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Rosuvastatin is a unique member of the statin family. It is a hydrophilic statin, meaning it has an affinity for water and tends to stay in the bloodstream rather than deeply penetrating muscle and other tissues. This property is thought to contribute to a lower risk of side effects, especially muscle-related symptoms, compared to some other statins (3).
When prescribing or taking rosuvastatin, it’s important to consider not only its cholesterol-lowering properties but also its broader impact on cardiovascular health—and the timing of when it’s taken. Like other statins, rosuvastatin has effects that go far beyond lowering cholesterol. Many of these additional benefits help reduce overall cardiovascular risk (2, 3, 4, 7).
A growing body of evidence shows that statins reduce mortality across a wide range of heart conditions—including heart failure—and can even lessen the extent of damage after a heart attack. Remarkably, many of these benefits occur independently of their cholesterol-lowering effects, thanks to the pleiotropic actions of statins. These additional benefits include (2, 3, 4, 7):
Stabilising cholesterol deposits (atherosclerotic plaques), making them less likely to rupture and cause blood clots. This involves reducing inflammation, oxidative stress (from free radicals), and overactivity in the immune system.
Improving blood vessel function by helping them dilate more effectively and reducing blood viscosity, which supports smoother, more efficient circulation.
Cholesterol production in the liver follows a natural daily rhythm, peaking between 8 p.m. and midnight—with activity up to four times higher than in the morning (12). As a result, taking statins at night—especially shorter-acting ones—can help maximise their cholesterol-lowering effects.
Explore PGX for CardiovascularStatins like rosuvastatin may be prescribed for several reasons (5):
Elevated cholesterol levels that haven’t responded sufficiently to lifestyle changes such as a healthy diet and regular physical activity.
Primary prevention of cardiovascular events in people at high risk of heart disease or stroke.
Secondary prevention after a heart attack or stroke. This is a common use of rosuvastatin, although it may be considered off-label in some regions. It is, however, strongly supported by clinical evidence.
How and when to take it
Rosuvastatin is typically taken once a day, with or without food. Your starting dose and how it increases depends on your age, ethnicity, and reason for treatment. Adjustments are usually made at 4-week intervals (5).
For High Cholesterol Not Responding to Lifestyle Changes:
General population: Start with 5–10 mg once daily, increasing if needed to 20 mg
Patients of Asian origin: Start with 5 mg once daily, increasing up to 20 mg
Adults aged 70 and over: Start with 5 mg once daily, increasing up to 20 mg
For Preventing Cardiovascular Events:
Adults aged 18–69 years: Start with 20 mg once daily
Patients of Asian origin: Start with 5 mg once daily, with increases to 20 mg over time
While rosuvastatin is generally well tolerated and widely prescribed, like all medications, it can cause side effects in some individuals. Understanding the most common and less common reactions can help you monitor your response and know when to seek advice.
Rosuvastatin is a hydrophilic statin, meaning it doesn’t penetrate body tissues—including muscle and brain—as deeply as some other statins. This doesn’t reduce its ability to lower cholesterol or inflammation, but it does lower the risk of side effects, especially muscle-related ones (3, 6).
That said, muscle symptoms are still the most common side effects of statin therapy (5, 6, 7), including:
Pain, soreness, or tenderness not linked to exercise or illness
Typically affecting both thighs, calves, or hip flexors
Occurring in an estimated 10–29% of patients (6)
Leading to statin discontinuation in many cases
If you notice muscle discomfort that isn’t related to physical activity or a viral infection, speak with your GP or pharmacist. These may be early signs of statin-related muscle symptoms—and early support can help.
Certain factors increase the likelihood of developing muscle symptoms while taking statins (11):
Age over 60
Diabetes
Hypothyroidism
Multisystem diseases
Vitamin D deficiency
Strenuous physical activity
Alcohol consumption
Major surgery
Higher statin doses — the strongest known risk factor, increasing risk sixfold
There have also been increasing reports of memory problems, especially at higher statin doses. Although research findings are mixed, if you notice memory lapses, low mood, or trouble concentrating after starting or changing your dose, speak to your GP (8, 9).
If you have myasthenia gravis and experience worsening symptoms while on rosuvastatin, inform your doctor. Although rare, statins have been reported to aggravate this condition, and any changes should be reviewed promptly.
While less common, rosuvastatin may also cause:
Painful joints
Fatigue or lack of strength
Dizziness
Sleep disturbances
Liver enzyme changes
Memory problems
Rosuvastatin is considered the most hydrophilic statin, meaning it tends to stay in the bloodstream and penetrates less into tissues like muscle, liver, and brain. This property is believed to contribute to its lower risk of side effects, especially muscle-related symptoms, compared to more lipophilic statins (3, 6).
However, understanding your individual risk of side effects from statins can still be challenging. A pharmacogenomics (PGx) test in the UK can reveal how your genes influence your response to medications like rosuvastatin, enabling safer, more personalised medicine through genetic testing for medication response.
Explore PGX for CardiovascularRosuvastatin’s journey through the body—how it’s absorbed, distributed, metabolised, and eliminated—is shaped by both biological processes and your genetic makeup. These areas of study are known as pharmacokinetics and pharmacogenetics, and they help explain why the same medication can affect different people in different ways (10).
Rosuvastatin has unique properties compared to other statins. It is the most hydrophilic statin, meaning it has a strong affinity for water and exists in a water-soluble salt form. This contributes to its targeted action and limited tissue penetration. Its oral bioavailability is approximately 20%—comparable to atorvastatin, pravastatin, and fluvastatin, and higher than simvastatin and lovastatin.
Rosuvastatin undergoes minimal liver metabolism. It is taken up into liver cells (hepatocytes) via several transporters, including:
OATP1B1 (encoded by the SLCO1B1 gene)
OATP1B3
OATP2B1
Once in the liver, it is processed by enzymes such as UGT1A1 and UGT1A3, primarily through a process called lactonization. Two transport proteins, BCRP (Breast Cancer Resistance Protein) and P-glycoprotein (P-gp), are mainly responsible for moving rosuvastatin into the bile for excretion.
Rosuvastatin has the longest half-life of any statin—about 19 hours. Around 90% of the drug is eliminated in the faeces, making it efficient and long-lasting in effect.
Genetic variation can significantly affect how well rosuvastatin works—and your likelihood of experiencing side effects. Key genes involved:
SLCO1B1 (encodes OATP1B1 transporter)
Critical for moving rosuvastatin into liver cells.
Reduced function variants (such as the c.521T>C polymorphism) can lead to higher statin levels in the blood and increase the risk of muscle-related side effects.
ABCG2 (Breast Cancer Resistance Protein / BCRP)
Expressed in tissues like the liver, intestine, and blood-brain barrier.
Helps transport rosuvastatin out of cells.
The minor A allele is associated with 30–40% lower protein expression and higher plasma levels of rosuvastatin, increasing the risk of side effects.
These pharmacogenetic insights are also relevant for other statins, particularly:
Atorvastatin
Simvastatin
Pravastatin
1. https://pmc.ncbi.nlm.nih.gov/articles/PMC3108295/ 2. https://pmc.ncbi.nlm.nih.gov/articles/PMC11660731/ 3. https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2021.687585/full 4. https://pmc.ncbi.nlm.nih.gov/articles/PMC2694580/ 5. BNF – British National Formulary 2025: https://www.nice.org.uk/about/what-we-do/evidence-and-best-practice-resources/british-national-formulary--bn 6. https://pubmed.ncbi.nlm.nih.gov/39681285/ 7. https://www.mdpi.com/1999-4923/16/2/214 8. https://pmc.ncbi.nlm.nih.gov/articles/PMC5830056/ 9. https://pmc.ncbi.nlm.nih.gov/articles/PMC5005588/ 10. https://www.sciencedirect.com/science/article/pii/S2405844025000088 11. https://pubmed.ncbi.nlm.nih.gov/35152405/ 12. https://www.jlr.org/article/S0022-2275(20)32008-3/fulltext 13. https://www.ncbi.nlm.nih.gov/books/NBK532919/ 14. https://pmc.ncbi.nlm.nih.gov/articles/PMC3303484/ 15. https://pmc.ncbi.nlm.nih.gov/articles/PMC10506175/ 16. https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2012.00335/ful 17. https://pmc.ncbi.nlm.nih.gov/articles/PMC4408357/