do not exceed 10mg.
Active liver disease or unexplained persistent transaminase elevation: contraindicated.
FDA Adverse Event Reports
Patient-filed reports from the FDA FAERS database · refreshed daily
Community Reports
User-reported experiences — anonymous & anecdotal
Medical Disclaimer
The information on this page is compiled from publicly available clinical trial data, FDA prescribing information, and peer-reviewed literature. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations. Individual responses to medications vary. Always consult a qualified healthcare provider before starting, stopping, or changing any medication.
Metabolic & Lifestyle Alternatives
Cardiovascular Risk & Lipids: The Particle Size Reality
LDL-C (the number statins are prescribed to lower) is not the same as cardiovascular risk. The atherogenic fraction is small dense LDL — driven primarily by excess carbohydrates and de novo lipogenesis in the liver, not by dietary fat. Carbohydrate restriction shifts LDL from atherogenic small dense particles to benign large buoyant particles, lowers triglycerides 40–50%, raises HDL, and improves flow-mediated dilation — addressing the root metabolic driver that LDL-C alone misses.
Important context: Evidence quality varies across these approaches. Some are well-studied with randomized controlled trial data; others are based on observational or smaller studies. These interventions are not guaranteed to replace medication for all patients. Discuss with your doctor whether any of these are appropriate for your clinical situation.
Low-carbohydrate / Ketogenic Diet
Eliminates the refined carb/excess glucose load that drives hepatic de novo lipogenesis (DNL) → triglycerides → small dense LDL (sdLDL)
Shifts LDL particle pattern from atherogenic small dense (Pattern B) to benign large buoyant (Pattern A); lowers triglycerides 40–50%; raises HDL; improves flow-mediated dilation. LDL-C may rise modestly — but NMR particle analysis and cardiovascular risk markers consistently improve.
Aerobic exercise + Zone 2 training (150 min/week)
Improves endothelial nitric oxide bioavailability and mitochondrial fat oxidation
Directly improves flow-mediated dilation (FMD) — a more accurate endothelial risk marker than LDL-C alone. Network meta-analysis: equivalent to statin therapy for all-cause mortality in primary prevention.
Omega-3 EPA (prescription-grade, 2–4g/day)
Directly suppresses hepatic VLDL/triglyceride synthesis; reduces sdLDL production at the source
REDUCE-IT: 25% reduction in CV events; lowers triglycerides 25–45%; improves flow-mediated dilation. Attacks the DNL → sdLDL pathway upstream.
Bergamot polyphenol extract (1000mg/day)
Natural HMG-CoA reductase inhibitor — same enzyme targeted by statins
RCT: LDL -23%, HDL +22%, triglycerides -30%, without muscle toxicity. Improves the full lipid panel without the metabolic side effects of pharmaceutical statins.
Mediterranean diet (fat-inclusive)
Olive oil, fatty fish, nuts — emphasis on what PREDIMED actually tested: adding fat, not restricting it
PREDIMED: 30% reduction in cardiovascular events. Critically, benefit came from adding olive oil and nuts — increasing fat intake — not from a low-fat protocol. Dietary fat was protective.
Key Studies
Global Prescribing & Pricing
US prescribes Crestor and statins for primary prevention at 2–3× the rate of Europe — despite similar cardiovascular mortality
United States
$15–40 (generic)/mo
ACC/AHA guidelines: treat at 10-year CV risk ≥7.5% — captures many "borderline" patients
JUPITER expanded prescribing to normal-cholesterol patients with elevated CRP; no lifestyle prerequisite for primary prevention
Usually covered
United Kingdom
~$2–5/mo
NICE: 10-year CV risk ≥10% threshold for primary prevention treatment
QRISK3 calculator required; explicit lifestyle intervention documented before treating borderline-risk patients
Fully covered by NHS
Germany
~$10–25/mo
ESC guidelines: treat based on overall CV risk plus LDL level combination
Lifestyle program with 3-month compliance check required before statin for primary prevention per DGK guidelines
Covered by GKV
Japan
~$12–28/mo
Lower statin prescribing; CAC scoring used before treating borderline cases
Coronary artery calcium (CAC) scoring eliminates borderline prescriptions; diet counseling standard before any statin initiation
Covered by JHIS
Australia
~$8–18 (PBS)/mo
PBS restricts statin use to higher-risk patients per NHF guidelines
Absolute cardiovascular risk calculation required; lifestyle counseling for 6 months mandatory for low-to-moderate risk
Covered by PBS with criteria
The JUPITER trial — funded by AstraZeneca — justified prescribing Crestor to people with normal cholesterol but elevated CRP. This dramatically expanded the treatable population. Independent re-analyses found JUPITER overstated benefits by 50–200% due to premature trial stopping. The lead researcher held a patent on the CRP test used. Europe requires a 10% 10-year CV risk threshold; the US treats at 7.5%.
Clinical Trials & Funding
Understanding who funds research helps contextualize results. Industry-funded trials are not automatically invalid — they undergo the same FDA review — but declared conflicts and sponsor effects are worth knowing. All linked trials can be verified on ClinicalTrials.gov.
Funding Sources
AstraZeneca funded the JUPITER trial — the study that dramatically expanded Crestor's market by demonstrating benefit in people with NORMAL cholesterol but elevated CRP (inflammation marker). JUPITER was stopped early, which statistically inflates apparent benefit. The lead investigator received substantial AstraZeneca funding. The trial was criticized for stopping before cardiovascular mortality benefit was established, and for including a composite endpoint that obscured which outcomes were actually improved.
Declared Conflicts of Interest
AstraZeneca's JUPITER trial was controversial among independent cardiologists. The lead investigator (Dr. Paul Ridker) held a patent on the hsCRP test used to select patients — creating a significant conflict of interest in a trial that justified widespread testing and prescribing. Multiple independent re-analyses found JUPITER overstated benefits by 50–200% due to early stopping.
Key Efficacy Results
44% relative risk reduction in CV events in JUPITER (from 1.8% to 0.9% absolute — 0.9% absolute risk reduction); 50% LDL reduction at standard doses
Referenced Studies
Each study carries a Cochrane RoB-2 risk-of-bias badge — tap the badge for details.
Evidence & Transparency
Cochrane RoB-2 (Risk of Bias)
Badges reflect an editorial assessment using Cochrane's RoB-2 tool domains: randomization, intervention deviation, missing data, outcome measurement, and selective reporting. These are not certified Cochrane reviews. Learn more ↗
CMS Open Payments
Manufacturer payment disclosures are reported via the CMS Sunshine Act. Disclosure is legally required and does not imply bias or misconduct. Language uses "may," "suggests," or "appears" — never definitive clinical claims. CMS Open Payments ↗
Live Clinical Trials
Live from ClinicalTrials.gov · refreshed every 4 hours
Currently enrolling, active, and recently completed studies involving Rosuvastatin Calcium. Data is pulled directly from the U.S. National Library of Medicine.
Recent Research
Live from PubMed · peer-reviewed literature · refreshed every 4 hours
Most recently indexed clinical trials and systematic reviews mentioning Rosuvastatin Calcium in PubMed.
Source Documentation
Structured citations for referenced clinical trials
Each referenced trial is listed with its registry ID, funding source, and bias assessment. Use the copy button to generate a formatted citation.
| Trial | Registry ID | Cite |
|---|---|---|
| JUPITER Trial (AstraZeneca) | NCT00239681 | |
| JUPITER Results (NEJM) | PMID:18997196 | |
| HOPE-3 Statin Trial | PMID:20585568 |
Bias ratings use Cochrane RoB-2 methodology. Editorial assessment — not a certified Cochrane review.
Our MethodologyMedical Disclaimer
The information on this page is compiled from publicly available clinical trial data, FDA prescribing information, and peer-reviewed literature. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations. Individual responses to medications vary. Always consult a qualified healthcare provider before starting, stopping, or changing any medication.
Stopping This Medication Safely
Statins do not cause physical dependence and can be stopped without tapering. LDL will return toward baseline within 4–6 weeks of stopping. This is medically expected, not a rebound.
What Published Research Shows About Stopping This Medication
This summarizes what published research documents — it is not personal medical advice. Any changes to your medication require discussion with your prescribing physician.
- ·Research shows no pharmacological taper is needed for statins
- ·Research supports discussing with a prescriber before stopping, particularly in secondary prevention (known heart disease)
- ·Clinical guidelines suggest rechecking the lipid panel 6–8 weeks after stopping to assess baseline return
- ·Research supports checking CK levels in patients stopping due to muscle pain and allowing 4–6 weeks for recovery before considering a different statin
Warning Symptoms — Contact Your Doctor If You Experience:
- If you have established heart disease: stopping statins abruptly has been associated with rebound inflammation — discuss with cardiologist
- Severe muscle pain, weakness, or dark urine (possible rhabdomyolysis — seek care even after stopping)
- Rapid onset of chest pain after stopping statin in secondary prevention patients
Never change or stop a medication without consulting your prescribing physician.
Questions for Your Doctor
Questions to Ask
- 1.Can we do a calcium scan of my heart arteries (called a CAC score) first, to actually confirm I have plaque before starting a statin?
- 2.Can we test the SIZE of my LDL particles, not just the total number? Small, dense LDL is the type that causes harm — and a standard cholesterol panel doesn't tell you which kind you have.
- 3.I'm in or past menopause — could lower estrogen be the reason my LDL went up? Estrogen helps your body clear cholesterol. Should hormone therapy be considered before a statin?
- 4.Has my thyroid been tested? Low thyroid raises cholesterol and is a fixable cause that doesn't need a statin.
- 5.Could sugar, refined carbs, or alcohol be driving my cholesterol numbers? These foods raise the harmful, small, dense LDL — more than eating fat does.
- 6.Out of 100 people exactly like me, how many will actually avoid a heart attack if they take this for 5 years? I want the real number, not just the percentage reduction.
- 7.Have I already had a heart attack or stroke, or is this to prevent one from ever happening? The benefit is very different in each case.
- 8.If I develop muscle pain, memory problems, or my blood sugar increases, what do we do?
Lab Tests to Request
- Fasting lipid panel — ask about LDL particle size (NMR) if available
- hsCRP (inflammation marker)
- Fasting glucose and HbA1c — statins can raise blood sugar
- Liver enzymes (ALT, AST) — baseline before starting
- TSH (thyroid) — underactive thyroid raises cholesterol and is treatable
- Calcium scan (CAC score) — confirms whether plaque is actually present
- CoQ10 level — statins lower CoQ10, which can cause muscle problems
Medical Disclaimer
The information on this page is compiled from publicly available clinical trial data, FDA prescribing information, and peer-reviewed literature. It is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment recommendations. Individual responses to medications vary. Always consult a qualified healthcare provider before starting, stopping, or changing any medication.
Frequently Asked Questions About Crestor®
- What is Crestor® used for?
- Crestor® (Rosuvastatin Calcium) is a Statin (HMG-CoA Reductase Inhibitor) manufactured by AstraZeneca / Generic. FDA-approved indications include: Primary hyperlipidemia (LDL reduction); Mixed dyslipidemia; Cardiovascular risk reduction; Familial hypercholesterolemia; Primary prevention in high CRP + multiple risk factors (JUPITER indication).
- What are the common side effects of Crestor®?
- Common side effects of Crestor® include: Muscle pain (myalgia) (10%); Liver enzyme elevation (3%); New-onset diabetes (9% relative increase); Cognitive effects / memory fog (4%); Proteinuria at high doses (3% (at 40mg)).
- How much does Crestor® cost?
- Crestor® list price is approximately $300+ (brand). With insurance it typically costs $10–30; without insurance approximately $15–40 (generic).
- Who funded the clinical trials for Crestor®?
- AstraZeneca funded the JUPITER trial — the study that dramatically expanded Crestor's market by demonstrating benefit in people with NORMAL cholesterol but elevated CRP (inflammation marker). JUPITER was stopped early, which statistically inflates apparent benefit. The lead investigator received substantial AstraZeneca funding. The trial was criticized for stopping before cardiovascular mortality benefit was established, and for including a composite endpoint that obscured which outcomes were actually improved.
- How strong is the clinical evidence for Crestor®?
- Key studies: JUPITER trial (2008), CORONA trial, HOPE-3 trial. 44% relative risk reduction in CV events in JUPITER (from 1.8% to 0.9% absolute — 0.9% absolute risk reduction); 50% LDL reduction at standard doses Potential conflicts of interest: AstraZeneca's JUPITER trial was controversial among independent cardiologists. The lead investigator (Dr. Paul Ridker) held a patent on the hsCRP test used to select patients — creating a significant .
- Are there non-drug alternatives to Crestor®?
- LDL-C (the number statins are prescribed to lower) is not the same as cardiovascular risk. The atherogenic fraction is small dense LDL — driven primarily by excess carbohydrates and de novo lipogenesis in the liver, not by dietary fat. Carbohydrate restriction shifts LDL from atherogenic small dense See the Alternatives tab for full details.
Get notified when we update Crestor®
We'll email you when new evidence, safety updates, or alternatives are added.
No spam. Unsubscribe anytime.