⚕️ Educational information only — not medical advice. Read the full disclaimer

Can Statins Cause Joint Pain? What the Evidence Shows

Aching muscles and stiff joints are the most common reasons people give for stopping a statin. The honest answer is more interesting than "yes" or "no." Statins can cause muscle symptoms in a minority of people, and very rarely they cause serious muscle damage. But large blinded trials show that most aches people feel on a statin turn up almost as often on a dummy pill. A direct effect on the joints is much less certain. Joint pain while taking a statin often has another cause, such as osteoarthritis, which becomes common at the ages when statins are started. This page goes through the trials, the rare serious problems, the risk factors and the options a doctor can try, so that you keep the heart and stroke protection a statin offers.

Important: This page is general educational information, not medical advice. Statins are prescribed to prevent heart attacks and strokes. Do not stop, skip or change the dose of a statin without speaking to the prescriber or a pharmacist. If you have new muscle or joint pain on a statin, book a review. Your doctor can look for the cause and adjust treatment without leaving your heart unprotected. Seek urgent care for severe muscle pain or weakness or dark urine (see when to see a doctor).

Key takeaways

  • Statins lower the risk of heart attack and ischaemic stroke. Each 1 mmol/L (about 39 mg/dL) fall in LDL cholesterol cuts major vascular events by about a fifth. Strong
  • In 19 double-blind trials (about 124,000 people), muscle pain or weakness was reported by 27.1% on a statin vs. 26.6% on placebo. In year 1, only about 1 in 15 muscle reports among statin users was actually due to the statin. Strong
  • In blinded crossover trials of people who had quit statins because of side effects (SAMSON, StatinWISE), symptoms were about as bad on placebo as on atorvastatin. This is the nocebo effect. Strong
  • Observational studies link statin use with somewhat more musculoskeletal and joint complaints, but they cannot fully separate the drug from who takes it or what people expect. Contested
  • Rhabdomyolysis and anti-HMGCR immune-mediated necrotizing myopathy are real but rare. The warning signs are marked weakness, a very high CK or dark urine. Strong
  • CoQ10 for statin muscle pain has mixed trial results, and vitamin D did not prevent statin muscle symptoms in a large randomized trial. Contested
  • Most people with symptoms can stay protected by switching statin, lowering the dose, dosing less often, or adding or switching to ezetimibe, a PCSK9 inhibitor or bempedoic acid. Strong

Why statins matter Strong

Statins block HMG-CoA reductase, the rate-limiting enzyme in the liver's cholesterol-making (mevalonate) pathway. The liver responds by pulling more LDL cholesterol out of the blood. In a meta-analysis of 26 randomized trials with about 170,000 participants, each 1.0 mmol/L reduction in LDL cholesterol lowered the yearly rate of heart attack, revascularisation and ischaemic stroke by just over a fifth (rate ratio 0.78). All-cause death fell by 10% per mmol/L, with no rise in cancer.1 The American Heart Association's safety review concluded that, for people whose guidelines recommend a statin, the benefits greatly outweigh the risks.2

~22%fewer major vascular events per 1 mmol/L LDL lowered
~1 in 15muscle-pain reports on statins in year 1 actually due to the drug
0.90SAMSON nocebo ratio: placebo symptoms vs. statin symptoms
<0.1%risk of serious statin muscle injury, including rhabdomyolysis

This matters for joint pain because stopping a statin is not a neutral choice. In a cohort of more than 28,000 patients with a recorded statin reaction, people who kept getting statin prescriptions had fewer heart attacks, strokes and deaths over four years (12.2% vs. 13.9%). This was an observational study, so it cannot prove cause and effect.19

Muscle symptoms (SAMS) vs. joint pain Strong

Doctors use the term statin-associated muscle symptoms (SAMS) for aching, cramps, heaviness or weakness in the muscles of people taking a statin. SAMS usually come with a normal or only slightly raised creatine kinase (CK), the enzyme that leaks from damaged muscle. Registries and observational studies report SAMS in 7–29% of users.3 The European Atherosclerosis Society panel describes the typical pattern: symmetrical aching of large muscle groups that is linked in time to starting the statin, settles after stopping, and comes back when the statin is restarted.3

Arthralgia (joint pain) is different. Pain that sits in a joint, especially with swelling, warmth, morning stiffness or a pattern that affects some joints but not others, points to arthritis (osteoarthritis, rheumatoid arthritis, gout) or a local problem more than a drug effect. People often find it hard to tell muscle from joint pain around the hips, shoulders and knees. Part of a good review is working out which one it is.

Clues that help separate statin muscle symptoms from arthritis
FeatureSuggests statin muscle symptomsSuggests arthritis or another cause
LocationBoth sides, large muscles (thighs, buttocks, calves, upper arms, back)Inside specific joints. May be one-sided or in a pattern (small hand joints, a knee, the big toe)
CharacterAching, cramping, heaviness, tiredness of musclesJoint swelling, warmth, grinding, locking or reduced range of motion
TimingStarts after beginning a statin or raising the dose. Eases after a supervised pause and returns on rechallengePresent before the statin, or unrelated to dose changes
StiffnessNot typically prominentMorning stiffness over 30–60 minutes suggests inflammatory arthritis. Brief stiffness after rest is typical of osteoarthritis
Blood testsCK usually normal or mildly raisedRaised CRP/ESR, positive RF/anti-CCP, or high uric acid may point to inflammatory arthritis or gout

Other conditions common in the same age group can mimic either pattern. These include an underactive thyroid, low vitamin D, polymyalgia rheumatica (shoulder and hip-girdle stiffness in people over 50), and side effects of other medicines. See rheumatoid arthritis symptoms and inflammatory markers for context.

What blinded trials show: the nocebo effect Strong

The key question is not "do people on statins have aches?" Many people over 60 do, with or without a statin. The question is whether they have more aches than similar people who do not know whether they are taking the drug. Blinded, placebo-controlled trials answer that.

Cholesterol Treatment Trialists' meta-analysis (Lancet 2022)

The CTT Collaboration pooled individual data from 19 double-blind statin-vs-placebo trials (123,940 people, about 4.3 years of follow-up). Muscle pain or weakness was reported by 27.1% of those on a statin and 26.6% on placebo (rate ratio 1.03). In the first year there was a 7% relative excess, about 11 extra reports per 1,000 person-years. That means only about 1 in 15 muscle reports among statin users was actually caused by the statin. After year 1 there was no significant excess. Higher-intensity regimens (atorvastatin 40–80 mg, rosuvastatin 20–40 mg) carried slightly more risk. The authors concluded that more than 90% of muscle-symptom reports in statin users were not due to the statin.4

SAMSON (NEJM 2020; JACC 2021)

SAMSON recruited 60 people who had stopped statins because of side effects. Each received 12 monthly bottles: four with atorvastatin 20 mg, four with placebo and four empty. They scored symptoms daily on an app. Average symptom scores were 8.0 in no-tablet months, 16.3 in statin months and 15.4 in placebo months, with no significant difference between statin and placebo. So about 90% of the symptom burden of taking a statin was also produced by taking a placebo. The timing of symptoms on starting or stopping did not distinguish statin from placebo either. Six months later, half the participants were back on a statin.56

StatinWISE (BMJ 2021)

In 200 UK primary-care patients who had stopped or were thinking of stopping statins because of muscle symptoms, StatinWISE ran a series of individual "n-of-1" trials: six blinded two-month periods of atorvastatin 20 mg or placebo. There was no overall difference in muscle symptom scores (mean difference −0.11 on a 0–10 scale). Withdrawals for intolerable symptoms were similar (9% during statin vs. 7% during placebo periods). Two-thirds of those who finished planned to restart statins.7

Blinded vs. unblinded in the same people (ASCOT)

In the ASCOT trial, muscle-related adverse events were reported at the same rate on atorvastatin and placebo while treatment was blinded (2.03% vs. 2.00% per year). In the open-label extension that followed, when people knew what they were taking, statin users reported 41% more muscle-related events. They also reported more musculoskeletal and connective-tissue complaints, which include joint problems (8.69% vs. 7.45% per year).8 The pill did not change between phases. Knowing that it was a statin did.

What "nocebo" does and does not mean

Nocebo means that the expectation of harm produces real symptoms. It does not mean the pain is imagined, and it does not mean statins never cause muscle problems. The CTT data show a small true excess, mostly in year 1 and at higher doses, and genuine statin myopathy exists.4 The practical point is that symptoms on a statin should lead to a careful review rather than an assumption. People often find it reassuring to learn that their own symptoms may not come from the drug, and many go on to restart successfully.67

Most of these trials measured muscle symptoms, not joint pain specifically. So the strongest evidence concerns SAMS. For joints, the evidence is thinner and mostly observational (next section). The AHA statement found no convincing evidence that statins cause tendonitis.2

Observational data on joints and musculoskeletal conditions Contested

The study most often quoted on statins and joints is a 2013 JAMA Internal Medicine cohort from a US military health system. It compared 6,967 statin users with 6,967 propensity-matched non-users. Statin users had higher odds of any musculoskeletal diagnosis (odds ratio 1.19), of sprains, strains and dislocations (1.13), and of drug-associated musculoskeletal pain (1.09). For the category of arthropathies (joint disorders), the odds ratio was 1.07 (95% CI 0.99–1.16), which narrowly missed statistical significance in the main matched analysis.9 The authors called for more research, especially in physically active people.

Studies like this are useful for spotting signals, but they have known limits. People prescribed statins differ from non-users in ways that matching cannot fully capture. They see doctors more often, so more diagnoses get recorded. And they may expect side effects. The ASCOT comparison above shows how much open-label reporting can inflate musculoskeletal complaints.8 The fairest summary is that a small effect of statins on joint or soft-tissue complaints in some people cannot be ruled out, but it has not been shown in blinded data, and it is much smaller than the cardiovascular benefit for people who need a statin.

Rare but serious: rhabdomyolysis and anti-HMGCR myopathy Strong

A small group of people have genuine, measurable statin muscle injury. The European Atherosclerosis Society estimates that statin myopathy with a significantly raised CK affects about 1 in 1,000 to 1 in 10,000 people on standard doses.3 The AHA puts the risk of serious statin muscle injury, including rhabdomyolysis, at under 0.1%.2 Rhabdomyolysis is rapid muscle breakdown that releases muscle proteins into the blood and can damage the kidneys. It typically causes severe muscle pain and weakness, sometimes with dark, cola-coloured urine. It is a medical emergency.

Immune-mediated necrotizing myopathy (IMNM) with antibodies against HMG-CoA reductase (anti-HMGCR) is rarer still, estimated at around 2–3 per 100,000 statin-treated patients.11 Unlike ordinary statin side effects, it is an autoimmune disease. Statins appear to raise HMGCR expression and can trigger the immune system to attack muscle. It causes progressive weakness of the hip and shoulder muscles with very high CK, and it persists or worsens after the statin is stopped. In a Johns Hopkins myositis centre, 6% of patients with myopathy had anti-HMGCR antibodies, and 92% of those aged 50 or over had taken a statin.10 IMNM needs specialist care, usually immunosuppressive treatment. A blood test for anti-HMGCR antibodies helps with diagnosis.1011

These are uncommon, but they are why new muscle weakness on a statin should never be ignored. Weakness, as in difficulty climbing stairs, rising from a chair or lifting your arms, is a different signal from aching. It needs prompt medical assessment and a CK blood test.

Risk factors for true statin muscle effects Strong

Genuine statin muscle problems are more likely when more statin reaches the muscle, or when the muscle is already vulnerable. Risk factors described by the EAS and AHA include:23

  • Higher doses and higher-intensity regimens. The CTT excess was larger with atorvastatin 40–80 mg or rosuvastatin 20–40 mg.4
  • Drug interactions that raise statin blood levels. Examples include some medicines that block the liver enzyme CYP3A4 (certain macrolide antibiotics, azole antifungals and HIV protease inhibitors), ciclosporin and gemfibrozil. Large amounts of grapefruit juice also raise levels of simvastatin, lovastatin and, to a lesser degree, atorvastatin. Not every statin is affected the same way, so ask a pharmacist to check your full medicine list.2
  • Untreated hypothyroidism. An underactive thyroid can itself cause muscle aches, stiffness and a raised CK, and it raises statin muscle risk.3
  • Older age, small body size, kidney or liver disease, heavy alcohol use and very strenuous exercise.3 In the VITAL cohort, female sex and younger age (50–64) were independent predictors of reporting SAMS.26
  • Genetics. A common variant in the SLCO1B1 gene, which controls how the liver takes up statins, raised myopathy risk about 4.5-fold per copy in people taking simvastatin 80 mg. Around 15% of the population carries the variant.12
  • Low vitamin D. People with statin myalgia had lower vitamin D levels in observational studies.16 However, supplementation did not prevent symptoms in a randomized trial (below).

CoQ10 and vitamin D Contested

Coenzyme Q10 Contested

The idea makes biological sense. CoQ10 is made in the same mevalonate pathway that statins block, it helps mitochondria produce energy, and statins lower blood CoQ10 levels. The trials, however, disagree. A 2018 meta-analysis of 12 small trials (575 patients) reported less muscle pain, weakness and cramps with CoQ10.15 A 2020 meta-analysis of 7 trials (321 patients) found no benefit for myalgia and no improvement in staying on statins.14 In one of the more rigorous trials, researchers first confirmed statin myalgia with a blinded statin-vs-placebo crossover. Only 36% of people with reported statin myalgia actually had symptoms on the statin but not on placebo. In those confirmed cases, 600 mg/day of ubiquinol raised blood CoQ10 about fourfold but did not reduce pain or improve strength.13 This site's medications page discusses the statin and CoQ10 link in the context of drug-induced nutrient depletion.

CoQ10 is generally well tolerated. Some people try it after discussing it with their doctor, but the current evidence does not support relying on it. Supplements can interact with other medicines, so check with a pharmacist first. See supplement safety and interactions.

Vitamin D Contested

Observational data link low vitamin D with statin myalgia. A meta-analysis of 7 studies (2,420 patients) found levels about 9 ng/mL lower in those with symptoms.16 But in the randomized VITAL trial, 2,083 people who started a statin while taking 2,000 IU/day of vitamin D or placebo reported SAMS at the same rate (31% in both groups), and statin discontinuation was the same (13% each). Results were similar whatever their starting vitamin D level.17 Correcting a genuine deficiency is still worthwhile for bone and muscle health in general (see vitamin D on the supplements page and 25-OH vitamin D testing). It just has not been shown to prevent statin muscle symptoms.

What your doctor can do Strong

Lipid specialists recommend a structured approach that aims to keep LDL cholesterol controlled rather than abandon treatment. The National Lipid Association now says that at least two statins, including one at the lowest approved daily dose, should be tried before someone is labelled statin-intolerant. It also explicitly recognises the nocebo effect.18 The EAS panel suggests trying at least three different statins and using the maximally tolerated dose combined with non-statin therapy if needed.3 Steps your doctor may consider include:

Options to discuss with your prescriber (never make these changes on your own)
StepWhy it helpsEvidence
Characterise the symptoms and examine youSeparates muscle symptoms from joint disease, nerve pain or other causesStrong
Check CK, thyroid function (TSH), kidney and liver tests, and vitamin D where relevantA very high CK or weakness needs urgent action. Hypothyroidism is treatable and raises muscle riskStrong
Review interactions, including grapefruitRemoving an interacting drug can resolve true statin toxicityStrong
Supervised pause and rechallenge, or a blinded n-of-1 approachShows whether symptoms really track the statin. Many people restart successfullyStrong
Switch to a different statinStatins differ in how they are metabolised and how much they interact with other drugsStrong
Lower the dose, or use alternate-day or less frequent dosingLess statin exposure while keeping some LDL lowering. Recommended as a strategy by the NLAEmerging
Add ezetimibeLowers cholesterol absorption. Reduced cardiovascular events when added to a statin (IMPROVE-IT), with similar muscle side effects to placeboStrong
PCSK9 inhibitor (e.g. evolocumab)Injectable. Lowered LDL by 59% and reduced cardiovascular events (FOURIER)Strong
Bempedoic acidReduced major cardiovascular events in statin-intolerant patients (CLEAR Outcomes). Note that it slightly raised uric acid and goutStrong

The non-statin evidence comes from large outcome trials. In IMPROVE-IT, adding ezetimibe to simvastatin after an acute coronary syndrome cut the primary endpoint from 34.7% to 32.7% over seven years, with similar rates of muscle side effects.20 In FOURIER, evolocumab lowered LDL cholesterol by 59% and reduced the composite of cardiovascular death, heart attack or stroke (5.9% vs. 7.4%).21 In CLEAR Outcomes, which enrolled 13,970 statin-intolerant patients, bempedoic acid reduced major adverse cardiovascular events (11.7% vs. 13.3%). It also raised the rate of gout (3.1% vs. 2.1%), which is worth knowing if you have a history of gout or high uric acid.22 See the gout page for other urate-raising drugs.

Before your appointment: note where the pain is (muscle or joint), when it started relative to any statin or dose change, whether you have true weakness, any new medicines or supplements, and how much grapefruit you eat or drink. A simple symptom log, like the site's flare tracker, makes the conversation more productive.

Statins in rheumatoid arthritis Emerging

For people with inflammatory arthritis, statins may do more than lower cholesterol. Statins have anti-inflammatory effects. In the TARA trial, 116 people with rheumatoid arthritis (RA) took atorvastatin 40 mg or placebo alongside their usual disease-modifying drugs. After six months, disease activity (DAS28) improved modestly with atorvastatin (difference −0.52), CRP fell by 50% relative to placebo, and swollen joint counts dropped.23 In an Israeli cohort of over 211,000 statin users, those who took their statins most consistently had a 42% lower risk of developing RA (hazard ratio 0.58). A weaker association with osteoarthritis (HR 0.85) suggests that "healthy adherer" bias accounts for part of this.25

RA raises cardiovascular risk roughly 1.5- to 2-fold (see what RA is), so the cardiovascular role of statins matters most here. The TRACE RA trial randomized 3,002 people with RA to atorvastatin 40 mg or placebo. It was stopped early because fewer events occurred than expected. Cardiovascular events were 1.6% vs. 2.4% (a 34% reduction that did not reach statistical significance), CRP was lower, and adverse events were similar (19.8% vs. 19.5%).24 Statins are not a treatment for arthritis and do not replace DMARDs. See RA complementary measures for how cardiovascular risk fits into RA care.

When to see a doctor Strong

Seek urgent, same-day medical care if you take a statin and have:
  • severe muscle pain or tenderness, especially with fever or feeling very unwell;
  • dark, tea- or cola-coloured urine or passing much less urine (possible rhabdomyolysis);
  • new or worsening weakness, such as trouble climbing stairs, rising from a chair or lifting your arms;
  • symptoms that began soon after starting a new medicine (for example an antibiotic or antifungal) alongside your statin;
  • a hot, red, swollen joint, especially with fever, which needs same-day assessment to rule out infection.
Do not wait to see if these pass, and tell the clinician you take a statin.23

Book a routine appointment with your prescriber or pharmacist if you:

  • have aching muscles or joints that you think may be linked to your statin;
  • are thinking about stopping your statin, or have already stopped it (it is never too late to talk it through);
  • have joint swelling, prolonged morning stiffness or pain in a pattern that could be arthritis;
  • are starting a supplement such as CoQ10, red yeast rice (which contains a natural statin) or St John's wort, all of which can interact or duplicate treatment.

Frequently asked questions

Can statins cause joint pain?

Statins can cause muscle aches in a minority of people, and some observational studies link statin use with more musculoskeletal and joint complaints. But in large blinded trials, muscle symptoms were almost as common on placebo as on a statin, and a direct effect on joints is not well established. Joint pain while taking a statin often has another cause, such as osteoarthritis, which becomes common at the ages when statins are started. This is educational information, not medical advice.

Is statin muscle pain all in my head?

No. The symptoms are real, but blinded trials show that most of them are not caused by the drug's chemistry. In SAMSON, symptoms in placebo months were about 90% as intense as in statin months, and the 2022 CTT meta-analysis estimated that only about 1 in 15 muscle-pain reports among statin users in the first year was actually due to the statin. Expectation (the nocebo effect), other conditions and normal aches of ageing explain much of the rest. A small number of people do have true statin muscle effects, and rare cases are serious.

Should I stop my statin if my joints or muscles hurt?

Do not stop a statin on your own. Statins prevent heart attacks and strokes, and stopping can raise that risk. Contact the prescriber, who can check for other causes, order a CK or thyroid test, and adjust the dose, switch statin or add another cholesterol-lowering drug. Get urgent care if you have severe muscle pain or weakness, dark or cola-coloured urine, or feel very unwell.

Does CoQ10 help statin muscle pain?

The evidence is mixed. Statins do lower blood CoQ10, and one 2018 meta-analysis of small trials reported less muscle pain with CoQ10, but a 2020 meta-analysis and a randomized trial in people with confirmed statin myalgia found no benefit over placebo. CoQ10 is generally well tolerated, but ask your doctor or pharmacist before taking it, and do not rely on it in place of a proper review.

What are the alternatives if I really cannot take a statin?

Most people who think they cannot take statins can tolerate a different statin, a lower dose or less frequent dosing. If not, non-statin drugs with cardiovascular outcome trials include ezetimibe, PCSK9 inhibitors such as evolocumab, and bempedoic acid. Which option fits depends on your cardiovascular risk, and that decision belongs with your doctor.

Can statins help rheumatoid arthritis?

Possibly, but modestly. In the small TARA trial, atorvastatin slightly lowered disease activity and CRP in people with rheumatoid arthritis, and some cohort studies link statin use with lower RA risk. Statins are not an arthritis treatment. Their main role in RA is reducing cardiovascular risk, which is raised in the disease.

References

  1. Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376:1670–1681. PubMed 21067804
  2. Newman CB, Preiss D, Tobert JA, et al. Statin safety and associated adverse events: a scientific statement from the American Heart Association. Arterioscler Thromb Vasc Biol. 2019;39:e38–e81. PubMed 30580575
  3. Stroes ES, Thompson PD, Corsini A, et al. Statin-associated muscle symptoms: impact on statin therapy — European Atherosclerosis Society Consensus Panel statement on assessment, aetiology and management. Eur Heart J. 2015;36:1012–1022. PubMed 25694464
  4. Cholesterol Treatment Trialists' Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022;400:832–845. PubMed 36049498
  5. Wood FA, Howard JP, Finegold JA, et al. N-of-1 trial of a statin, placebo, or no treatment to assess side effects. N Engl J Med. 2020;383:2182–2184. PubMed 33196154
  6. Howard JP, Wood FA, Finegold JA, et al. Side effect patterns in a crossover trial of statin, placebo, and no treatment. J Am Coll Cardiol. 2021;78:1210–1222. PubMed 34531021
  7. Herrett E, Williamson E, Brack K, et al. Statin treatment and muscle symptoms: series of randomised, placebo controlled n-of-1 trials (StatinWISE). BMJ. 2021;372:n135. PubMed 33627334
  8. Gupta A, Thompson D, Whitehouse A, et al. Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial–Lipid-Lowering Arm (ASCOT-LLA). Lancet. 2017;389:2473–2481. PubMed 28476288
  9. Mansi I, Frei CR, Pugh MJ, Makris U, Mortensen EM. Statins and musculoskeletal conditions, arthropathies, and injuries. JAMA Intern Med. 2013;173(14):1318. PubMed 23877079
  10. Mammen AL, Chung T, Christopher-Stine L, et al. Autoantibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase in patients with statin-associated autoimmune myopathy. Arthritis Rheum. 2011;63:713–721. PubMed 21360500
  11. Mammen AL. Statin-associated autoimmune myopathy. N Engl J Med. 2016;374:664–669. PubMed 26886523
  12. SEARCH Collaborative Group. SLCO1B1 variants and statin-induced myopathy — a genomewide study. N Engl J Med. 2008;359:789–799. PubMed 18650507
  13. Taylor BA, Lorson L, White CM, Thompson PD. A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. Atherosclerosis. 2015;238:329–335. PubMed 25545331
  14. Kennedy C, Köller Y, Surkova E. Effect of coenzyme Q10 on statin-associated myalgia and adherence to statin therapy: a systematic review and meta-analysis. Atherosclerosis. 2020;299:1–8. PubMed 32179207
  15. Qu H, Guo M, Chai H, et al. Effects of coenzyme Q10 on statin-induced myopathy: an updated meta-analysis of randomized controlled trials. J Am Heart Assoc. 2018;7:e009835. PubMed 30371340
  16. Michalska-Kasiczak M, Sahebkar A, Mikhailidis DP, et al. Analysis of vitamin D levels in patients with and without statin-associated myalgia — a systematic review and meta-analysis of 7 studies with 2420 patients. Int J Cardiol. 2015;178:111–116. PubMed 25464233
  17. Hlatky MA, Gonzalez PE, Manson JE, et al. Statin-associated muscle symptoms among new statin users randomly assigned to vitamin D or placebo. JAMA Cardiol. 2023;8:74–80. PubMed 36416841
  18. Cheeley MK, Saseen JJ, Agarwala A, et al. NLA scientific statement on statin intolerance: a new definition and key considerations for ASCVD risk reduction in the statin intolerant patient. J Clin Lipidol. 2022;16:361–375. PubMed 35718660
  19. Zhang H, Plutzky J, Shubina M, Turchin A. Continued statin prescriptions after adverse reactions and patient outcomes: a cohort study. Ann Intern Med. 2017;167:221–227. PubMed 28738423
  20. Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary syndromes (IMPROVE-IT). N Engl J Med. 2015;372:2387–2397. PubMed 26039521
  21. Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease (FOURIER). N Engl J Med. 2017;376:1713–1722. PubMed 28304224
  22. Nissen SE, Lincoff AM, Brennan D, et al. Bempedoic acid and cardiovascular outcomes in statin-intolerant patients (CLEAR Outcomes). N Engl J Med. 2023;388:1353–1364. PubMed 36876740
  23. McCarey DW, McInnes IB, Madhok R, et al. Trial of Atorvastatin in Rheumatoid Arthritis (TARA): double-blind, randomised placebo-controlled trial. Lancet. 2004;363:2015–2021. PubMed 15207950
  24. Kitas GD, Nightingale P, Armitage J, et al. A multicenter, randomized, placebo-controlled trial of atorvastatin for the primary prevention of cardiovascular events in patients with rheumatoid arthritis (TRACE RA). Arthritis Rheumatol. 2019;71:1437–1449. PubMed 30983166
  25. Chodick G, Amital H, Shalem Y, et al. Persistence with statins and onset of rheumatoid arthritis: a population-based cohort study. PLoS Med. 2010;7:e1000336. PubMed 20838658
  26. Gonzalez PE, Hlatky MA, Manson JE, et al. Statin-associated muscle symptoms in the VITamin D and OmegA-3 TriaL (VITAL). Am Heart J. 2022;252:39–41. PubMed 35717999