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.
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!)
In 2015, https://pubmed.ncbi.nlm.nih.gov/26551272/ showed that medicating all of the way to normal works out better than medicating down to stage 1 hypertension, then insisting on diet and exercise. And yet my request in 2018 to be medicated down to normal blood pressure was refused, because the professional guidelines followed by the experts was to only medicate down to stage 1 hypertension, then get the patient to engage with diet and exercise. The expert standard of care was literally the opposite of what research had shown that they should do.
I agree that experts should not be accountable for my laziness. But can you agree that experts should be accountable for following standard of care guidelines that are in direct conflict with medical research? And (as in my case) refusing the patient's request to be treated in a way that is consistent with what medical research says is optimal?
My advice would be to "shop around" for doctors, establish a relationship where you demonstrate openness to what they say, try not to step on their toes unnecessarily, but also provide your own data and arguments. Some of the most "life-changing" interventions in terms of my own healthcare have been due to my own initiative and stubbornness, but I have doctors who humor me and respect my inputs. Credentials/vibes help here I think: in my case "the PhD student from the brand name school across the street who shows up with plots and regressions" is probably a soft signal that indicates that I mean business.
Thanks for posting this. While I would generally advise a healthy dose of skepticism for any individual study, this one was very large and seems to be both well designed and executed. While there was a (statistically) significant increase in side effects with more intensive treatments, only about 1% more patients had adverse effects versus the standard treatment group, which seems like a very reasonable risk given the improved outcomes.
I've been trying to get my blood pressure under control recently and was thinking getting down to 12x/8x was good enough, but this has me rethinking that.
You've communicated that by ignoring or dismissing the question of whether better outcomes are possible through other means than demanding that everyone follow doctors' orders and blaming them if they don't.
"Who cares if better outcomes are possible, so long as blame is in the right place"? Is that how we want to approach this?
She wanted to change, tried a many multiple of times and it failed. Fault, guilt, blame are useless concepts to use on the Other. And only in moderation should they be applied to the Self. There deep disconnects between what we think, know and do.
Bob the gambler wants to quit and wants to wager, sometimes sequentially and sometimes simultaneously.
The question isn't whether the whole Bob "means it", but which version of Bob we want to ally-with to war against the other, and what conditions or limitations we put on that assistance.
Statins, GLP-1 antagonists, etc isn’t magic, but it changes people’s behavior and bodies in such as way as to diminish the importance of willpower. Thus, it’s not that people are lacking instead our medicine is simply to primitive to help with a wide range of issues.
This strongly suggests that genetics definitely slips a thumb on the scale, but ultimately we are able to also impact our personal behavior.
More importantly, research such as https://pubmed.ncbi.nlm.nih.gov/31270766/ shows that there are techniques (such as mindfulness practices) that have been demonstrated to improve our abilities in practice. I have personally seen these have an impact.
Of course if you have a condition such as severe ADHD, you might not be able to reach the same level as is possible for someone with good genetics. But you still have the ability to move the needle. If you have a condition such as traumatic brain injury, even your ability to move the needle may be lacking.
But most of us should be able to make a positive change.
If it's 30-60% heritable, that leaves 70-40% to split between personal decisions and environment. It does not guarantee that personal decisions matter much at all...
And then further followed up with a link to research showing that it is, in fact, possible to change. With advice on how to change it.
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).
I would be immensely skeptical of this unless he was talking about something much more narrow, like how there's a fraction of people who have really unfortunate genetics and can only improve their blood lipids with medication.
We have mountains of data showing that diet can massively improve lipids, and the combination of diet and exercise are our largest levers for reducing the risk of heart disease for most people. (There are always some fraction of people who can do everything right but have outlier genetics that require medication anyway, just as some people have outlier genetics and can smoke a pack a day their whole lives and reach their 90s.)
I'd check out the Barbell Medicine podcast for anything related to the intersection of lifestyle and health. They're extremely evidence based with a preference for measurable improvements in outcomes over hypothetical mechanisms.
Relevant to this thread are their episodes on testing and screening, hypertension / high blood pressure, cholesterol, fiber, and the new PREVENT heart disease risk calculator.
I'd also check out the episodes on diabetes, Alzheimer's, fatty liver disease, and health priorities.
I am one of those unfortunate genetic people, sadly, and have had high cholesterol numbers since my early 20s. Most of my older grandparents passed from heart disease. Now in my 40s, have a decent diet, and my numbers are < 100 for LDL. Current (and previous) PCPs have indicated to me that diet will have little effect for me, and that I will likely be on statins for most of my life. Experiments with stopping the statins have shot my LDL numbers through the roof.
The good news is that it's a pretty low dose with decently high effect.
I'm familiar with the genetically high cholesterol thing and when you look at that you see parents/grandparents having heart attacks in their 40's. nothing like any of that in my family.
anyway yes im on the statins and probably need to boost my dose a little more to be below 200.
They are unlikely to get lipid levels down low enough to reach soft plaque regression levels. You need to get sustained levels below 50 to 70 depending on genetics, Lp(a), etc.
If you've lived a healthy life in general and don't have genetically bad Lp(a) this advice is probably enough for you staying that way. If you've spent a significant portion of it with bad lipids for whatever reason, you almost certainly need to go on a combo therapy to get to regression levels.
These effects were first demonstrated in 1953. And has been confirmed over and over again since.
So don't discount the value of diet and exercise just because losing weight didn't fix your cholesterol.
still doesnt explain what my cardiologist was talking about, though. he's not the first dr. to tell me that "diet isn't really going to help you much". one dr. said, "if you went totally vegan, maybe it would have a slight effect". so no I didnt go totally vegan.
i think the idea is diet/exercise can make a 20 point dent in your total cholesterol but in practice, not much more than that, if you have total cholesterol over 250 kind of thing.
i don't know how to source that but I recall a few 20 points lower diets making the news over the years
Accepted medical guidelines not long ago said to bring blood pressure from the dangerous range, to elevated, then encourage patients to engage in diet and exercise. Research such as https://pubmed.ncbi.nlm.nih.gov/26551272/ demonstrated that it is better to medicate all of the way to the normal range.
I personally had specialist in blood pressure follow the old advice around 2018. I asked for further medication, and he refused to give it. In so doing, he was following accepted practice, per professional guidelines. This left me with elevated blood pressure for several years. This despite the fact that when I was personally physically fit (when my blood pressure problems were discovered, I still had my crossfit bod), that did not help my blood pressure.
Guidelines are continuing to evolve. Even today, guidelines about how far down to take blood pressure are somewhat vague in the USA. Many countries stick to the older, higher, targets in who even gets medicated in the first place.
It wasn't until about 2 years ago that I encountered a doctor who was willing to medicate me all of the way into the normal range. Given the 2015 research, I'm very happy about this. But it is far from a guarantee that a random person on HN with high blood pressure will encounter a doctor who is willing to do the same.
That's why I believe that this is not a strawman position. I'd be curious to hear your case explaining why you wrongly assumed that it was.
Second, you are just giving your opinion about doctors. You are not providing evidence. In fact what you claim about doctors is just straight up wrong.
I already gave you a link to a 2015 study that demonstrates what the standard of care was at that point. Here is https://www.aafp.org/pubs/afp/issues/2018/0115/p72.html demonstrating that in 2018, the year I had my interaction, the standards were shifting. With not all major medical organizations endorsing bringing blood pressure down to what the 2015 study said they should.
In fact if you look at the actual AAFP guidance, see https://www.aafp.org/pubs/afp/issues/2018/0315/p413.pdf. Read to the last page and look for "Follow up". This matches my experience. I was brought to stage 1 hypertension, then "nonpharmological interventions" were recommended. Namely diet and exercise.
And now it is apparent that you were dead wrong. My doctor in 2018 was not some rogue jerk. My doctor was exactly following the recommended standard of care put forth in that year by a major medical association.
While the USA has evolved their standards further, that 2018 standard in the USA is still common in many other countries.
But look on the bright side. You just were given the opportunity to learn something.
It's more accurate to say that certain statins have significant side effects in certain patients. Atorvastatin made me dizzy. But I switched to Pravachol and that went away. I switched again to Rosuvastatin and it stayed away.
Not all statins are the same.
Some statins have significant side effect in some patients.
We have many "new" statins that the overwhelming majority of people have no side effects on. Exceedingly small amounts of people have issues with things like rosuvastatin and pitavastatin, and for people that do, repatha and other pcsk9 inhibitors often work fine.
> 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.
There is a downside to delaying treatment, and particularly so when they are far out of range, or have spent an extended amount of time out of range.
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...
No doctor wants their patient to have a stroke. But they also only get to meet patients where they are.
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.
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.
I think only recently have insurance companies started covering APoB testing in your annual exams (or that may just be my insurance…).
But if they're employed by a health system and fail to follow company policy then yes, they could be fired.
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.
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 :/
A zero is still a zero though, and is associated with low risk of heart disease in the near future.
I turned 50 fairly recently...
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.
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.
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.
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.
Financed by who?
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
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.
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.
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.
Most with efficacy determined by the proxy variable of LDL-C levels, and with even more questionable results in actual lifetime improvement.
I too really wanted not to be that skeptical about medicinal research. But if I had high cholesterol and a doctor recommended newer statins to me, I don't think I would take them.
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.
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...
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.
https://www.bmj.com/campaign/statins-open-data
So no settled science here.
Unless you consider the BMJ a trash journal of course.
I pointed to this BMJ reference because in the article there is the following: "To help drive down our ApoB, we have statins which do miracles for lipid management. Some people believe that everyone should be on a statin so long as they don’t have adverse side effects."
Most statins prescribed today are not for secondary prevention.
A lot of doctors prescribe a statin immediately on seeing just one measure of "high" LDL without looking at any other parameter or context.
Sorry, that's nonsense. It is a dangerous drug with plenty of side effects. If it had no side effects it would be sold over the counter. The brain needs cholesterol to function. If you artificially remove cholesterol this is what happens: https://www.health.harvard.edu/cholesterol/new-findings-on-s...
And considering serum cholesterol cannot pass the blood brain barrier and that it is all synthesized de novo in the brain makes it an even sillier claim. Your serum cholesterol level does not have impact on your brain's cholesterol levels.
Quite a few organs have the ability to synthesize cholesterol as needed and can do so just fine. Another area where we make use of cholesterol is for synthesizing hormones... but those organs can all synthesize it de novo just fine too.
The new pkcs9 inhibitors have gotten people down to extremely low levels of LDL (<30 and <10!) and found no impact to cognition, hormone production, etc. We have mendelian randomization studies looking at people that genetically do not produce pkcs9 and have basically nonexistent serum levels of LDL, no impact to cognition, hormone production, etc.
https://pubmed.ncbi.nlm.nih.gov/36779348/
https://www.ahajournals.org/doi/10.1161/ATV.0000000000000164
https://www.acc.org/Latest-in-Cardiology/Clinical-Trials/201...
https://www.acc.org/Latest-in-Cardiology/Clinical-Trials/201...
https://www.fda.gov/drugs/drug-safety-and-availability/fda-d...
FDA requires statins to have warnings about potential memory issues.
There are risks associated with extremely low cholesterol: https://www.webmd.com/cholesterol-management/cholesterol-too...
The human body creates cholesterol because it is essential for several vital biological functions. Cholesterol is a key structural component of cell membranes, providing rigidity and fluidity necessary for cellular function.
People reporting things doesn't mean much, because as your own original link mentions, people tend to overreport stuff when they are going to the doctor already for other things. What do actual studies that have controls show? We have human RCTs here that have looked at this very thing - and found no evidence of it.
A random article on webmd also says very little when it contradicts the data we have from human RCTs and provides no sources. The trials I linked specifically looked at the common concerns that people have raised as being possibly related to low cholesterol - and didn't find them.
No one is saying that cholesterol isn't essential - your brain literally won't work without it, among many other things. But there is a difference between serum cholesterol levels and its use in in your body. You do not need high serum LDL-C levels for your body to create cholesterol where it needs it.
Those studies I linked quite specifically check for these concerns on people with way lower LDL-C from PKCS9 inhibitors than even combo therapy of statins and ezetimibe will get most people.
If you want to trust individual anecdotes over RCTs while scare quoting the primary way we advance science in these fields, be my guest.
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.
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.
(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.
The PKCS9 inhibitor monoclonal antibodies are an option for most people if they show intolerance to multiple statins - insurance will usually relent at that point.
If your doctor isn't willing to work with you to find the medication that works best for you, then find a new doctor.
It sometimes seems like if you get one, you get the others. That's because all these diseases feed into each other.
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.
Or you could take statins and prevent it from becoming an issue in the first place.
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.
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.
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
Unfortunately American retail prices might as well be generated by a PRNG, and do not mean much.
On Ulta, a basic lipid panel vs an ApoB test are $22 and $36 respectively. Looking at Indian lab prices, (approx. INR->USD), both are under $10 there.
https://www.ultalabtests.com/test/cholesterol-and-lipids-tes... https://www.ultalabtests.com/test/cardio-iq-apolipoprotein-b...
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.
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.
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...
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 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.
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.