Comment by Buttons840

9 months ago

I am not a statin skeptic--or rather, I don't want to be a statin skeptic. I've done the research and it makes sense to me, but I still feel some social and psychological pressures to reject statins.

When I see that it is widely accepted that ApoB is better to measure than LDL-C, but the industry continues to measure LDL-C, but not ApoB, I wonder why. It makes me skeptical.

When I see that the purpose of statins is to reduce plaque buildup in the arteries, and that we have the ability to measure these plaque buildups with scans, but the scans are rarely done, I wonder why. Like, we will see a high LDL-C number (which, again, we should be looking at ApoB instead), and so we get worried about arterial plaque, and we have the ability to directly measure arterial plaque, but we don't, and instead just prescribe a statin. We're worried about X, and have the ability to measure X, but we don't measure X, and instead just prescribe a pill based on proxy indicator Y. It makes me skeptical.

In the end statins reduce the chance of heart attack by like 30% I think. Not bad, but if you have a heart attack without statins, you probably (70%) would have had a heart attack with statins too. That's what a 30% risk reduction means, right?

As you can see, I'm worried about cholesterol and statins.

If you fix it without statins through better lifestyle and diet, that is the preferrable route.

As to why medicine is like this, it's because it's conservative, usually about 17 years behind university research[0], and doctors are shackled to guidelines in most health systems or risk losing their licenses. It isn't a coincidence that the article author had his out-of-pocket concierge doctor tell him the more up-to-date stuff.

[0] https://pmc.ncbi.nlm.nih.gov/articles/PMC3241518/

  • I have an objection to the "better lifestyle and diet" approach.

    Sure, it is absolutely true that better lifestyle and diet has a huge effect. However it is absolutely certain that the vast majority of people who are told to improve their lifestyle and diet, won't.

    The result is doctors giving advice that they know won't be followed. And thereby transferring potential fault from the doctor to the patient, with no improvement in actual outcomes. "I told the patient to lose weight and maintain that with a controlled diet." And yet, most people when told to diet, won't. Most people who start a diet won't complete it. And most people who lose weight on a diet, have the weight back within 5 years. Where each "most" actually is "the overwhelming majority". And the likelihood of the advice resulting in sustained weight loss probably being somewhere around a fraction of a percent.

    What, then, is the value of the doctor giving this lecture?

    (Disclaimer. I have lost 20 of the pounds I gained during COVID, and am making zero progress on the remaining 30. A few months ago I successfully started a good exercise routine. Given my history, I would expect to only follow it for a few years before falling off the wagon. I believe that this poor compliance puts me well above average. But do you know what I do reliably? Take my prescribed medicine!)

    • Your health is ultimately your own responsibility - it's your body. You have free will, and your appetite for risk is yours alone. You can choose to ignore expert advice and refuse to wear a seatbelt, skip your rehabilitation exercises, invest all-in on crypto, or smoke cigarettes. None of this responsibility should fall on the expert if they communicated the risks clearly.

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    • > Sure, it is absolutely true that better lifestyle and diet has a huge effect.

      not for me. My cholesterol was hovering in the high 200's, then finally hit 300 and I completely freaked out, radically changed my diet, and lost 22 pounds (from 180 to 158).

      What did my high cholesterol do ? It did absolutely nothing. ticked down to like, 280.

      So I'm on the statins. my total cholesterol went from high 200's to about 150 in a month and was impacting my liver function. so we reduced the statins to a very low dose (5mg three times a week, crazy low). My total cholesterol hovers around 200 now. My cardiologist tells me that the conventional wisdom of "diet and exercise" is almost entirely disproven to have any meaningful effect on lipids these days (though i havent researched deeply).

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    • I think people use it as cudgel to blame people and as a crutch to avoid action. And we ignore the psychological and other factors that make improving lifestyle and eating better difficult.

      No doctor wants their patient to have a stroke. But they also only get to meet patients where they are.

    • You're arguing against a strawman. The reality is that most doctors will tell the patient their options and let them pick. While statins have some significant side effects in many patients, there is no downside to a better diet and frequent hard exercise (assuming proper technique). So it usually makes sense to at least try lifestyle modification as the initial therapy. And if that doesn't work for whatever reason then prescribe the drugs.

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    • That is because dietary advice they give is actually bad. It mostly boils down to "limit calories while eating standard western diet" but that is impossible to follow long-term as SWD and similar (e.g. food pyramid) diets are nutrient-deficient.

      How many doctors recommend things like paleo diet, intermittent fasting and so on? Not many, I think - most simply focus on calories, combined with the advice that is either extremely generalized ("avoid sugar") or outright counterproductive ("eat 5 - 6 meals a day"). And then they wonder why people can't follow their diet.

      Here I described my own experiences: https://ketoview.wordpress.com/2025/11/09/low-fodmap-keto-di...

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  • >doctors are shackled to guidelines

    To expand, one of the coverage pillars of malpractice insurance (in the US) is the "standard of care". This is basically what most doctors and their associations consider acceptable, which by definition excludes new, better techniques.

    This is both a bug and a feature. A move fast and break things philosophy would cause more harm than good, but it also prevents rapid adoption of incremental improvements.

    • You are conflating two different things. The standard of care in a malpractice lawsuit is not necessarily the same as clinical practice guidelines. In reality doctors are free to rapidly adopt incremental improvements, especially when they are evidence based.

    • 17 years is far from rapid or move fast and break things. ApoB has been known about for quite a long time, since the 90s its effects have been obvious, and showed up in research in the 70s-80s!!! It's still not part of standard testing!!!

      Guidelines also leads to standards of care being random and heavily driven by politics & financial reasons disguised as medical best practice. South Korea and India are "parallel testing" places, which saves time, while the USA & others are serial testing places mostly because of their funding models.

      Talk to any American doctor and they will give you a bunch of emotionally wrapped cope about why it's bad because the cognitive dissonance sucks and there are liability reasons to avoid admitting your wrong. I would argue that in many cases, parallel testing is cheaper because $300 of tests is cheaper than 4 chained $500 doctor visits. But whatever.

  • There is virtually zero chance that a doctor will lose their medical license for diverging from the from the usual clinical practice guidelines around statins. Check the state medical board disciplinary records.

    But if they're employed by a health system and fail to follow company policy then yes, they could be fired.

    • Different countries are different, some are far more trigger happy about it like Canada. What you suggest as an alternative other than 'git gud' diet & exercise also changes it.

  • No, actually, you should improve your lifestyle and diet and also take statins.

    Ever cardiologist ever will tell you that statins work best when you make diet and lifestyle changes. They tell you that, to your face. It's not a secret. This actually goes for A LOT of medications. Usually, medication + diet and exercise is better than medication alone. They also test medications like this.

  • You can only do things to reduce your risk. And whatever intervention would be based on overall population statistics, since it's difficult to know your own personal risk. Heart disease kills marathon runners. You can't just "fix it". Someone who has naturally high cholesterol won't magically be okay by changing their lifestyle and diet.

  • Licensing but also insurance.

    I think only recently have insurance companies started covering APoB testing in your annual exams (or that may just be my insurance…).

    • Many commercial health plans will only cover an ApoB blood test for patients with certain conditions or risk factors. But if you want it you can pay out of pocket for like $70.

> When I see that it is widely accepted that ApoB is better to measure than LDL-C, but the industry continues to measure LDL-C, but not ApoB, I wonder why. It makes me skeptical.

ApoB is shaping up to be an incremental improvement in measurements, but health and fitness influencers have taken the marginal improvement and turned it into a hot topic to talk about.

This happens with everything in fitness: To remain topical and relevant, you always need to be taking about the newest, most cutting edge advances. If it’s contrarian or it makes you feel more informed than your doctor, it’s a perfect topic to adopt for podcasts and social media content.

ApoB is good, but it’s not necessarily the night and day difference or some radical medical advancement that obsoletes LDL-C. For practical purposes, measuring LDL-C is good enough for most people to get a general idea of the direction of their CVD risk. The influencers like to talk about edge cases where LDL-C is low but then ApoB comes along and reveals a hidden risk, but as even this article shows there isn’t even consensus about where the risk levels are for ApoB right now. A lot of the influencers are using alternative thresholds for ApoB that come from different sources.

> In the end statins reduce the chance of heart attack by like 30% I think. Not bad, but if you have a heart attack without statins, you probably (70%) would have had a heart attack with statins too. That's what a 30% risk reduction means, right?

30% reduction in a life threatening issue is huge. I don’t see why you would want to diminish that.

If you were given the choice of two different dangerous roads where one road had a 30% lower chance of getting into a life-threatening car crash, you would probably think that the choice was obvious, not that the two roads were basically the same.

  • numbers often quoted in favor of statins use relative instead of absolute risk. when seen in absolute terms there is little case for statins except in some possible particular cases. they also do little, if anything, when it comes to life extension — the expected lifespan of a statin user is often estimated to be four days longer than that of those who do not use them. not only is this essentially statistical noise, it discounts the lowered quality-of-life side effects experienced by many who have been put on statins.

    • This is all true. If you take a statin and it causes no issues, you're... maybe (30%, yay!) better off for it.

      If a statin makes you feel miserable, I think any doctor would sympathize with a calculated decision to stop them. There are many types of statins to try though, so hopefully one would work without side effects.

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    • AFAIK statins show better numbers for secondary prevention. For primary prevention its a toss up.

  • >If you were given the choice of two different dangerous roads where one road had a 30% lower chance of getting into a life-threatening car crash, you would probably think that the choice was obvious, not that the two roads were basically the same.

    You could absolutely think that they were basically the same, depending on the base rate. The differece between a one-in-a-million and 0.7-in-a-million is 30%, but it wouldn't be humanly perceivable. We're all likely faced with situations like that regularly. Differing airlines probably have much greater variances in their crash statistics, but it just doesn't matter in 99.99999% of flights.

https://jamanetwork.com/journals/jamainternalmedicine/fullar...

Meta-analysis conclusion: This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up.

  • A meta-analysis that only includes 11 studies on statins is immediately suspect.

    There have been a lot of studies on statins. If a meta-analysis comes along and only cherry picks a couple of them, something is up.

    • Have you read their methodology and understood how they did their selection? You could critique their actual methodology. Maybe their selection is backed by strong arguments, right? And if you think their methodology is weak, then please explain why.

      Not just throw a two-line comment disparaging the work of experienced specialists in the field.

      For the curious, here are the author affiliations for this study:

      Department of Public Health and Primary Care, University of Cambridge, Cambridge, England (Drs Ray, Seshasai, and Erqou); Department of Cardiology, Addenbrooke's Hospital, Cambridge (Dr Ray); Department of Clinical Pharmacology and Therapeutics, Imperial College, and National Heart and Lung Institute, London, England (Dr Sever); Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands (Dr Jukema); and Department of Statistics (Dr Ford) and BHF Glasgow Cardiovascular Research Centre, Faculty of Medicine (Dr Sattar), University of Glasgow, Glasgow, Scotland.

    • That’s fair.

      This is totally unsourced now but I did a deep dive quite a while ago now and it seemed to me that studies largely found that statins after a heart attack helped all cause mortality (though not by a ton), but if they were prescribed to someone before a heart attack it wasn’t nearly as clear. Considering how they often make people feel it seems like people should be a bit skeptical.

    • How many studies is enough? There were approx. 60k+ participants in them. If I got it right…

    • Ah, you were so close...

      If you actually read the article, you would find the selection criteria and the explanation for the criteria.

      First, a preface.

      The article was published in 2009. At the time, AstraZeneca, the maker of the controversial statin Rosuvastatin, had been engaged in a yearslong intensive campaign to promote the drug. The editor of The Lancet wrote "AstraZeneca's tactics in marketing its cholesterol-lowering drug, rosuvastatin, raise disturbing questions about how drugs enter clinical practice and what measures exist to protect patients from inadequately investigated medicines"; CEO Tom McKillop [1] angrily fired back. Consumer rights group Public Citizen tried to get the medicine withdrawn for safety reasons; the FDA denied the request [2.]

      AstraZeneca prevailed, and Rosuvastatin proceeded to make billions of dollars a year in sales. Today, 42 million Americans take it and in 2015 it was the most prescribed branded drug in America.

      Now, back to the article. Most new drugs focus on studying the most diseased patients first and then, if possible, attempt to expand to the (far larger and more lucrative) prevention markets later. Statins are no different. The overwhelming majority of research on statins has been industry-funded, done on patients with CVD. Pharma companies want to expand to a larger market, of course. So there are efforts on many fronts. One was to broaden the definition of CVD or other criteria for starting statins. For example, in 2017 the definition of high blood pressure was successfully changed from 140/90 to 130/80. That bumped up the proportion of US adults with CVD from 36% in 2011-2014 [3] to 48% in 2013-2016 [4], or in other words, added 30 million US adults to the market. Similarly, in 2013 the 2013 ACC/AHA guidelines encouraged starting statins for anyone with LDL-C ≥190 mg/dl "even in the absence of other risk factors" which increased statin use from 31 million to 92 million Americans from 2008-09 to 2018-19 [5.]

      Where did these changes come from, what motivated them? Studies, of course. Studies like the AstraZeneca-funded JUPITER trial, which claimed an improvement in the health of participants with even _low_ levels of LDL-C. A lot of this stuff was considered fairly strange, and it didn't seem to replicate. Thus the meta-analysis. Are statins truly useful for prevention?

      So, in short: Most studies investigating statins in real depth are funded or influenced by industry. They usually focus on the sickest patients, presumably to get a larger effect size, yet the industry is constantly trying to prescribe to a wider audience - the healthier patients - often on grounds that mainstream health authorities find weak. This meta-analysis was only able to include 11 studies because industry SOP is to study the sickest patients yet prescribe to a wider audience. And as you might then expect: "This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up."

      [1] If the name sounds familiar, it's because Tom McKillop was the CEO of RBS who "aggressively" pursued leveraged buyouts up until its collapse and bailout in 2008.

      [2] Here's the 10-year followup on that: https://www.bmj.com/content/350/bmj.h1388

      [3] https://www.ahajournals.org/doi/epub/10.1161/CIR.00000000000... "total CVD prevalence, age >20y, both sexes" from Table 12-1 is 36%/92.1M

      [4] https://www.ahajournals.org/doi/epub/10.1161/CIR.00000000000... "total CVD prevalence, age >20y, both sexes" from Table 13-1 is 48%/121.5M

      [5] https://pmc.ncbi.nlm.nih.gov/articles/PMC10203693/

  • https://www.lipidjournal.com/article/S1933-2874(25)00317-4/f...

    Guidance from the National Lipid Association, based on a review of the current understanding of the science across quite a few different meta-studies, analysis, etc. Many of the referenced studies are meta-studies significantly larger than the one here.

    We have mountains of studies showing the negative impact of LDL-C (and inflammation! Which statins also reduce) on health. We have mountains of studies showing positive impact from statins. We have specific mechanistic understanding of how LDL-C and other atherogenic particles cause heart disease. We have mountains of studies show that statins directly lower the amount of atherogenic particles you have.

    This has been studied enough and sliced enough ways that yeah, there is evidence on both sides. But one side is effectively a mountain range, and the other is a small hill. I know which way I'm going to land on it.

  • Concentration of ApoB-carrying lipoproteins in the bloodstream as the driver of heart disease is one of the most strongly proven facts in medicine. Statins are proven to lower LDL (a close-enough substitute for ApoB in most situations) by about 30%. I can't look at the study now, but most likely it's a situation where patients' cholesterol has not been lowered enough by medication to make a meaningful difference. If you have an LDL of 160, statins aren't going to be sufficient. The issue is doctors/patients not targeting a sufficiently low cholesterol level.

> When I see that it is widely accepted that ApoB is better to measure than LDL-C, but the industry continues to measure LDL-C, but not ApoB, I wonder why. It makes me skeptical

Because this is a recent understanding and healthcare tends to be a conservative industry that moves slowly. Sometimes too slowly.

And also because LDL remains an excellent measure. The risk with LDL isn’t false positives. If someone has high LDL they likely have an elevated risk of heart disease. The problem with LDL testing is that someone with low LDL may still have a high risk of heart disease which may be captured in APoB testing.

> When I see that it is widely accepted that ApoB is better to measure than LDL-C, but the industry continues to measure LDL-C, but not ApoB, I wonder why. It makes me skeptical.

Part of this is just that insurance coverage lags science. We've known that ApoB is more accurate than LDL since the 1990's or 2000's, but to be covered by insurance, several more steps have to happen.

First, the major professional societies (like the American College of Cardiology or National Lipid Associations) have to issue formal guidelines.

Then, the USPSTF (US Preventive Services Task Force) needs to review all of the evidence. They tend to do reviews only every 5 or 10 years. (Countries aside from the US have different organizations that perform a similar role.)

If the USPSTF issues an "A" or "B" rating, then insurance companies are legally obligated to cover ApoB testing. But that also introduces a year or two lag since medical policies are revised and apply to the next plan year.

The net effect is that the entire system is 17 years, on average, behind research.

  • ApoB blood tests are relatively cheap. You can pay out of pocket about $70 if you really want one and insurance won't cover it.

    Most commercial health plans will cover an ApoB test for members with certain cardiac risk factors or medical conditions. But they generally won't cover it as a preventive screening for all members. I don't think we have enough evidence to justify broad screening yet, although that may be coming.

> When I see that the purpose of statins is to reduce plaque buildup in the arteries, and that we have the ability to measure these plaque buildups with scans, but the scans are rarely done, I wonder why.

I'd love to know where to get the right advice on this topic.

I have high LDL-C, had a heart CT in hospital last week, yet the hospital's cardiologist phoned me yesterday to cancel a scheduled appointment to discuss the results(!), because she said I have zero arterial plaques and there's simply no need for us to meet.

I feel really quite lost with this stuff :/

  • If it was a calcium scan, it is expected to be zero until mid 40s. It doesn't really start to give a signal until then.

    A zero is still a zero though, and is associated with low risk of heart disease in the near future.

    • > If it was a calcium scan, it is expected to be zero until mid 40s.

      I turned 50 fairly recently...

  • How old are you? I was told that they're not considered diagnostic until somewhat later in life (>50) because the plaque may not have calcified yet, which could cause a false negative.

I was found to have high cholesterol in my late 20s. At the time the doctors (my cardiologist, then a second one brought in for advice) determined that the source was hereditary, but the effects would be the same. So they put me on statins. It's been 40 years now. I changed the statins three times since, when the actual one, at a specific time was no longer able to keep the values within acceptable limits. Approximately 8-9 years ago (I think) I ended up on Rosuvastatin 20mg, which I'm still taking every day. I do not maintain any diet (it'd be very hard, as I'm a heavy meat eater) and cholesterol levels are still staying within acceptable limits. Of course YMMV

  • No heart attacks or strokes? I'm in the same boat (hereditary issue), and altering my diet has never had any substantial effect on my numbers. I'm not overweight and rarely eat red meat, but have had trouble keeping onto a primary care physician long term (the people I keep picking seem to move between clinics constantly) in order to retain consistent access to a statin prescription, but as I continue to age I've been getting increasingly anxious that my time is coming.

    • So far everything is good. I only had more of a logistic issue, once, when moving to France from the US, a few years back (retirement) and when my new doctor told me that the French do not recommend statins for people at my age and overall good shape (active, fit, etc. ), even if the numbers are high. I asked her to give me a referral to a cardiologist, to whom I mentioned my 35 years of statins in the US, and who was of the opinion that after such a long time and with no apparent side effects, he would recommend continuing on this type of médication. And that was it, so I'm now getting the prescription renewals almost "automatically", even as my cholesterol is staying within limits (under the assumption that it may increase, should I stop, especially considering the amazing cuisine and products to which I now have access :) )

I haven't had to touch statins to get my lipids profile much better. I used zepbound to lose about 50lbs and then weaned myself off that. I was a little afraid my “completely normal after 8 months of weight loss” blood panel status at the end of my zepbound journey would go back to the “bad” region, but I have maintained going on a year with a much better whole foods/lean meats based diet and moderate exercise (I do let myself have some red meat on Saturdays, otherwise I would explode from hamburger desires). So it was done through a combination of lifestyle changes and zepbound to help me bury the hunger monster long enough to learn new habits and get to a new normal. Him suggesting that “probably” most people should be on statins whether they need them or not seems like covering up the source of the problem. I do know that some people just naturally have lipid issues even when doing “all the healthy things” though. My mom is one of them.

I ALSO want to not be a statin-skeptic but, like you, these things look very weird to me. The most prescribed drugs in the country and we don't even try to check if they are addressing the actual problem?

  • We have checked to see if they are addressing the problem more than probably any drug in history. The idea that we haven't is the result of skeptics cherry picking results that back up their point while ignoring the huge quantities of evidence supporting the efficacy of statins and other LDL lowering medications like ezetimibe, pcks9 inhibitors, etc.

    Statins are so good at what they do they even reduce the risk in people who are already at low risk for heart disease.

    https://www.thelancet.com/journals/lancet/article/PIIS0140-6...

There are plenty of statin skeptics and for good reasons; see prior discussion here: https://news.ycombinator.com/item?id=45430939

  • > and for good reasons

    That prior discussion gives no good reasons. The linked medium posts are, to be frank, trash.

    Statins are well-tolerated drugs with little to no noticeable side effects. You might have to try a few. You may need to combine ezetimibe to maintain a moderate statin dosage level, and that's it. (Like the author of this article)

    Source: Leading cardiologists worldwide, and doctors of the rich and famous.

I'm a big statin sceptic so just putting that up front.

I think things haven't changed because most people underestimate how slow institutional scale change is. There is a reason why HR departments and consultants have Change Management experts. The inertia is huge. Young people don't appreciate this because they thrive on new ideas. Old folks don't and will subconsciously push back, like a form of institutional homeostasis.

Also, while I believe your heart attack stats are correct, I'm more interested in all cause mortality. I believe there statins are a net negative.

Statins also raise your blood sugar and lower your GLP-1, increasing your risk of diabetes?

They also tend to be continued well into old age (off label) despite increasing fall risk, which is way more dangerous to an 80 year old.

  • A single study showed a single statin reducing GLP-1 levels and ascribed it to gut microbiome changes that could be totally resolved with UDCA supplementation.

    If this even ends up being reproduced it at most says there is an easy fix for people taking atorvostatin and that it might be a concern with other statins, but this should be treated with the same health skepticism of any other single study finding.

    Not all statins raise blood sugar either - pitavastatin usually shows an improvement in insulin sensitivity.

    • How many doctors are cycling through all the statin classes to find the least-bad option for each patient?

      (I'll rant about one guy I know.. was any of this related to statin over perscribing? who can know)

      Now that we have your LDL under management isn't it easier to just add metformin and gabapentin into the mix? I mean what are the chances you're not also put on a calcium blocker too?

      Now you've got brain fog and sleepiness? weird! we have some modafinil for that but now that you're developing early-stage dementia know that it's progressive.

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one better simple indicator than large panels, if you can't get access to them or don't have them is simply your triglycerides/hdl ratio. aim to be under 2 if using mg/dl and under 0.87 if using mmol/L. it's one of the strongest correlated indicators of cardiovascular disease. way better than any classic cholesterol ratios.

Statins can be effective for many patients (and there are multiple different statins with varying effects) but there are also alternative or additional drugs such as Leqvio (inclisiran) and Repatha (evolocumab). Patients should do their research and talk to their doctors. It might take some trial and error to figure out what works best.

5mg daily Crestor (a very small dose) cut my ApoB in half from ~130 mg/dL to 61. I’ve had no negative side effects.

The general advice is that the scans are only useful sometimes. That is, they can show a problem. But a clear scan doesn’t mean you’re fine. So don’t base anything on a clean scan, be proactive with all the rest of it. My two cents, by the way: Repatha is pretty amazing.

There is no reason take statins, ever. They will destroy your muscles, then cause diabetes and thus indirectly kill you. They will prevent a heart attack by... four days.

If biomarkers are elevated, the question must always be, "why is this elevated", and "is there a natural change in habit and diet that can reverse this elevation".

Artifically lowering the marker with a drug is like pasting duct tape on a leaking pipe - the leak is still there and it will likely quietly get worse over time and then eventually kill you anyways.

I find it unbelievable that our society swallows any drug without second thought. You body produces cholesterol on purpose. There must be reason why it produces it. "Ah well, who cares, let's just throw in a wrench and make it stop producing the cholesterol" and hope for the best...

  • Arguing against nonsense like this gets so exhausting.

    Statins do not destroy your muscles. Newer statins make this already exceedingly rare side effect even rarer, but let's look at them as a general class:

    https://pubmed.ncbi.nlm.nih.gov/36049498/

    Blinded RCT/Meta-analysis shows about 11 complaints per 1k patient years, with 90% of them not actually being due to the statin. But because people act like they're common, they mistakenly believe it was the statin, which just reinforces this idea. And that's for muscle pain.

    https://www.ahajournals.org/doi/10.1161/atv.0000000000000073

    https://academic.oup.com/eurjpc/article-abstract/26/5/512/59...

    https://pubmed.ncbi.nlm.nih.gov/15572716/

    For actual significant muscle injury? Even lower. 1 or less per 10,000 patient years.

    Effectively, you might get one muscle ache per year per 100 people and at most a 1 in 10,000 chance of serious myotoxicity.

    As for diabetes, rosuvstatin usually has a neutral to positive impact on insulin sensitivity, and pitvastatin almost always has a positive impact. Some statins do have negative impact, but it's not universal.

    It's not like duct tape on a leaking pipe - it's like removing items in a pipe that damage the pipe walls. Yeah, ideally they're not in the pipe to begin with, but removing them is better than letting them stay, and diet and exercise only do so much to remove said items.

    Your body can synthesize LDL de novo in the organs that use it, and one of the heaviest users, the brain, can't get cholesterol out of your diet/serum levels at all - LDL cannot pass the blood brain barrier.

    There are people with genetic mutations that mean they don't produce LDL, or at least not at high levels - their increased longevity and incredibly rare incidents of ASCVD is what drove the creation of PKCS9 inhibitors.

    Statins also lower LDL-C levels - they don't make your body stop producing cholesterol in general, or even LDL-C. Even if your body couldn't make it on-demand where needed, statins aren't going to drop your serum levels to 0.

    • I feel like statins are harder to accept than vaccines. With vaccines we can say it is just training our existing immune system to recognize and fight something. So how would you straightforwardly explain statins to a scientifically literate adult so they can make an informed decision. But part of that means honestly acknowledging whatever scientific unknowns and uncertainties there are in this area of human biology.

> When I see that it is widely accepted that ApoB is better to measure than LDL-C, but the industry continues to measure LDL-C, but not ApoB, I wonder why.

That's pretty simple to explain. No conspiracy.

LDL-C is much much cheaper to measure. ApoB costs 36x times as much, so Insurance Companies don't like to pay for it

My wife had high cholesterol numbers, so her doctor wanted to give her statins. She asked about a scan, he begrudgingly said well, I guess you could do that. Her scan showed 0 plaque.

  • Plaque won't show as calcium until it has been in your arteries for decades and has calcified. It is a delayed indicator.

    For anyone under 40, it's expected to have zero calcium. Even a measure of 1 or 2 when you're below 40 would be a bad sign.

  • Was it a CAC or CTA?

    It was almost certainly the former, and the former is is basically an indicator that the damage is already done.

    Soft plaque takes a long time to calcify. But soft plaque is the stuff that ruptures, and will clog up your arteries just as much.

    Statins are best used as a preventative measure - once the plaque is there it's difficult to regress it even while soft, and as far as we know effectively impossible once it is calcified.