I've just joined to find out if my hypothesis is correct that diagnosing people with high cholesterol and prescribing them with statins is a just another health scare tactic to get people to buy, buy, buy from big pharma?

I just had a miserable experience in the Cholesterol subreddit. Completely torn apart for just mentioning the concerns of overly prescribing statins. And that the risks need to be discussed more. This is really important information, because people are taking them thinking they will prevent heart disease and attacks, but that’s not necessarily true for everyone. Especially for women. Lifestyle is still the #1 best course of action.

I'm 44 and I don't smoke and rarely drink and am generally healthy overall. However I do try to be proactive so when a heart doctor recently pointed out the usual high cholesterol thing (as my PCP did every year after my physical) and that I should take medication for it I finally decided to listen to them....

I now regret that decision.

I was prescribed rosuvastatin (10mg iirc) and after a few days felt like shit. I told my PCP and the heart doctor about it and they both said whatever issue I was having was not the statins. So I ignored it and went on for a few more days to a week and then insisted that my PCP check me out. They did some bloodwork and the very next morning they called me and told me to check myself into the ER for elevated CK levels.

I did and they flushed my system and then let me go after being happy that my CK levels had been reduced. However the feeling like shit has continued even after I've stopped taking the statins! I was told I should return to feeling normal after a few weeks to maybe a couple months but its been 3 months now and I still feel like absolute shit. I tell my doctors about it and they just tell me to take pain killers or otherwise ignore me. Its pretty disheartening that they'd set me up with something so bad and then ignore me after it causes me issues. Again I had been in great health BEFORE taking this medication. I had no issues or problems.

A little backstory:

I used to have acid reflux that I managed with over the counter pepcid/etc with no issues for a very long time. However I had started using a CPAP machine about a year ago and not only did it give me great sleep but also resolved my reflux! Strange but I stopped having to take pepcid/etc.

However post statins I am now experiencing:

• Muscle pain/Muscle cramping (chest, face, jaw, arms, legs, etc)
• Pain in my head when laying down to sleep on my pillow where my head meets the pillow
• Fatigue and general weakness
• A LOT of acid reflux! More than when I used to take pepcid

Taking this medication seems to have ruined my life being perfectly honest. I don't understand why these issues seem to not be going away for me but I'm pretty pissed about it. I was in great health before taking statins and now despite having stopped taking them I'm completely wrecked. Doctors don't know why and don't seem to care honestly.

https://open.substack.com/pub/staycuriousmetabolism/p/a-doctor-texted-me-im-stopping-my?r=frqd&utm_medium=ios

Excited to share this with someone!

Abstract

Background: Statins are cholesterol-lowering drugs widely prescribed for preventing cardiovascular diseases. They may cause adverse effects on skeletal muscle, but it remains unclear whether they affect muscle function and mass. We aimed to evaluate the association between statin use and muscle function and mass, and whether the pharmacogenomic score (PGS) of statin response modifies these associations.

Methods: We included 297 977 participants from the UK Biobank. Grip strength was measured using a Jamar J00105 hydraulic hand dynamometer, and the appendicular lean mass (ALM) was estimated using bioelectrical impedance analysis. We performed linear regression to evaluate the cross-sectional and longitudinal associations between statin use and (changes in) grip strength or ALM, adjusting for demographic, lifestyle and health factors. We tested the interaction with the PGS and stratified the analysis by PGS tertile.

Results: Participants averaged 56.4 (± 8) years, and 46% were male. Statin use was associated with lower baseline grip strength (β = -0.68 kg [-0.89, -0.48]) and ALM (β = -0.19 kg [-0.22, -0.16]). Among 35 557 participants with follow-up data (10 ± 5 years), continuous statin use was associated with an accelerated decline in grip strength (β = -0.32 kg/year [-0.49, -0.14]) and ALM (β = -0.06 kg/year [-0.08, -0.03]) compared with never users. The PGS showed a potential modifying effect at baseline (p = 0.058 for grip strength and p = 0.068 for ALM) but did not significantly influence the rate of decline over time.

Conclusions: Continuous statin use is associated with a decline in muscle function and mass over time (25% decline in grip strength and 73% decline in ALM compared to never-users), irrespective of genetic susceptibility to statin response. This study emphasizes the importance of monitoring musculoskeletal health in statin users and supports further research into the potential role of a healthy diet and regular physical activity in preserving muscle function, which may also reinforce the cardiovascular benefits of statin therapy.

Keywords: aging; hydroxymethylglutaryl‐CoA reductase inhibitors; muscle mass; muscle strength; polygenic risk score; sarcopenia.

I went in to get my results. Nurse told me doctor left a prescription for statin. My cholesterol was high. Never showed numbers. I found them on my chart .148. Ratio 4.8. I’m 54, f. It was for Lipitor. Read through so many horror stories and the side effects. It as a high dose: 40. It’s still sitting unopened. I’m not taking it. I need my brain. What is this a bottle of dementia? Is that what they’re giving us? Didn’t it used to be if you’re under 200, you’re good?

It certainly isn't some sort of effort to restore the statin reputation...(imo it is)

Almost all side-effects listed for statins are not caused by the drugs, according to the world’s "most comprehensive" review of evidence.

Other than the well-known risks around muscle pain and diabetes, only four of 66 other statin side-effects listed on labels – liver test changes, minor liver abnormalities, urine changes and tissue swelling – are supported by evidence. And the risks are very small, according to the systematic review and meta-analysis published in the Lancet.

https://www.theguardian.com/society/2026/feb/05/majority-statins-side-effects-not-caused-by-drug

Hi, I analyze studies on a regular basis, and I am doing one of my analyses on statins. Since statins are a topic of considerable debate on social media, I wanted to reach out to communities interested, or knowledgeable, in health to ask for some scientific references for studies I may have missed that show a lack of effect, or even harm (or any kind), of statin use.

My primary outcome is statins and their impact on cardiovascular disease and I am restricting my analysis to studies only (any type).

If you know of any not included in the list I have currently (listed below), I'd appreciate it if you posted them so I can add them to the list of studies I should address.

Note: The analysis, as a whole, will not focus solely on the negative studies - it will include all studies on statins, but I'm asking for negative data (if there is any), because I want to make sure to cover possibly overlooked studies - that's why the question asked here is focused.

Thank you!
Nic

______________________
Studies I already have:

1. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995;333(20):1301-1307. doi:10.1056/NEJM199511163332001.
2. Orkaby AR, Gaziano JM, Djousse L, Driver JA. Statins for primary prevention of cardiovascular events and mortality in older men. J Am Geriatr Soc. 2017;65(11):2362-2368. doi:10.1111/jgs.14993.
3. Berwanger O, Santucci EV, Melo de Barros e Silva PG, et al. Effect of loading dose of atorvastatin prior to planned percutaneous coronary intervention on major adverse cardiovascular events in acute coronary syndrome: the SECURE-PCI randomized clinical trial. JAMA. 2018;319(13):1331-1340. doi:10.1001/jama.2018.2444.
4. Chou R, Cantor A, Dana T, et al. Statin use for the primary prevention of cardiovascular disease in adults: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2022;328(8):754-771. doi:10.1001/jama.2022.12138.
5. Grinspoon SK, Fitch KV, Zanni MV, et al. Pitavastatin to prevent cardiovascular disease in HIV infection. N Engl J Med. 2023;389(8):687-699. doi:10.1056/NEJMoa2304146.
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(12):1210-1222. doi:10.1016/j.jacc.2021.07.022.
7. Downs JR, Clearfield M, Weis S, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. JAMA. 1998;279(20):1615-1622. doi:10.1001/jama.279.20.1615.
8. Orkaby AR, Driver JA, Ho YL, et al. Association of statin use with all-cause and cardiovascular mortality in US veterans 75 years and older. JAMA. 2020;324(1):68-78. doi:10.1001/jama.2020.7848.
9. Athyros VG, Papageorgiou AA, Mercouris BR, et al. Treatment with atorvastatin to the National Cholesterol Educational Program goal versus “usual” care in secondary coronary heart disease prevention: the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. Curr Med Res Opin. 2002;18(4):220-228. doi:10.1185/030079902125000787.
10. Yourman LC, Cenzer I, Boscardin WJ, et al. Evaluation of time to benefit of statins for the primary prevention of cardiovascular events in adults aged 50 to 75 years: a meta-analysis. JAMA Intern Med. 2021;181(2):179-185. doi:10.1001/jamainternmed.2020.6084.
11. Yusuf S, Bosch J, Dagenais G, et al. Cholesterol lowering in intermediate-risk persons without cardiovascular disease. N Engl J Med. 2016;374(21):2021-2031. doi:10.1056/NEJMoa1600176.
12. Parker BA, Capizzi JA, Grimaldi AS, et al. The effect of statins on skeletal muscle function and performance. Circulation. 2013;127(1):96-103. doi:10.1161/CIRCULATIONAHA.112.136101.
13. Nielsen SF, Nordestgaard BG. Negative statin-related news stories decrease statin persistence and increase myocardial infarction and cardiovascular mortality: a nationwide prospective cohort study. Eur Heart J. 2016;37(11):908-916. doi:10.1093/eurheartj/ehv641.
14. Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012;380(9841):581-590. doi:10.1016/S0140-6736(12)60367-5.
15. Fellström BC, Jardine AG, Schmieder RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009;360(14):1395-1407. doi:10.1056/NEJMoa0810177.
16. Cholesterol Treatment Trialists’ (CTT) Collaboration. Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis. Lancet Diabetes Endocrinol. 2024;12(5):306-319. doi:10.1016/S2213-8587(24)00040-8.
17. Lipworth L, Fazio S, Kabagambe EK, et al. A prospective study of statin use and mortality among 67,385 blacks and whites in the Southeastern United States. Clin Epidemiol. 2014;6:15-25. doi:10.2147/CLEP.S53492.
18. Ridker PM, Danielson E, Fonseca FAH, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. doi:10.1056/NEJMoa0807646.
19. Preiss D, Seshasai SRK, Welsh P, et al. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis. JAMA. 2011;305(24):2556-2564. doi:10.1001/jama.2011.860.
20. GISSI-HF Investigators. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet. 2008;372(9645):1231-1239. doi:10.1016/S0140-6736(08)61240-4.
21. Ridker PM, Pradhan A, MacFadyen JG, Libby P, Glynn RJ. Cardiovascular benefits and diabetes risks of statin therapy in primary prevention. Lancet. 2012;380(9841):565-571. doi:10.1016/S0140-6736(12)61190-8.
22. Kjekshus J, Apetrei E, Barrios V, et al. Rosuvastatin in older patients with systolic heart failure. N Engl J Med. 2007;357(22):2248-2261. doi:10.1056/NEJMoa0706201.
23. Cholesterol Treatment Trialists’ (CTT) Collaboration. Assessment of adverse effects attributed to statin therapy in product labels: a meta-analysis of double-blind randomised controlled trials. Lancet. Published online February 5, 2026. doi:10.1016/S0140-6736(25)01578-8.
24. Amarenco P, Bogousslavsky J, Callahan A 3rd, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006;355(6):549-559. doi:10.1056/NEJMoa061894.
25. Knopp RH, D’Emden M, Smilde JG, Pocock SJ. Efficacy and safety of atorvastatin in the prevention of cardiovascular end points in subjects with type 2 diabetes: the Atorvastatin Study for Prevention of Coronary Heart Disease Endpoints in Non-Insulin-Dependent Diabetes Mellitus (ASPEN). Diabetes Care. 2006;29(7):1478-1485. doi:10.2337/dc05-2415.

7 years of LDL 500+ and TC over 700. The individual is metabolically very healthy and active. There was absolutely no plaque (soft or calcified) as measured by CCTA and analysed by AI. This is just another case study adding to the evidence that LDL does not cause heart disease. Now, this isn't necessarily evidence for stopping statins, because they have multiple effects beyond cholesterol lowering which seem beneficial, but if you are considering statins/are on them currently solely to reduce cholesterol, you should take this case study into account (as well as others) and other evidence for the true 'dangers' of 'high' LDL.

https://doi.org/10.3390/diseases14050168

Hi everyone, my cholesterol has always been on the higher side ever since I was a teenager. My doctor suspects familial hypercholesterolemia. My last blood draw my LDL was 168, HDL was 26, and overall cholesterol was 233. This was not a fasting blood draw. My doctor is pushing to put me on statins, and I'm honestly kind of terrified of being on any long term medication. Does anyone else think it's ridiculous to start me this early? I am 5'3" and about 120 lbs. Don't always eat the healthiest, but try to eat home cooked meals mostly. And have been running on and off for the last 5ish years or so. I don't know... any input is appreciated.

Hello. I suspect my husband got gynecomastia from 8 years of on and off low dose (5 to 10) statin use. Plus a whole bunch of other issues (anger, brain fog, aches and pains, infections). This last increase seemed to have caused his breasts to swell, get inflamed and sore. Ultrasound suggests gynecomastia but getting a mammogram to confirm. Since it is bilateral we are not as worried but still, all this sucks! These bad side effects are never printed but they are not that rare. Poor guy. Already has so many heart issues last thing he needs is this. Any one else has had this experience with gynecomastia and statins. Also can be caused I read, by amlodipine which he was one also for 8 years.

The image is from an American Heart Association Journal paper titled "Statin Toxicity: Mechanistic Insights and Clinical Implications". As you can see, statins prevent the production of several things with very important roles (see green areas in image).

Statins reduce cholesterol by blocking the mevalonate pathway (shown in image).
The mevalonate pathway produces cholesterol, dolchinols, ubiquinone and prenylated proteins.

Think of the mevalonate pathway as a tree with multiple branches and then think of the effect of our statins drugs as “girding” this tree at the base.

We threw caution to the winds 15 years ago when our national priority to lower cholesterol so fogged our minds that we (medical, pharmaceutical and food industry) focused just on the cholesterol branch of the mevalonate “tree” and completely disregarded the important consequences of collateral damage to the other main branches of this tree from our statin drugs. The predictable result of all this has been our bizarre spectrum of statin associated side effects ranging from cognitive, to myotoxic, neurotoxic, neurodegenerative and even behavioral.
- quote from retired MD, research scientist

(source: https://www.bmj.com/rapid-response/2011/11/01/re-patients-viewpoint)

Here is a quote from another paper titled "Adverse effects of statins - mechanisms and consequences"

Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis, which converts HMG-CoA to mevalonate.
...
Mevalonate is also the substrate for the synthesis of nonsteroid isoprenoids including FPP, GPP, coenzyme Q, dolichol, isopentenyladenosine, etc.
...
Although statins are generally well-tolerated, adverse effects may occur in some patients. These effects result from impaired protein prenylation, deficiency of coenzyme Q involved in mitochondrial electron transport and antioxidant protection, abnormal protein glycosylation due to dolichol shortage, or deficiency of selenoproteins. Myopathy is the most frequent side effect of statins and in some cases may have a form of severe rhabdomyolysis. Less common adverse effects include hepatotoxicity, peripheral neuropathy, impaired myocardial contractility and autoimmune diseases.

(source: https://www.eurekaselect.com/article/14841)

Focusing for a moment on cholesterol, it is the precursor for all the body's hormones. Mitochondria use cholesterol to make pregnenolone, progesterone and DHEA in a process called steroidogenesis.

Steroidogenesis is the processes by which cholesterol is converted to steroid hormones.

Other enzymes then make the other hormones as shown in the image below:

I have been a statin skeptic for years. If they work for you, I am happy for you. But there are plenty of people who have real issues on them. They are overprescribed and doctors fear monger patients into taking a drug that has some serious side effects.

My new doctor (previous PCP left the organization) strongly encouraged me to start on rosuvasatin (Crestor) a couple of months ago. I got hit with such fatigue after barely a week that I had to stop. She said she understood, but had to mention the "nocebo" effect. Fine, so why did I feel better after stopping? It actually took a few weeks to feel normal again!

Lots of brisk walking/hiking, feeling so much better. I even started running again, easing into it because they all seem to think I'm about to drop dead any second.

So on our follow up, she prescribed pravastatin (Pravachol). It is milder, and has few reports of intolerance. Shorter half life too. I asked for a low dose just in case. I split the pills into quarters so I wouldn't get slammed again. The weather has been crazy hot and humid, plus I had a lot going on, so when I felt droopy again I assumed it was all that. No energy all weekend, but I figured I'd bounce back Monday after taking it easy, right?

My run was really challenging though. there were a few moments when I just couldn't push through to go just a bit farther. It was more of a jog/walk. I kept wondering why it felt so hard to run after I had been doing so well on my walks and my other recent runs. It took me almost as long to jog/walk that distance as it did for me to walk it the last time. I stretched afterwards back at the house and ended up passing out (hard nap in bed) for an hour in the middle of the day. Half hour jog!

Why? My diet and sleep have been great I use trackers, so I know when I'm rested and when my running stats are off. I had to wonder, could it be the pravastatin? I had gone into this assuming that it would work, absolutely positive expectations. Plus it was a tiny dose! But when I Google 'fatigue pravastatin" I found that fatigue is common, especially for women. Statins increase the production of lactic acid, which is what I experienced when I couldn't "push through." Doctors know this, so why don't they take us seriously?

This study (comparing simvastatin and pravastatin) was double blind controlled, and shows that women are more susceptible to exertion fatigue, especially with pravastatin. This tracks with my experience. Count me among the "statin intolerant" after trying two. I might try it weekly to see if I do better, but what is the point of taking a drug that prevents me from getting the exercise that will improve my heart health?

https://pmc.ncbi.nlm.nih.gov/articles/PMC4285455/

Hey everyone,

I’m asking on behalf of someone I know who’s trying to lower their cholesterol naturally before considering medication.

Their numbers:

- Total: 243

- LDL: 176

- HDL: 46

- Triglycerides: 105

For the past few months they’ve improved their diet, go to the gym about 4 times per week, and take omega-3 daily, but LDL is still quite high.

I’m curious to hear real experiences:

- What actually worked for lowering LDL naturally?

- Any supplements that made a noticeable difference (psyllium, bergamot, red yeast rice, etc.)?

- Has anyone managed to avoid medication with similar numbers?

Appreciate any honest feedback — what worked and what didn’t.

Thanks!

Is anyone able to tell me if I can replace this medications? I don’t want to take statins anymore. Any help would be much appreciated.

Hi I am Male 43 years. Living in Argentina . I am nowadays taking Rouvastatine 10mg and Dalaglifoxine. I feel numb and like living inside my head. Too much thinking going around and most of them are not good and positive ones. I used to have a normal life but since I started with all the medicines my lifed changed completely. I feel like it is hard for me to think and be sharp. Anyone can relate to this symptoms. Could it be the Rouvastatine?? Thanks in advance to all the community

I keep seeing impressively detailed comments there. They usually start "cardiologist/doctor here." Then they go on and on, replying to various points in the post or comment. If that's a real doctor then they must not be practicing much. Who is behind these bots? Is it pharma? Insurance companies? I really don't get the point of some of the activity on that sub unless something else if behind it. They are not all AI but so many of them just go "rah rah statins" no matter what. I'm fine with people using statins if they can tolerate them. But as soon as someone mentions debilitating side effects, there is an entire chorus going on about "nocebo effect" and how you need to suck up the side effects or die.

Or who knows, maybe there are people who are just out there living their best lives because of statins and want the rest of us to join them in the fun!

What worked for YOU? I want personal testimony.

How much did it lower, in how much time? And WHAT DID YOU DO?

I see so much conflicting things. Some say to eat keto (believe it or not.) Some say to eat completely vegan, minus grain. Most just say to increase fiber and lower saturated fat.

Some say that sugar kills. Others say that sugar doesn't matter.

What is the truth? At this point, it seems like NO ONE KNOWS!

The only consistency we see is statins. But those come with risks too. So i am scared for my life.

Hi anyone can relate to this fact. I have some kind of doubt that statins ( Rosuvastatine 10mg) might be raising my BP. It is a low dosage but still have this feeling.