Statins may grow part of your brain while simultaneously shrinking your testosterone levels. That’s not a theoretical trade-off – it’s what researchers found when they analyzed genetic data from 340,000 people taking cholesterol-lowering medications. The study, led by Kitty Pham, a Ph.D. student at the University of South Australia, was the first of its kind to compare both statins and a newer drug class called PCSK9 inhibitors against a wide range of body and brain measurements. What emerged was a picture far more complicated than “lower your cholesterol, protect your heart.”
The University of South Australia study, published in the British Journal of Clinical Pharmacology, compared cholesterol-lowering drugs to a range of clinical, heart, and brain MRI biomarkers, drawing on genetic data from 340,000 UK Biobank participants. The researchers weren’t running a traditional drug trial. Chief investigator Professor Elina Hypponen, Centre Director of the Australian Centre for Precision Health at the University of South Australia, explains that using genetic information made it possible to compare drug outcomes across a sample size that would never be practical in a conventional clinical trial.
The headline finding got a lot of attention: a class of drugs millions of people have never heard of may be silently affecting their lungs. But the statin findings – body weight, hormones, and brain tissue – were just as striking, and they touch the lives of far more people. More than 200 million people around the world take statins or other medications for high cholesterol. For that many people, “side effects beyond cholesterol” is not a footnote. It’s a conversation worth having.
Cholesterol Drugs Side Effects: What the Research Actually Found
One unexpected benefit of statin use emerged from the study: some people saw an increase in brain volume in the hippocampus, the region of the brain central to memory and emotional regulation, which may reduce the risk of dementia and depression. That’s a genuinely counterintuitive finding. Statins are a cholesterol-blocking drug. The brain is the most cholesterol-rich organ in the body, so the assumption has long been that reducing cholesterol activity might harm brain tissue rather than protect it.
The picture isn’t entirely rosy, though. The brain does rely heavily on cholesterol for myelination – the insulating of nerve fibers – and neuronal function, and some statins can cross the blood-brain barrier, potentially affecting cholesterol synthesis within the brain itself. A 2025 study in ScienceDirect found that statin use was associated with increased cortical thickness in multiple brain regions across healthy controls and people with early Alzheimer’s disease, suggesting a potential neuroprotective effect. But a separate 2024 paper published in Brain Communications found statin users also showed higher volumes of white matter hyperintensities – small lesions that can signal vascular stress in the brain – alongside lower grey matter volumes. The effects of statin use on brain structure remain largely unknown, and studies have yielded conflicting results. The takeaway for statin users isn’t panic, but it is reason to flag any noticeable cognitive or mood changes with a doctor, particularly when starting or changing doses.
Muscle Pain, Weight, and Testosterone
Muscle aches are the side effect most people on statins already know about. What’s less understood is exactly why they happen. Genetic variants reflecting statin use were found to correlate with higher BMI and body fat, as well as reduced testosterone. Both of those findings matter practically: testosterone affects energy, muscle mass, mood, and libido, and changes in body composition can influence long-term cardiovascular risk – the very thing statins are prescribed to manage.
On testosterone specifically, the science has sharpened in recent years. A 2024 meta-analysis in the PMC database confirmed that statins are associated with a small but statistically significant reduction in total testosterone across cross-sectional studies. The effect is modest for most men, but it can matter for those who are already on the lower end of normal or who are experiencing fatigue and reduced drive without an obvious explanation.
The weight connection is equally worth understanding. A 2014 study found that statin users gained an additional 3- 5 kg over a 10-year period vs those who did not. That number sounds trivial, but the mechanism behind it is not. Statins may alter bile acid metabolism, gut microbiota, or lower GLP-1 hormone levels – GLP-1 being the same appetite-regulating hormone that newer weight-loss drugs like semaglutide are designed to mimic. In other words, statins may gently work against appetite control at the same time as they protect the heart.
The muscle pain story got a significant update in early 2026. Research reported by ScienceDaily discussed the ryanodine receptor in muscle cells as the likely mechanism behind statin-induced muscle pain, and suggested that redesigning statins so they no longer bind to that receptor could one day eliminate this side effect entirely. That’s still a future possibility, not a current solution. For now, atorvastatin and simvastatin are associated with higher incidences of myopathy compared to pravastatin, according to a report from US Pharmacist – so if muscle pain is a problem, switching statin type rather than stopping therapy is often the better conversation to have with a prescriber. Severe cases are rare: the most serious form of muscle breakdown, rhabdomyolysis, affects approximately 1 in 10,000 statin patients, according to a study in the British Journal of Pharmacology.
For people concerned about how their statin may be affecting CoQ10 levels and muscle energy – a related and frequently overlooked issue – this deep look at statin-related nutrient depletion covers the biochemical connection clearly.
What Statins Do Beyond Cholesterol
The conversation about the side effects of cholesterol drugs often focuses on what statins take away, but they also add something. A 2026 paper in the Journal of Clinical Lipidology found that statins improve endothelial function, reduce vascular inflammation, and help stabilize atherosclerotic plaques – the fatty deposits inside artery walls that can rupture and cause heart attacks. These are effects that happen separately from the cholesterol-lowering itself, which is why researchers call them “pleiotropic effects” (meaning effects beyond the primary target).
One of the most clinically meaningful of these is inflammation control. Statins lower C-reactive protein (CRP), a key inflammation marker, independently of their effect on cholesterol levels, according to a 2022 network meta-analysis in Frontiers in Cardiovascular Medicine. CRP is one of the most widely used markers of systemic inflammation, and elevated levels are associated with a higher risk of heart attack, stroke, and even some cancers. Getting that number down – regardless of what cholesterol is doing – is a meaningful benefit.
For years, there was some concern that statins could potentially affect kidney health. However, that fear has largely been put to rest. According to a 2025 study, “statin therapy was not associated with improved or worsened kidney function.” For people who have avoided or delayed statin therapy out of concern for their kidneys, that finding offers some reassurance.
The PCSK9 Inhibitor Question
PCSK9 inhibitors – drugs like evolocumab (Repatha) and alirocumab (Praluent) – work differently from statins. While statins inhibit the production of cholesterol, PCSK9 drugs work by destroying cholesterol already present in the cells. They are newer, considerably more expensive, and prescribed mainly for people who can’t tolerate statins or whose cholesterol remains dangerously high despite statin use.
Their cardiovascular credentials are strong. A 2025 study published in the European Heart Journal found that PCSK9 inhibitors combined with statins reduced the risk of heart attack by 21 percent compared to statins alone. Separately, 2025 research published in Frontiers in Endocrinology found that PCSK9 inhibitor use was associated with a 35 percent reduction in all-cause mortality in patients with type 2 diabetes and dyslipidemia (abnormal blood fat levels) – a substantial signal in a high-risk population.
But the side effect picture for PCSK9 inhibitors is still being written. Research from the University of South Australia found that PCSK9 inhibitors could impair lung function, and further studies are needed on their long-term side effects. The mechanism isn’t fully understood yet. PCSK9 is a protein that plays roles beyond cholesterol metabolism – it’s expressed in lung tissue – and when drugs suppress it systemically, the consequences for the lungs may be an unintended consequence.
Beyond the lungs, a 2023 analysis of the FDA adverse event database found that PCSK9 inhibitors showed a musculoskeletal adverse event signal 5.92 times higher than in non-users, suggesting muscle-related complaints are not exclusive to statins. And emerging real-world evidence suggests that PCSK9 inhibitors may increase the risk of infections, with respiratory tract infections the most frequently reported type, according to a 2025 paper in PMC. On the inflammation side, the 2026 paper in the Journal of Clinical Lipidology found that PCSK9 inhibition reduces specific vascular inflammation markers without broadly altering the global immune response – a finding that suggests the drugs are more targeted in their anti-inflammatory effects than statins.
Read More: Cholesterol Drug Could Have Serious Side Effects in Some People, Health Authorities Say
What Does This All Mean?
The core tension in all of this research is that both drug classes do exactly what they’re supposed to do – lower LDL cholesterol and reduce cardiovascular risk – while also producing effects on tissues and systems that have nothing to do with cholesterol. That’s not unusual for any medication, but it is a reason to treat prescribing as an ongoing conversation rather than a one-time decision.
If you take a statin and have noticed muscle aches, weight creep, low energy, or mood changes, discuss them with your doctor. Never stop any prescribed treatment from your doctor. Switching from atorvastatin or simvastatin to pravastatin may reduce muscle-related side effects. Asking about CoQ10 supplementation is reasonable given the biochemical pathway involved. If you’re on a PCSK9 inhibitor and notice any change in breathing, especially shortness of breath or a persistent cough, flag it early – the lung connection from the University of South Australia research is still being investigated, and your report could matter.
The broader message from this body of research is precision. As Kitty Pham, the lead researcher of the University of South Australia study, put it: the findings on lung function and brain size may influence how these drugs are prescribed or repurposed in the future. One pill does not fit every body, and the growing body of evidence on cholesterol drugs side effects is the basis for asking better questions – not for avoiding treatment, but for tailoring it. Statins still largely have a net benefit for anyone taking them.
Disclaimer: The author is not a licensed medical professional. The information provided is for general informational and educational purposes only and is based on research from publicly available, reputable sources. It is not intended to constitute, and should not be relied upon as, medical advice, diagnosis, or treatment. Always consult a licensed physician or other qualified healthcare provider regarding any medical condition, symptoms, or medications. Do not disregard, avoid, or delay seeking professional medical advice or treatment because of information contained herein.
AI Disclaimer: This article was created with the assistance of AI tools and reviewed by a human editor.
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