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Atorvastatin is a member of the statin family, originally inspired by natural compounds produced by fungi. The first statins were identified in nature as biochemical “weapons” that fungi use in their battle against bacteria—natural enemies of fungal organisms. These compounds inhibit cholesterol synthesis—a mechanism that proved lethal to certain microbes. This microbial interaction provided the original basis for using statins to lower cholesterol in humans (1).
When prescribing or taking atorvastatin, it's important to consider not just its cholesterol-lowering properties, but also its broader impact on cardiovascular health and the timing of its use. Like other statins, atorvastatin has effects that extend well beyond lowering lipids—many of which play a key role in reducing 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 cardiovascular disease—and can even limit the extent of heart damage after a heart attack (3, 4). Remarkably, many of these benefits occur independently of their cholesterol-lowering effect. These additional actions are known as the pleiotropic effects of statins. Some of these added benefits include (2, 3, 4, 7):
Stabilising cholesterol deposits (atherosclerotic plaques): Statins make these fatty deposits less likely to rupture and trigger clots, partly by reducing inflammation, oxidative stress (from free radicals), and immune system overactivity.
Improving blood vessel function: Statins help blood vessels dilate more effectively and reduce blood viscosity, which supports smoother, more efficient circulation.
Stronger anti-inflammatory effects in certain statins: Atorvastatin, a lipophilic statin, tends to show stronger anti-inflammatory and lipid-lowering effects compared to hydrophilic statins like rosuvastatin and pravastatin.
Cholesterol production in the liver follows a natural daily rhythm. It typically peaks between 8 p.m. and midnight—up to four times higher than in the morning hours (12). Because of this, taking statins at night—especially shorter-acting ones—can help maximise their effectiveness in reducing cholesterol levels.
Explore PGX for CardiovascularStatins like atorvastatin may be prescribed for several reasons, including:
Elevated cholesterol levels that haven’t responded enough to lifestyle changes such as a balanced diet and regular physical activity.
Primary prevention: To lower the risk of a first heart attack or stroke in people considered at high risk of developing cardiovascular disease.
Secondary prevention: To reduce the chances of another cardiovascular event after a heart attack or stroke. While this is a common use, it is considered off-label in some regions—meaning not officially licensed for this purpose—but it is strongly supported by clinical evidence.
How and when to take it:
Atorvastatin is usually taken once a day, with or without food. Taking it at the same time each day—preferably in the evening—may help optimise its effect.
Atorvastatin is generally well tolerated and widely prescribed. However, like all medications, it can cause side effects in some people. Knowing what to expect—especially the common and less common effects—can help you stay informed and seek advice if needed.
Atorvastatin is a lipophilic statin, meaning it easily penetrates body tissues, including muscles and the brain. This property enhances its ability to lower cholesterol and reduce inflammation—but it also increases the likelihood of certain side effects (3).
Muscle-related symptoms are the most commonly reported side effects of statin therapy, experienced by a significant number of patients. However, compared to simvastatin, atorvastatin has been shown to cause fewer statin-associated muscle symptoms (SAMS) (5, 6, 7).
If you experience muscle pain, soreness, or tenderness that isn’t clearly linked to physical activity or a recent viral infection, speak with your pharmacist or GP. These could be early signs of statin-related muscle symptoms.
Muscle-related side effects occur in an estimated 10–29% of patients (6) and are in fact the leading reason why people stop taking statins.
The most commonly affected areas include the thighs, calves, and hip flexors, and symptoms are usually symmetrical (6).
Certain factors can increase the risk of developing statin-associated muscle symptoms. These include (11):
Age over 60
Diabetes
Hypothyroidism
Multisystem diseases
Vitamin D deficiency
Excessive or strenuous physical activity
Alcohol consumption
Major surgery
Higher statin doses — this is the strongest risk factor, increasing the risk sixfold compared to lower doses
There are also increasing reports of memory issues associated with statins—particularly at higher doses. Although clinical evidence remains mixed, if you’ve recently started or increased your dose and notice memory lapses, difficulty focusing, or low mood, consult your pharmacist or GP (8, 9).
If you have myasthenia gravis and notice a worsening of symptoms while taking statins, speak with your GP. Although rare, statins have been reported to aggravate this condition, so any changes should be reviewed promptly (5).
In addition to muscle-related symptoms, atorvastatin may cause a range of other side effects (5). These are generally less common but still important to be aware of—especially if they persist or begin to affect your quality of life:
Painful joints
General lack of energy or strength
Dizziness
Sleep disturbances
Liver disorders
Memory problems
Understanding your individual risk of side effects—especially from statins—can be challenging. A pharmacogenomics (PGx) test in the UK can help identify how your genes influence your response to medications like atorvastatin, supporting safer, more personalised medicine through genetic testing for medication response.
Explore PGX for CardiovascularAtorvastatin’s journey through the body—how it’s absorbed, distributed, metabolised, and eliminated—is shaped by both biological processes and your genetics. These areas of study are called pharmacokinetics and pharmacogenetics, and they help explain why the same medication can affect different people in different ways (10). This is a key part of what makes personalised medicine possible.
Thanks to its fat-loving (lipophilic) nature, atorvastatin is quickly absorbed from the gut after oral administration.
As a fat-soluble medicine, atorvastatin can penetrate tissues such as the liver, muscles, and brain. This improves its ability to lower cholesterol but may also increase the risk of side effects. It enters liver cells primarily through the OATP1B1 transporter, with additional roles played by OATP1B3 and OATP2B1.
Atorvastatin undergoes extensive metabolism in both the gut and liver, resulting in a total oral bioavailability of around 14%. It is processed by the CYP3A4 and CYP3A5 enzymes into active metabolites, which are responsible for about 70% of its therapeutic activity. Its half-life is approximately 14 hours.
The drug and its metabolites are mostly eliminated via the bile into the faeces. This elimination process is driven by the P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) transporters.
Genetic variation can affect both how well atorvastatin works and your risk of side effects. One of the most important genes involved is SLCO1B1, which encodes the OATP1B1 transporter. This protein helps move statins like atorvastatin into the liver, where they carry out their cholesterol-lowering effects (10, 11).
Key points about SLCO1B1 and statin response:
SLCO1B1 is essential for the liver uptake of statins.
Reduced transporter function can lead to higher levels of statins in the bloodstream and a greater risk of muscle-related side effects.
The c.521T>C variant (rs4149056) is strongly linked with statin-induced myopathy.
People with two copies of the C allele (C/C genotype) are at significantly higher risk of muscle damage—especially from simvastatin and lovastatin.
Pharmacogenetic factors may also be important for other statins, particularly:
Simvastatin
Rosuvastatin
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/