Statins and Muscle Loss: What a New Study Really Shows

Statins have been prescribed for decades because lowering atherogenic cholesterol can substantially reduce cardiovascular events in appropriately selected patients.

Muscle has always been part of the statin conversation. Muscle aches, weakness, reduced exercise tolerance, and, rarely, serious muscle injury are well-recognized problems. A harder question is whether years of statin therapy can affect the gradual loss of muscle mass and strength that comes with aging.

A large UK Biobank study published in the Journal of Cachexia, Sarcopenia and Muscle adds some important data to that discussion.

One-Minute Read

A 2025 UK Biobank study involving nearly 298,000 adults found that statin users had slightly lower grip strength and appendicular lean mass after researchers adjusted for a long list of health and lifestyle differences. Among roughly 35,500 participants with repeat measurements over an average follow-up of about 10 years, continuous statin use was associated with a faster decline in both measures.

One number from the study has attracted particular attention and is easy to misread. The frequently cited “73% decline in lean mass” does not mean statin users lost 73% of their muscle. It refers to a 73% greater rate of decline compared with the modeled rate in people who never used statins.

The study also has real limitations. It was observational. Muscle mass was estimated with bioelectrical impedance rather than DEXA. The researchers did not know the participants' statin doses or how long they had been taking them before entering the study. Statin users also differed medically from people who were not taking statins. Newer 2026 research has also found no significant association between statins and sarcopenia, muscle mass, grip strength, or physical performance.

The study raises a legitimate question about long-term muscle health. It does not establish that statins cause sarcopenia. For patients taking lipid-lowering medication for many years, however, muscle mass and strength are worth following along with cardiovascular risk.

What the UK Biobank Study Found

Researchers evaluated 297,977 UK Biobank participants with an average age of about 56. Grip strength was measured with a hand dynamometer. Appendicular lean mass, which estimates lean tissue in the arms and legs, was calculated from bioelectrical impedance measurements.

After adjusting for age, sex, body mass index, physical activity, diet, smoking, alcohol use, diabetes, hypertension, coronary heart disease, kidney disease, and other variables, statin use was associated with slightly lower grip strength and appendicular lean mass at baseline.

The long-term data were more notable. Among 35,557 participants with follow-up measurements roughly 10 years later, continuous statin use was associated with an additional annual decline of approximately:

• 0.315 kilograms of grip strength per year
• 0.057 kilograms of appendicular lean mass per year

Both differences were statistically significant.

Statistical significance does not establish cause and effect, particularly in an observational study. It does give researchers a signal worth investigating more carefully.

What the “73%” Number Actually Means

The study estimated that appendicular lean mass declined by approximately 0.078 kilograms per year among people who never used statins. Continuous statin use was associated with an additional decline of approximately 0.057 kilograms per year.

The additional 0.057-kilogram decline is about 73% of the 0.078-kilogram annual decline seen in never-users. That is the source of the 73% figure.

That is not the same as losing 73% of your muscle.

Grip strength was reported in a similar way. Never-users had a modeled decline of approximately 1.256 kilograms per year, while continuous statin use was associated with an additional decline of approximately 0.315 kilograms per year. The additional decline was about 25% of the background rate.

These percentages describe differences in the modeled rate of decline. They do not represent the percentage of total muscle or total strength lost.

The Long-Term Pattern Is More Complicated

The longitudinal model contains another detail that is easy to overlook. Continuous statin users began with higher predicted grip strength and appendicular lean mass. Their modeled decline was steeper, and the trajectories crossed at roughly 10 years.

The study therefore does not describe rapid muscle wasting after starting a statin. The concern it raises is more gradual: whether long-term exposure might influence the trajectory of muscle aging over many years.

That remains an open question.

This Was an Observational Study

People who take statins are medically different from people who do not take them. They are more likely to have cardiovascular disease, insulin resistance, diabetes, hypertension, obesity, and other conditions that can also influence muscle health.

The researchers adjusted for many of these differences and used propensity-score analyses to make the groups more comparable. That improves the analysis, but it cannot remove every source of confounding. Coronary heart disease, in particular, remained imperfectly balanced.

The investigators also lacked detailed information about statin dose and previous duration of treatment.

A participant taking a low dose of rosuvastatin for several years could not necessarily be separated from someone taking a higher dose of atorvastatin or another statin for a much longer period.

As a result, the study cannot tell us whether the observed association differs by drug, dose, statin type, or cumulative exposure.

Lean Mass Was Not Measured by DEXA

Appendicular lean mass was estimated with bioelectrical impedance rather than measured directly with DEXA. The researchers reported a strong correlation between impedance and DEXA measurements in a subset of participants, so the method has value, especially in a study this large.

For a question involving small changes in muscle mass over many years, however, direct longitudinal body-composition measurement would provide stronger evidence.

This is one reason DEXA body-composition testing can be useful in longevity medicine. A whole-body DEXA establishes objective measurements of total and regional lean mass that cannot be seen on a scale or calculated from BMI.

Other Studies Have Not Found the Same Association

The UK Biobank study is not the only evidence we have on statins and muscle aging.

A 2026 study involving 2,282 adults age 75 and older examined grip strength, skeletal muscle mass, and physical performance. Nearly half were taking statins. Over two years, researchers found no significant difference between statin users and nonusers in loss of grip strength, skeletal muscle mass, or physical performance. Higher statin doses were not associated with worse muscle outcomes either.

A separate 2026 systematic review and meta-analysis included 10 observational studies involving 9,080 older adults. Statin use was not significantly associated with an increased risk of sarcopenia. The studies varied considerably in design and results, which limits how confidently that finding can be applied.

Another long-term observational study published in 2026 used DEXA to evaluate muscle mass along with grip strength and physical performance and found no clear adverse association with long-term statin use.

At present, the evidence is mixed. The UK Biobank findings deserve attention, but they have not established a consistent pattern across studies.

Statin-Associated Muscle Symptoms Are Real

The uncertainty around long-term sarcopenia should not be confused with the better-established problem of statin-associated muscle symptoms.

Some patients develop muscle pain, cramps, weakness, or reduced exercise tolerance while taking a statin.

A large individual-participant meta-analysis of randomized, double-blind statin trials involving more than 150,000 participants found a small excess of muscle pain or weakness among people assigned to statins, particularly during the first year of treatment and with more intensive therapy.

The absolute increase was much smaller than many patients assume. Most muscle symptoms reported by people taking statins were not caused by the statin itself. Still, genuine statin-associated muscle symptoms occur and should not be dismissed.

New weakness, persistent muscle discomfort, or an unexplained decline in exercise capacity deserves clinical evaluation, particularly when symptoms appear after starting a statin or changing the dose.

Why Statins Could Affect Muscle

There are plausible biological reasons why statins could affect skeletal muscle in susceptible people.

Statins inhibit HMG-CoA reductase and reduce activity in the mevalonate pathway. That pathway is involved in more than cholesterol production. It also contributes to molecules involved in mitochondrial function, cellular signaling, and energy metabolism.

Researchers have investigated several possible mechanisms behind statin-associated muscle effects, including changes in mitochondrial energy production, CoQ10 availability, calcium handling, oxidative stress, and muscle-cell signaling.

Those mechanisms help explain why muscle effects are biologically plausible. They do not show that most people taking statins will gradually lose muscle because of the medication.

Protecting Arteries and Preserving Muscle

Atherosclerotic cardiovascular disease remains one of the leading causes of death and disability. In appropriately selected patients, lowering ApoB-containing lipoproteins can significantly reduce cardiovascular risk.

Muscle deserves the same long-term attention. Skeletal muscle is central to glucose disposal, insulin sensitivity, mobility, balance, bone loading, and physical independence. Loss of muscle mass and strength increases the risk of frailty, falls, fractures, metabolic dysfunction, and loss of function with age.

Protecting cardiovascular health should not come at the expense of ignoring muscle health. Both can be followed.

That is part of the broader HormoneSynergy® preventive cardiology approach, where lipid treatment is considered alongside insulin resistance, inflammation, body composition, exercise, and other factors that shape long-term cardiovascular health.

What Is Worth Monitoring?

For someone who may remain on lipid-lowering therapy for years or decades, a cholesterol panel provides only part of the picture.

Depending on the patient, useful measures may include:

• Strength and functional performance
• Changes in exercise tolerance
• Lean mass and appendicular lean mass
• Protein intake and nutritional status
• Resistance-training volume
• Thyroid function when clinically indicated
• Vitamin D status when clinically relevant
• Glucose regulation and insulin resistance
• Medication dose and statin type
• New muscle pain, weakness, or cramping

Body composition can be especially useful because body weight cannot tell us whether a person is gaining or losing muscle.

Our Body Composition and Longevity Medicine guide explains why lean mass, visceral fat, and muscle distribution are clinically useful measures of aging and metabolic health.

Should Someone Stop a Statin Because of This Study?

No. An observational study showing an association is not a reason to abruptly stop a medication that may be substantially reducing cardiovascular risk.

The more useful questions are whether the statin is indicated, whether the dose fits the patient's cardiovascular risk, whether lipid targets are being reached, and whether the treatment is being well tolerated.

For patients with genuine statin-associated muscle symptoms, the 2026 ACC/AHA dyslipidemia guideline recommends looking for other possible causes of the symptoms and adjusting treatment when necessary. Depending on the patient, that may involve a different statin, a lower tolerated dose, an altered dosing schedule, or nonstatin lipid-lowering therapy.

There is no reason to treat statin therapy as an all-or-nothing decision. Cardiovascular risk, medication tolerance, muscle health, metabolic health, and the alternatives available to the patient all belong in the same discussion.

The HormoneSynergy® Perspective

This study does not persuade us that statins routinely cause sarcopenia. It does give us another reason to pay attention to muscle in patients who may remain on lipid-lowering therapy for decades.

ApoB, LDL cholesterol, and plaque burden matter. So do glucose regulation, inflammation, bone density, body composition, muscle strength, exercise capacity, and the ability to remain physically independent with age.

If cardiovascular risk markers are improving and muscle mass and strength remain stable, that is reassuring.

If cardiovascular markers improve while strength, lean mass, or exercise capacity steadily deteriorate, we want to know that too.

The response should be measurement, not panic.

Muscle mass and strength already decline with age. A treatment that might accelerate that decline deserves scrutiny. Untreated atherosclerosis deserves scrutiny as well.

Long-term preventive care should account for both.

Frequently Asked Questions

Do statins cause muscle loss?

Statins can cause muscle symptoms in some patients, but it is still unclear whether long-term statin therapy routinely accelerates age-related loss of muscle mass. One large UK Biobank study found an association with faster decline, while several other studies have found no significant adverse effect.

Did the new study show that statins cause a 73% loss of muscle?

No. The 73% figure describes the relative difference in the modeled rate of appendicular lean-mass decline compared with never-users. It does not mean participants lost 73% of their muscle.

Can statins cause muscle weakness even if CK is normal?

Yes. Statin-associated muscle symptoms can occur without a major elevation in creatine kinase. CK is particularly important when symptoms are severe or significant muscle injury is suspected, but a normal CK does not automatically exclude statin-associated symptoms.

Should I stop taking a statin if I notice muscle weakness?

Do not abruptly discontinue cardiovascular medication based on an article or an isolated symptom. New or progressive weakness should be discussed with the prescribing clinician so the medication, dose, other possible causes, and cardiovascular risk can be reviewed.

Can DEXA track muscle loss?

Yes. Whole-body DEXA can measure total and regional lean mass, including appendicular lean mass. Repeating the study under similar conditions can help identify meaningful changes in body composition over time.

What helps preserve muscle with aging?

Progressive resistance training, adequate protein intake, sufficient calories, regular physical activity, restorative sleep, and treatment of relevant medical or hormonal problems are among the foundations of preserving muscle with age. These measures remain important whether or not someone takes a statin.

References and Further Reading

• Gentreau M, et al. Statin Use Is Associated With a Decline in Muscle Function and Mass Over Time, Irrespective of Statin Pharmacogenomic Score. Journal of Cachexia, Sarcopenia and Muscle. 2025.
• Fazel SD, et al. Statin use does not impair muscle health in older adults: findings from the SCOPE study. Aging Clinical and Experimental Research. 2026.
• Mondéjar-Barrios MD, et al. Effect of statin use on the development of sarcopenia in older adults: A systematic review and meta-analysis. Experimental Gerontology. 2026.
• Aydoğan TMI, et al. Long-term intake of statins or renin-angiotensin system inhibitors: associations with sarcopenia-related parameters in older people. GeroScience. 2026.
• Cholesterol Treatment Trialists' Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomized, double-blind trials. The Lancet. 2022.
• Parker BA, et al. Effect of statins on skeletal muscle function. Circulation. 2013.
• 2026 ACC/AHA Guideline on the Management of Dyslipidemia.

Medical Disclaimer: This article is for educational purposes only and does not constitute medical advice or establish a physician-patient relationship. Decisions regarding statin therapy or other cardiovascular medications should be individualized with a qualified healthcare professional.