Inflammation Now Predicts Heart Disease More Strongly Than Cholesterol
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A recent article suggests that inflammation is now a stronger predictor of heart disease than cholesterol, sparking debate among HN users about the implications and potential biases of this new information.
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Read the primary article or dive into the live Hacker News thread when you're ready.
The American College of Cardiology just started recommending that everyone measure hs-CRP, a blood test for inflammation. Why? Because inflammation now predicts cardiovascular events more accurately than cholesterol — especially in people already on statins or those without traditional risk factors.
In some ways, cholesterol has become a victim of its own success. With routine screening and statins, most heart attack patients now have artificially lowered cholesterol. That leaves the remaining risk hidden in non-traditional biomarkers — beyond the usual SMuRFs (standard modifiable risk factors).
I think there's supposed to be some kind of green highlight for comments by the poster but that's missing as well.
Mea culpa.
(There are some people who dispute whether cholesterol is causative, but most cardiologists believe LDL cholesterol, or ApoB, causes heart attacks and strokes --based on both mechanistic evidence and randomized control trials.)
2. Having now read the article, i see that my question was indeed already addressed in the article — sorry for asking silly questions
3. Your good-natured, approachable response is great marketing for your company! I’m not the target audience, but I did click through your marketing material, and probably trust it more because of your response.
TLDR: women who would otherwise be missed by current algorithms might be picked up by this inflammatory marker (hs-CRP)
Lp(a) is a largely distinct risk factor from “ordinary” cholesterol and cannot be changed by diet or exercise. Survey papers show practically no effective treatment (statins help all cause mortality in patients but do not lower lp(a)). There are two (iirc) ongoing trials for new, effective drugs. But those are not available yet and will probably be prohibitively expensive, going by the advertisements that the companies run.
So yeah, get an Lp(a) test once (it doesn’t vary too much over time) and reduce your other risk factors, but don’t put too much hope into an easy solution to this specific cause yet.
edit: found the two papers that were a good read:
Kamstrup, P. R. (2021). Lipoprotein(a) and Cardiovascular Disease. Clinical Chemistry, 67(1), 154–166. https://doi.org/10.1093/clinchem/hvaa247
Schwartz, G. G., & Ballantyne, C. M. (2022). Existing and emerging strategies to lower Lipoprotein(a). Atherosclerosis, 349, 110–122. https://doi.org/10.1016/j.atherosclerosis.2022.04.020
Burying the lede a little, here. The ACC has decided on a standard way to measure inflammation, which decades ago was a centerpiece of some very woo-woo "following the squizledoff diet will decrease your gomperblorp"-style health 'advice'. "Systemic inflammation" was a very tricky physiological parameter to nail down.
https://zellavie.ch/wp-content/uploads/2020/06/Nature-Medici...
Try meditation? Not the religious stuff, just breathing exercises and trying to clear your mind
That is what I have never been able to figure out. At face value, I believe some people are just 'built' more resilient that others, but that is purely conjecture.
I've tried meditation, but it never really provided any relief. Sure, in the moment, it might reduce stress or a bit, but at least for me, the relief isn't really persistent. If I mediate for 10 minutes, then I get 10 minutes of relief and then after 30 minutes, I am back to where I was before meditating. Same with any other methods I have attempted. How do you reduce stress? How effective are your methods?
Huberman has done a few episodes on it: https://www.hubermanlab.com/episode/tools-for-managing-stres...
https://cancerblog.mayoclinic.org/2025/02/17/want-to-reduce-...
https://health.clevelandclinic.org/anti-inflammatory-diet
https://health.clevelandclinic.org/foods-that-can-cause-infl...
https://www.heartandstroke.ca/articles/the-anti-inflammatory...
https://health.osu.edu/health/general-health/how-fragrances-...
https://pmc.ncbi.nlm.nih.gov/articles/PMC9163252/
https://www.amjmed.com/article/S0002-9343(25)00549-2/abstrac...
> Grains (mainly whole grains): 7-8 servings > 1 slice bread
Who the heck is eating 7-8 slices of bread -- A DAY??? (or the equivalent)... Of a healthy bread that's about 900 calories just from breads...
That's like 2 bowls of cereal for breakfast, 2 sandwiches for lunch, and 2 servings of pasta for dinner, whoa.
https://www.heartandstroke.ca/healthy-living/healthy-eating/...
> People at highest risk are those who work in environments where they’re continuously exposed to fragrances, such the cleaning industry, cosmetics industry or agriculture industry. You also may be at slightly higher risk if you are continuously exposed to fragrance through personal overuse.
I am 5 months into NSAID Gastritis. Would not recommend.
The impact has been significant. Small servings of non-irritating food for months. I’m told the stomach lining does heal given time, and my symptoms are better now than a few months ago. The post I originally replied to sounded like a recommendation to take Aspirin speculatively as a preventative, which is exactly the mistake I made. Gastro resistant tablets might have helped, but the general advice is to be very careful with NSAIDs on the stomach (although I still use topical Ibuprofen gel when needed).
https://youtu.be/bDGA82wts2g?t=2015&si=lmZeD_KE1F7TvOPA
also they list a big list of drugs that are in various stages
I don't even know. But exercise is the god-tier reigning champion of all things health. You can count on it pretty reliably to show up as a positive effect source in any health study.
"Just exercise" should be a meme at this point.
To get a statin you have to go to the doctor, get a blood test, get a prescription for the statin, and start taking it, get blood retested, adjust dose (possibly), etc. Then you have to go to the pharmacy, pay for it and take it every single day.
To exercise you literally have to walk for 30 minutes. That's it.
If you have high cholesterol, you probably have to change your diet to put any real dent in it, like reduce consumption of your favorite foods.
Meanwhile a low dose statin can drop your cholesterol by 30%.
For the record adding a statin reduced my (genetically very high) cholesterol by over 50%, and I will almost certainly take it for the rest of my life. Diet and exercise changes led me to lose over 80lbs, required 0 doctor visits, cost $0, and has completely changed my life and my likely health trajectory.
So yes take statins, but no statins aren't 'easy' unless you are very well integrated into a health care system and actively having checkups where your cholesterol levels are being checked and reviewed, which is only true of a very low % of people in the US, even those with gold plated healthcare coverage.
It might for all-cause mortality, but it is unlikely to reduce ASCVD mortality more than a statin, or statin + ezetimibe would. Even if your high LDL isn't genetic, once you've done the damage to your arteries, it is basically going to stay there, and treatment targets for preventing further damage at that point (or some regression, if you get really aggressive with combo therapy and get down below 50) aren't often possible with lifestyle changes alone.
People at risk for ASCVD should also realistically just be doing both. It shouldn't be an either/or.
All of this is fine, having your response take the shape of a rebuttal was silly.
It's only hard because we make it hard.
There's people that live even closer that drive their kids to school. One of them lives literally 19 houses down the street from it.
I also have a rule where if I can go somewhere within 20 minutes on a bike, I'm taking my bike. Most places I go fall under this rule, and I live in what most would call a suburban hellscape.
My wife used to drive to work. Driving took longer than walking. But she still drove.
I think it's less about easy vs hard and more about the culture around driving in the US.
I tried biking to work for a while - 13 miles. During summer/fall, it was pretty nice, I'd go early in the morning, shower at the gym, and then bike home. 2 workouts a day when the weather was fair.
The sweaty part, you'll get less sweaty as you get more in shape, both exerting less and retaining heat less efficiently due to lower BMI. But - you'll probably never not be sweaty if the distance is anything significant like, say, 13 miles.
Let's talk about colder climates. I was a consultant for a few years, and got to travel all over. I recall visiting Calgary in the winter, and some maniac dev manager biked to work every day, rain, snow or shine. 6 miles he said (helpfully translating units for me).
[0] I heard this claim a long time ago, but according to Wikipedia (https://en.wikipedia.org/wiki/Plato#Life) it's apocryphal. The Talk page has a decent argument for it not being the case.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7498668/
What lowers oxidative stress is nutrition, specifically selenium, vitamin C, manganese, zinc, and copper.
And avoiding putting stuff in your body that makes your immune system react like air pollution, microplastics, hyper processed foods
Good luck avoiding either of those. For the first one, if you live in a heavily industrialized or urban area and can't just leave for X reasons, should you perhaps breathe less?
As for microplastics, from all I've read about them, they're now in nearly everything and many modern humans who haven't spent their lives living and eating/drinking entirely off the land in the deep remote country are unavoidably saturated with them to the point where (need to find the source again) the average modern adult human in the developed world has something like a teaspoon worth of microplastic inside their body. They've become essentially impossible to avoid if you eat or consume any modern food item.
There is no free lunch or magic bullet (yet) to health. We're all going to die.
Not sitting a lot (more than 1 hour at a time), walking or cycling everywhere, not eating a kot of sugar/refined carbs..
https://www.derekthompson.org/p/why-does-it-seem-like-glp-1-... (Control-F "Theory 2: GLP-1 is a miraculous “moderation molecule,” and it has docking portals all throughout the body that reduce inflammation.")
https://www.health.harvard.edu/diseases-and-conditions/do-gl...
Novo Nordisk purchased Corvidia Therapeutics in 2020 [1] for their IL-6 antibody and will read out the first of three Phase 3's in 2026 [2]. Their programs, however, are focused on individuals with higher risk factors like chronic kidney disease (2026 topline), a couple kinds of heart failure (2027), and a prior myocardial infarction (heart attack; 2027). These trials notably are on top of "standard of care" existing therapies, so they're looking for additional benefit beyond what is commonly sought, like LDL reduction (highlighted in other comments).
Novartis recently announced an intended acquisition of Tourmaline Bio for their IL-6 antibody [3]. So attention to the biological target is heating up.
Another target mentioned in the comments is Lp(a). Genetic studies suggest a heightened risk of cardiovascular disease. Therapeutics aimed at reducing Lp(a) levels are being explored separate from IL-6 for a similar end goal of avoiding cardiovascular events (i.e. heart attacks, death).
Novartis will read out a Phase 3 of an Lp(a) reducing therapeutic in the first half of 2026 [4]. Amgen will likely read out theirs likely sometime thereafter [5]. These have been a long time coming: Amgen in-licensed their asset from Arrowhead in 2016 [6], Novartis in-licensed their asset from Ionis/Akcea in 2017 [7].
If any of these work, there's a chance that they'd be explored in patients with less pronounced risk than the original studies in these Phase 3's. Amgen has already announced an intent to explore their Lp(a) drug in a Phase 3 with participants with elevated Lp(a) at "high risk" for a first cardiovascular event in 2H25/1H26.
[1] https://ml-eu.globenewswire.com/Resource/Download/e7e162e5-a... [2] Page 113 - https://cdn.ipaper.io/iPaper/Files/ffd0326c-1fa6-41e5-a82d-0... Page 225 - https://investor.novonordisk.com/q2presentation2025/?page=22... [3] https://ir.tourmalinebio.com/news-releases/news-release-deta... [4] https://ir.ionis.com/static-files/66c5e90a-3651-480d-a596-1c..., https://clinicaltrials.gov/study/NCT04023552 [5] https://clinicaltrials.gov/study/NCT05581303?rank=1, Page 15 - https://investors.amgen.com/static-files/27fcb898-9cee-48db-... [6] https://www.amgen.com/newsroom/press-releases/2016/09/amgen-... [7] https://ir.ionis.com/news-releases/news-release-details/ioni...
tl;dr: Exercise, sleep, and diet. Plus a zillion different supplements and medicines as adjuncts to a healthy lifestyle.
First, consider what inflammation is. It's fundamentally an immune response designed to attack unhealthy tissue and to facilitate repair of healthy tissue - the effects of inflammation are largely driven by cytokines like TNF-alpha (which is responsible for killing unhealthy cells and recruiting immune cells), IL-1 (which recruits immune cells), and IL-6 (which drives cRP production - the biomarker that you usually look for to gauge systemic inflammation). The production of these is mediated by nuclear factor kappa B (NF-kB).
Other major factors are things like reactive oxygen species (or "free radicals"), which can oxidize all sorts of things in the body and cause damage (which is good when the thing being damaged is a pathogen or damaged cell, bad when it's healthy tissue). Damaged tissue provokes immune responses.
So, if you want to "reduce inflammation", you want to:
1. Reduce stimuli or downregulate processes which are causing the production of inflammatory cytokines
2. Upregulate the production of anti-inflammatory cytokines
3. Ensure sufficient antioxidant capacity to deal with ROS production and oxidative stress
If you've got a chronic illness or autoimmune disorder, you're dealing with inflammation just because your "make immune defenses" signals are stuck on. But you can also have chronic inflammation through too much fat (adipose tissue is an endocrine organ!), environmental or diet factors, or just behaviors which result in an imbalance between pro- and anti-inflammatory responses in the body (for example: smoking induces consistent tissue damage, which drives immune responses).
Exercise upregulates production of anti-inflammatory cytokines and improves mitochondrial efficiency, which results in less ROS production during cellular respiration. Sugar surges cause elevated ROS production, and chronically-elevated blood glucose results in insulin resistance, which promotes inflammatory cytokine production. Lipopolysaccharides from gut bacteria in the bloodstream stimulate immune responses. Insufficient sleep upregulates NF-kB directly, but also contributes to dysfunction of other systems which can upregulate NF-kB.
If you're sleeping plenty, eating well, and exercising, and you don't have a chronic health condition, your inflammation levels are probably pretty good. But you can generally further reduce them with supplementation of things like:
* Omega-3 fatty acids (which compete with omega-6 fatty acids - "seed oils", which produce inflammatory prostaglandins) - this is why your doctor wants you to take fish oil
* Turmeric, resveratrol, and green tea extracts (which contain compounds which inhibit NF-kB and are ROS scavengers),
* Vitamin D (which inhibits cytokine production and supports your natural antioxidant systems)
* NAC, which replenishes glutathione (the primary driver of the body's antioxidant systems)
There are medications, of course, like your regular old aspirin and ibuprofen, which reduce prostoglandin production (which is one upstream of NF-kB), corticosteroids (which block NF-kB), as well as more exotic entries such as GLP-1 peptides (which, among other things, improve insulin sensitivty and reduce adipose tissue, which results in reduced systemic inflammation) or BPC-157 peptides (which acutely inhibit NF-kB, upregulate antioxidant enzymes, and help regulate nitrous oxide, which is how they can help heal NSAID-induced leisons).
This is by no means comprehensive - there are plenty more mechanisms and interventions to explore - but it should be a pretty good clue as to why "diet and exercise" are standard health advice. You don't want to turn off your inflammation responses - they're responsible for taking out pathogens, killing tumors and maintaining a healthy body - but you don't want them chronically upregulated, either.
https://medium.com/@petilon/cholesterol-and-statins-e7d9d8ee...
> Of 1000 people treated with a statin for five years, 18 would avoid a major CVD event which compares well with other treatments used for preventing cardiovascular disease. Taking statins did not increase the risk of serious adverse effects such as cancer. Statins are likely to be cost-effective in primary prevention.
What the BMJ has to say on this very topic of statins:
https://www.bmj.com/campaign/statins-open-data
So no settled science here.
And remember that the largest ever study on saturated fat and cholesterol lowering was just not published by their original author because it didn't proove their hypothesis.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4836695/
Lowering cholesterol lowers the amount of oxidized cholesterol that is caused from inflammation. The fact is is that in inflammation is the fundamental disorder, not high cholesterol on its own.
pubmed.ncbi.nlm.nih.gov/18625445/
Oxidative modification of low-density lipoprotein (LDL) is one of the earliest events in atherosclerosis.
https://www.frontiersin.org/journals/cardiovascular-medicine...
The point of the original article is we should be focusing more on lowering oxidative stress (inflammation) instead of focusing on lowering cholesterol since 75% of people who have heart attacks have normal cholesterol.
Also, CVD mortality is lowered, but other causes of death increase.
We have MVMR studies that look at multiple variables
https://journals.plos.org/plosmedicine/article%3Fid%3D10.137...
https://www.thelancet.com/journals/lanhl/article/PIIS2666-75...
Some MR looking specifically at CRP actually dispute the idea of a causal link altogether
https://www.bmj.com/content/342/bmj.d548
https://www.ahajournals.org/doi/10.1161/01.atv.0000258869.48...
Factorial MR show strong evidence that the risk is additive, in the case of these that look at atherogenic particles and IL-6 signaling
https://www.ahajournals.org/doi/10.1161/JAHA.121.023277
MR looking at specific genes that reduce LDL-C through a variety of mechanisms, including some that lower inflammation, show basically identical reduction of risk per LDL-C lowered.
https://pubmed.ncbi.nlm.nih.gov/25770315/
https://www.nejm.org/doi/full/10.1056/NEJMoa1604304
However, I’m not aware of any evidence showing that higher oxLDL vs higher LDL entails greater risk. IIRC there is a paper that compared oxLDL to ApoB where ApoB was more strongly associated with risk, which doesn’t seem like it would be expected on your hypothesis.
The response to retention hypothesis and the mechanistic evidence supporting it point to oxidation being inevitable once ApoB tagged lipoproteins are trapped in the arterial wall. That being the case, it would be moot whether it entered the wall in an oxidised state or not.
So yes, oxLDL is one of the early stages of atherogenesis, but I’m not aware of any evidence that having LDL pre-oxidised before it’s trapped vs regular LDL increases risk.
I’m always open to new evidence that would change my view, but that’s my understanding of the research landscape at the moment.
> Fourteen trials recruited patients with specific conditions (raised lipids, diabetes, hypertension, microalbuminuria). All‐cause mortality was reduced by statins (OR 0.86, 95% CI 0.79 to 0.94); as was combined fatal and non‐fatal CVD RR 0.75 (95% CI 0.70 to 0.81), combined fatal and non‐fatal CHD events RR 0.73 (95% CI 0.67 to 0.80) and combined fatal and non‐fatal stroke (RR 0.78, 95% CI 0.68 to 0.89). Reduction of revascularisation rates (RR 0.62, 95% CI 0.54 to 0.72) was also seen.
So the evidence base is a collection of studies where most of the participants had at least one prior indicator of CVD or diabetes, and their outcome is a relatively weak benefit to all-cause mortality, CVD, CHD and stroke. For primary prevention, what you really want is a strong outcome in a study of people without any prior indication of disease [1].
I think the article posted by parent is exaggerating, but even the Cochrane review is pulling its punches here, saying specifically "cost-effective in primary prevention", instead of the stronger claim. Common jokes about putting statins in the water supply aside, there's not a ton of evidence for giving them to, say, otherwise healthy 20-somethings.
[1] Imagine the following, not-uncommon scenario: you have an otherwise healthy patient who is both pre-diabetic, as well as presenting with elevated cholesterol. Statins have a tendency to elevate blood glucose. So which risk do you choose?
The available evidence provides poor guidance.
Lack of data doesn't mean the treatment won't work. There is plenty of reason to think statins work for primary prevention even though it hasn't been proved yet. For most the side effects are acceptable, and the cost is low. Thus for most it is worth trying as primary prevention even if we don't have data to show it works. Remember you are playing with your own life here, and the best evidence we have is on the side of stains for primary prevention - this may change in the future when we get data of course.
In drug development, that is the default presumption, and rightfully so: almost nothing ever works.
> There is plenty of reason to think statins work for primary prevention even though it hasn't been proved yet.
Define "primary prevention" -- do you propose giving this to a healthy 20 year old with no other signs of illness? Younger? Should we "put it in the water", as they say? How about older patients? How old? Or, do you mean someone with symptoms? If so, then what about the case I cited (which is quite common in "primary prevention") where you have multiple things in tension?
The evidence provides no guidance here, and anyone who tells you otherwise is guessing. For what it's worth, though, we agree completely on the need for larger data. I think what drives me most batty about the "appeal to consensus" is that it's almost invariably used as a highbrow-lowbrow way of beating up on people who want to ask the question, which is the first step toward getting the answer!
https://www.bmj.com/campaign/statins-open-data
Extraordinary claims require extraordinary evidence. The cholesterol to heart disease link is one of the best attested in medical science [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15]
And yet when making this very extraordinary claim, the author fails to cite any quantitative data for or against. He does not even attempt to build a qualitative argument by proposing a mechanistic theory of why cholesterol is unlikely to be causative of heart disease. Then he goes on to claim that doctors don't have hard evidence to show that statins reduce the incidence of heart disease, despite the fact that such evidence exists [5]. The post is just 10 paragraphs of fluff that boil down to 'don't trust the medico-industrial complex'
Honestly, I think that blog post is a litmus test on scientific literacy - What convinces you more, data and numbers and charts and tests of statistical significance, or rail-against-the-machine rhetoric and a few scary sounding quotes provided without the associated context?
[1] https://jamanetwork.com/journals/jama/article-abstract/19216...
[2] https://pubmed.ncbi.nlm.nih.gov/25815993/
[3] https://jamanetwork.com/journals/jamacardiology/article-abst...
[4] https://www.ahajournals.org/doi/abs/10.1161/01.CIR.67.4.730
[5] https://jamanetwork.com/journals/jama/fullarticle/2678614
[6] https://pubmed.ncbi.nlm.nih.gov/32507339/
[7] https://www.tandfonline.com/doi/abs/10.1080/07315724.2008.10...
[8] https://pubmed.ncbi.nlm.nih.gov/18061058/
[9] https://www.jacc.org/doi/abs/10.1016/j.jacc.2022.03.384
[10] https://www.nature.com/articles/s41598-021-00020-3
[11] https://www.ahajournals.org/doi/full/10.1161/JAHA.123.030496
[12] https://www.nature.com/articles/s41467-024-46686-x
[13] https://www.sciencedirect.com/science/article/pii/S002191502...
[14] https://link.springer.com/article/10.1186/s12872-021-01971-1
[15] https://www.jstage.jst.go.jp/article/jat/31/3/31_64369/_arti...
The blog is merely pointers to, and excerpts from, other articles on sources such as New York Times and Bloomberg. The blog post can't be bad unless the original sources it cites are bad. Which ones are bad?
The blog post misrepresents some of the sources by exaggerating the certainty of the claims and ignoring any evidence contrary to the point it's making.
It's a bad blog post.
What about this:
Cholesterol lowering is not the reason for the benefit of statins. If it was, lowering cholesterol via any means should have produced the same benefit, but it doesn’t. One obvious way to confirm this is to find therapies that lower cholesterol by different means (i.e., other than statins) and see if they, too, prevent heart attacks. They don’t. See: https://www.nytimes.com/2008/01/27/opinion/27taubes.html (Some will discredit the author Gary Taubes without addressing the points he is raising.)
The main reason why statins work may not be because they lower cholesterol, but because they reduce the inflammation that leads to heart attacks: https://www.bloomberg.com/news/articles/2008-04-15/heart-dis...
This last link aligns with the new findings.
https://pmc.ncbi.nlm.nih.gov/articles/PMC6661243/
Your comment is an appeal to authority. While I have my problems with characterizing statins as dangerous drugs, the article is not particularly spicy. In particular, this part:
> Because the link between excessive LDL cholesterol and cardiovascular disease has been so widely accepted, the Food and Drug Administration generally has not required drug companies to prove that cholesterol medicines (such as statins) actually reduce heart attacks before approval. So drug companies have not had to track whether episodes like heart attacks are reduced.
...is true, and controversial only amongst people who don't know the evidence. Which, unfortunately, is many doctors and "experts".
In general, saying any variation on "experts disagree" is not a rebuttal to a question of medical evidence. You would perhaps be surprised to know how many practicing physicians have no idea what level of evidence backs the drugs that they prescribe.
I for one appreciated the clarification that it was not mainstream, since sneaking a random controversial take into a comment thread as if it was fact without noting that it's contentious is disingenuous.
No, they don't. If you don't know enough to argue on the merits, don't argue. A count of opinions is not an argument.
> sneaking a random controversial take into a comment thread as if it was fact without noting that it's contentious is disingenuous.
And again, you're justifying your judgment and dismissal based on hearsay. Saying "I refuse to believe it because experts disagree" is fine if you're unable or unwilling to look into an issue yourself, but in that case you have to realize you're basically ignorant.
I realize that we all go through life taking most things on faith, but that also means that you should not cling to the opinions of others as a substitute for thought.
edit: I see you added "I realize that we all go through life taking most things on faith, but that also means that you should not cling to the opinions of others as a substitute for thought."
Don't worry, nobody's doing that here. It's a question of weighting, not clinging. Maybe you mistook "this is not mainstream" to mean "this is definitely false because it's not mainstream"? It does not mean that. It is just helpful context for evaluating credibility.
You're asserting that a extremely well-known logical fallacy is not a fallacy. It's not an HN rule, it's argumentation 101.
The OP literally dismissed the parent based on nothing more than the opinions of others.
> When assessing the probable significance of an agglomeration of empirical data, it’s valuable to know what experts in the field think about the data and their consensus about the inferences we can draw from it—even if the consensus might be mistaken
I already conceded that, if you have no ability or capacity to think or investigate the issue yourself, it's perfectly fine to defer to the opinions of others. But in doing so, you remain ignorant on the matter.
> because the consensus is usually right.
No. I understand that's a comforting belief -- and even politically charged, today -- but it's just an assertion.
> I for one appreciated the clarification that it was not mainstream, since sneaking a random controversial take into a comment thread as if it was fact without noting that it's contentious is disingenuous.
(emphasis mine)
In other words, you didn't just passively ignore the parent (which would be fine), you posted about it, and not only that, you called it a lie. [1].
When you call something a lie like that, you're making an argument, so you'd better be prepared to bring the evidence.
[1] I realize that you're actually saying that it's "disingenous" that they posted this without some kind of disclaimer that it's a "controversial argument", but to the core of the issue: if you need that disclaimer, you aren't qualified to judge the content. For all you know, it isn't controversial at all.
But you have to separate the fallacy from it being supportive evidence of other data.
There is a difference from saying X must be true because Y person said it and they're an expert on Z. But when there is consensus between appropriate experts - such as researchers that specialize in this field - and it is in support of other specific evidence it is supporting evidence that the other specific evidence is compelling.
If I have 10 CPAs explaining a specific bit of the tax code to me and they are pointing out the specifics of the tax code, it is not fallacious to note that these people are experts and are pointing to specific evidence that supports their point.
The fallacy is where you use an authority in place of evidence. It is not fallacious to refer to consensus or experts.
Else, you end up basically in the "Do your own research"/vaccine denier/climate deniers/flat earth territory. Appeals to experts is not a logical fallacy. It's actually smart, because you get to leverage agreed facts (the earth is round) even though you've never actually been to space to see it for yourself.
There are two distinctly different fallacies of appeal to authority (which overlap, since all of the second are also the first), this form is the form which is a deductive fallacy (appeal to status), but not the form that is a fallacy in inductive argument (which is appeal to false authority). It is important to distinguish them because while deductive fallacies are much more clear cut, they are also far less relevant to most real world debate, which rarely is about proving something is true by logical necessity assuming some set of axioms, but that is the only place that deductive fallacies are inappropriate, since all a deductive fallacy is is a form of argument in which the conclusion does not follow from the premise by logical necessity.
People are far too willing, today, to defer their thinking blindly to a consensus of opinions, but worse, to accuse anyone who also doesn't defer of being malicious.
There are conflicting incentives here, and as usual we don't care about someone else's p value, we care about argmaxing our own utility functions.
It’s so obvious it doesn’t need to be stated dude.
As someone who lost the genetic lottery (has the high cholesterol gene) you bet I care. There is every reason to think that treating cholesterol will increase my lifespan - I'm hoping for quite a few more healthy years.
> Statins can be beneficial in patients who have already suffered heart attacks. Cholesterol lowering is not the reason for the benefit of statins. If it was, lowering cholesterol via any means should have produced the same benefit, but it doesn’t.
What a blatant lie! Ppcsk9 inhibitors have produced excellent results, even better than statins.
Vytorin is a combination of cholesterol-lowering drugs, one called Zetia and the other a statin called Zocor. Because the two drugs lower LDL cholesterol by different mechanisms, the makers of Vytorin (Merck and Schering-Plough) assumed that their double-barreled therapy would lower it more than either drug alone, which it did, and so do a better job of slowing the accumulation of fatty plaques in the arteries - which it did not.
See: https://www.nytimes.com/2008/01/27/opinion/27taubes.html
Do you have any?
Statins are not evil and they're not a scam, but we definitely need to replace them with something better.
Since 2010, however, the number of statin prescriptions has gone up 75%, and there have been proclamations that not only is the science "settled" because of a meta-analysis laundering past studies (that could never find a convincing benefit to lowered cholesterol), but that 1) twice as many people should be taking statins, and 2) maybe we should just put them in the water!*
What passes for science in medicine is usually bad, but it's exceptionally bad in the cases of the two classes of drugs that are the most prescribed, meant to be taken for the rest of your life, and coincidentally the biggest moneymakers: statins and SSRIs. They both also, even at best, claim very small benefits.
This thread is just going to consist of sloganeering and people calling you ignorant. Or a "denier," in order to compare disbelief in the tiny effect that statins claim (25-35%, under particular conditions) to disbelief in the Holocaust.
* Which was suggested every five years before any of these new, "conclusive" studies appeared. They'll just keep pitching it until they get that payday.
Why would we favour cross sectional data over that produced by more rigorous methodologies?
> the tiny effect that statins claim (25-35%, under particular conditions)
25-35% reduction in one of the west’s leading killers is tiny? Wild.
Regardless, the OP doesn't actually claim that cholesterol is not correlated with heart attack risk. If you read the entire article (not just the headline) it has a section explaining that the results are confounded by the fact that many patients were on statins already and therefore had lower measured LDL cholesterol than they would normally have due to their diet and lifestyle.
LDL isn't the only factor in determining heart disease risk. We've known this for a long time. Measuring LDL in heart attack patients can be misleading because it doesn't represent lifetime LDL area under the curve and they are more likely to be on LDL-lowering therapy than people with lower heart attack risk.
Correct, but if you read the news articles you'll see that they are reporting results from scientific articles and clinical trials. In other words, it is not the reporter's opinions.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5633715/
Can you expand on this? I don't understand.
So for some individuals with a super clean, low cholesterol diet, adding dietary cholesterol would significantly impact their serum cholesterol. But for many (arguably most), it won't make much of a difference, which is one of the reasons DC has moved down in importance in dietary guidelines.
Again, I'm not a doctor. I talk to my doctor and see what others hear from their doctors and am able to make some educated guesses off of that.
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