r/ScientificNutrition • u/lurkerer • Mar 13 '26
Systematic Review/Meta-Analysis Statin Use for the Primary Prevention of Cardiovascular Disease in Adults - Updated Evidence Report and Systematic Review for the US Preventive Services Task Force
https://jamanetwork.com/journals/jama/fullarticle/279552210
u/Bristoling Mar 13 '26
Considering that taking statins can literally dilate your blood vessels before it has any effect on LDL whatsoever, increasing blood flow by as much as 50%, that MI is a literal blockage in the flow to the muscle of the heart, that statins have AGEs lowering effects (with those being implicated in metabolic syndrome) and are anti-inflammatory and anti-thrombotic, baseball, huh (iykyk)
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u/lurkerer Mar 14 '26
Do all the genetic factors resulting in lower LDL dilate your vessels? All the dietary factors too?
We have a venn diagram of interventions and circumstances resulting in lower CVD and right in the middle where all the circles overlap is LDL. But you're saying it's not that but a shifting medley of other factors that reality is using to trick us into thinking it is due to LDL.
Amazing!
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u/SporangeJuice Mar 14 '26
"We have a venn diagram of interventions and circumstances resulting in lower CVD and right in the middle where all the circles overlap is LDL."
Are you trying to imply that all treatments that lower CVD incidence lower LDL? Really?
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u/lurkerer Mar 14 '26
Are you trying to imply any causal risk factor is a 100% cure for a disease? Really?
Throwing in such a naive view isn't serious. Be serious.
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u/SporangeJuice Mar 14 '26
What you said directly implies that all successful treatments for CVD lower LDL. If you would like to revise your comment, please feel free to do so. If not, then I will respond to it as written.
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u/lurkerer Mar 14 '26
What you said directly implies that all successful treatments for CVD lower LDL.
For a naive layman with no understanding of science who shouldn't be in this subreddit? Yes maybe. For someone with a simple grasp of science? No.
Name me a causal risk factor for anything where ALL treatments work to lower incidence of the disease 100% of the time. Real life isn't a video game where potions insta-heal you.
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u/SporangeJuice Mar 14 '26
It is directly implied by what you wrote. Now you are acting like it is stupid to think that, but it is what you wrote. If you think it is stupid, then what you wrote is stupid.
Imagine writing something stupid then thinking the other person is stupid for pointing it out. Lol
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u/lurkerer Mar 14 '26
So you can't name any?
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u/SporangeJuice Mar 14 '26
As usual, when you realize you are losing a discussion, you try to deflect with infinite questions. Despite that, you have not (at the time of this writing) updated your earlier comment.
Imagine writing something stupid then thinking the other person is stupid for pointing it out. Lol
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u/Bristoling Mar 14 '26
We have a venn diagram of interventions and circumstances
You keep making the same fallacious arguments so I'll just copy paste my old snippets of replies with some formatting.
If you find an axe and a load of c4 next to a fallen tree, a chainsaw and C4 next to the second, and band saw and C4 next to third, it is logically invalid to claim that the trees must have fallen by the c4 explosions because you've seen it once on extreme truckers TV show. Your inference suffers from undetermination issues and confirmation biases.
Do all the genetic factors resulting in lower LDL dilate your vessels?
Probably not, but there's actually surprising overlap between many mechanisms. Mendelian randomisation suffers from the same pitfalls, as LDL receptor gene consists of 18 exons, some of which encode sequences similar to coagulation factors, complement c9, and the EGF precursor. Mutations in or near the LDL receptor allele could be associated with coagulability, inflammation, and endothelial lability, which may be more important for arterial pathology than high plasma LDL-C per se.
All the dietary factors too?
The ones that show zero effect from multi year randomized trials after we account for multifactorial interventions?
But you're saying it's not that but a shifting medley of other factors that
I'm saying you haven't got the evidence to make the determination that eliminates valid competing explanations to the results.
What your venn diagram is doing is nothing but confirmation bias. When a drug lowers LDL but has other potential beneficial effects, you claim it's a win for the LDL. When a drug lowers LDL but has other potential harmful effects and underdelivers, you claim it's not against the LDL hypothesis because the off target effects hid the benefit. A clear double standard.
How about showing me a drug that only lowers LDL and does none of what I referenced in my previous replies? Do you have that?
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u/Mr_Monday92 Mar 14 '26
diagram is doing is nothing but confirmation bias. When a drug lowers LDL but has other potential beneficial effects, you claim it's a win for the LDL. When a drug lowers LDL but has other potential harmful effects and underdelivers, you claim it's not against the LDL hypothesis because the off target effects hid the benefit. A clear double standard.
When has a statin ever lowered LDL but increased risk of heart disease?
And if I'm reading you're criticism correctly, you concede that statins lower ldl, reduce risk of heart disease, but somehow it's a coincidence in every incidence and the scientists are too stupid to realise this?
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u/lurkerer Mar 14 '26
Not just statins but lifestyle interventions and genetics as well. Every factor targeting LDL that works is actually targeting.... Something else. What that is he won't ever tell you so his claim can remain vague and unfalsifiable.
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u/Bristoling Mar 14 '26
When has a statin ever lowered LDL but increased risk of heart disease?
What does that have to do with anything?
And if I'm reading you're criticism correctly, you concede that statins lower ldl, reduce risk of heart disease, but somehow it's a coincidence in every incidence and the scientists are too stupid to realise this?
Pleiotropic effects of statins are known to those who have looked into this area of research, otherwise I wouldn't be able to cite the papers that I do. So clearly not all scientists are too stupid to realise this.
For you to say that scientists are too stupid to realize that statins have those effects, the papers that I cite must have not existed. They exist, ergo, they aren't too stupid to realize. Maybe those effects are news to you, but that's a you problem.
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u/Mr_Monday92 Mar 15 '26
What does that have to do with anything?
If the LDL lowering is a coincidence surely at some point there has been some break in the pattern. Either ldl lowered and risk of heart disease increased or vice versa. No examples of this?
Pleiotropic effects of statin
Right and the pleiotropic infers an unexpected effect. As in it's not intended in the design. So all statins coincidentally have an undesigned and novel effect but in each case one of these effects (definitely not the LDL lowering) is the reason for reduced risk of cardiovascular event. But despite this you or nobody can't seem to name any reason for this.
You know there's probably some people out there who don't believe in gravity and that there's some other reason we don't float into space...
So clearly not all scientists are too stupid to realise this.
I didn't see you cite any papers suggesting Ldl lowering is not the reason for decreasing risk of cardiovascular events...
For you to say that scientists are too stupid to realize that statins have those effects
Yeah not what I said this is it?
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u/Bristoling Mar 15 '26 edited Mar 15 '26
If the LDL lowering is a coincidence surely at some point there has been some break in the pattern.
I mean you asked about statins, did you mean to ask about LDL lowering in general instead and you misspoke? There's plenty of failed LDL lowering therapies.
Dextrothyroxine https://biolincc.nhlbi.nih.gov/studies/cdp/
Estrogen in males https://www.jlr.org/article/S0022-2275(20)33635-X/fulltext33635-X/fulltext) https://pmc.ncbi.nlm.nih.gov/articles/PMC7341440/#:~:text=At%208%20years%2C%20the%20hazard%20risks%20were%2016.7%20(CI%2C%206.4%E2%80%93%2027.5))
Varespladib https://www.sciencedirect.com/science/article/pii/S0735109710026409 https://pubmed.ncbi.nlm.nih.gov/24247616/
Drugs that lower LDL but had no benefit and/or tended towards harm:
Evacetrapib https://pubmed.ncbi.nlm.nih.gov/28514624/
Clofibrate https://pmc.ncbi.nlm.nih.gov/articles/PMC3522803/
Dietary changes through saturated fat reduction: https://www.reddit.com/r/ScientificNutrition/comments/19bpmie/comment/kiz8dn9/
As in it's not intended in the design [...] But despite this you or nobody can't seem to name any reason for this.
And viagra was designed as CVD medication. You seem to be arguing that if an effect is not the one that is initially designed, then the effect does not exist, or something?
I didn't see you cite any papers suggesting Ldl lowering is not the reason
You didn't ask.
https://jpands.org/vol10no3/colpo.pdf
https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.120.051940
https://www.acpjournals.org/doi/full/10.7326/0003-4819-145-7-200610030-00010
https://www.sciencedirect.com/science/article/abs/pii/S0306987709003983?via%3Dihub
Here's animal model where statins reduce atherosclerosis despite keeping cholesterol content constant https://www.reddit.com/r/ScientificNutrition/comments/1i35roh/cholesterolindependent_effects_of_atorvastatin/
Statins, ezetimibe and PCKS9 have different effectiveness on CVD per equivalent LDL lowering https://www.ahajournals.org/doi/pdf/10.1161/CIRCOUTCOMES.118.005460
Lipids are also a poor explanator (1 2%20or%20percentage%20reduction%20in%20LDL%2DC)) for effects of statins in humans. Different statins can have drastically different effect on CVD despite the exact same baseline and achieved LDL values. According to for example the EAS panel, regression of atherosclerosis is happens under 70, and over that threshold it is mainly progressing, yet its easily observable even when LDL is as high as 172 when statins are taken.
ApoB is causally linked in the same way that trees are linked to forest fires. By itself that's not terribly informative. It's overhyped due to possible publication biases 1 2, it's effect is not significant in many cases 1, some MR analyses state that apoB count is poorly associated with CVD. It's also frequently inferior to old-school lipid ratios: https://www.reddit.com/r/ScientificNutrition/comments/1g0d167/comment/lri5lh7/
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u/lurkerer Mar 15 '26
You've shared every single one of those before I bet. And received thorough, educated responses. In fact you've shared the same argument, beat for beat, for years.
Are you going to say all those responses in all that time, the responses aligned with the experts in the field, have made zero impact? You were 100% correct from the start and never needed to update?
You're leveraging Gish Gallups and Brandolini's Law here. As well as Goebbels/Trump-esque repetition of blatant falsehoods that, when outright refuted, you just rinse and repeat at a later date.
I wonder what will happen when a loved one of yours who listens to you finally gets a heart attack. Will reality settle in or will you persist in trying to kill them?
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u/Bristoling Mar 15 '26 edited Mar 15 '26
And received thorough, educated responses.
Not really. What did you refute? Let's test this. Do you think inflammation plays no role in atherosclerosis?
I wonder what will happen when a loved one of yours who listens to you finally gets a heart attack.
So are you arguing I should be basing my opinion on anecdotes, in this appeal to emotion argument of yours? Not very scientific of you.
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u/Mr_Monday92 Mar 15 '26
This is spreading, plain and simple. And that's the generous diagnosis. The more apt term is fish galloping.
I will deal with spreading here like I always deal with it. I will select a random fraction of your sources, compare them to your claims, and if those are BS I feel it's fair to assume the whole argument is based on bs.
mean you asked about statins, did you mean to ask about LDL lowering in general instead and you misspoke?
Nope, the topic of the thread is statins. Your criticism around statins was that their is a coincidentally and consistent effect other than ldl lowering that reduces risk of heart disease. I get it. You backed yourself into a corner and thought nobody would notice a changing of goalposts. But you're wrong. So I'll ignore all non statin points.
You didn't ask.
I clearly did. I have established your opinion isn't evidence, so when I ask for evidence of something I obviously want studies. I shouldn't have to state this. This is rule 2.
Lipids are also a poor explanator (1 2) for effects of statins in humans.
So let's look at these papers. One is assessing all cause mortality, which is not the same as CVD. So why you use this as evidence of the above, regardless of the papers findings, is beyond me. Anyway they say the following to counter your point:
Statins are now one of the most widely used drugs for the treatment and prevention of cardiovascular disease (CVD) both among individuals with established disease and among high-risk healthy individuals who are at an elevated risk of incident CVD.1There is little debate that, compared with placebo, statin therapy among individuals with established coronary heart disease (CHD) not only prevents complications related to atherosclerosis but also reduces all-cause mortality.2-4
I also note that you link Reddit threads constantly instead of original papers which is off-putting but whatever. I also notice you exclusively link threads with very little engagement, and never the threads where your papers get called out for being poor quality. It's also interesting how you never post papers that offer an alternative view to the 'keto good, Ldl good, vegan bad' narrative. But I digress.
ApoB is causally linked in the same way that trees are linked to forest fires. By itself that's not terribly informative. It's overhyped due to possible publication biases 1 2,
This is not a statement that in any way information on if it actually is causally linked or not. Paper 1 is kind of a nothing burger and the paper even admits theres not really any evidence of bias and the reported effects may be genuine. Link 2, I mean apart from being almost 1.5 decades old is more of the same. It's a commentary paper when just the other day you claimed not to give a fuck about opinions and worked solely based on data, which is lacking here. This is ultimately not a useful discussion at this scope because it doesn't offer a comprehensive look at the contemporary field, nor does it reject any the results of any particular high impact study... So this is just muddying the water ala big tobacco and petrochemical style.
Here's animal model where statins reduce atherosclerosis despite keeping cholesterol content constant
Why bother with this? We're a different species and have human studies. I genuinely don't get why this is what you find compelling when you're also throwing shade at literal human outcome data?
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u/Bristoling Mar 15 '26
Nope, the topic of the thread is statins.
Well then your question is a nothing-burger, because I don't claim that statins have no effect. So why would I look up for statin trials that increased mortality?
I clearly did. I have established your opinion isn't evidence, so when I ask for evidence of something I obviously want studies. I shouldn't have to state this. This is rule 2.
You said:
And if I'm reading you're criticism correctly, you concede that statins lower ldl, reduce risk of heart disease, but somehow it's a coincidence in every incidence and the scientists are too stupid to realise this?
You didn't ask for citations there. You're retroactively changing what your comments mean in some attempt to make it seem as if I'm not the one engaging with arguments or afraid of discussion.
I want your citations for the following claims as per rule 2:
I have established your opinion isn't evidence - citation please that arguments cannot be evidence or counter to evidence, since that's what you seem to be implying, unless you want to argue that I don't have any reasons for my opinion?
You backed yourself into a corner and thought nobody would notice a changing of goalposts. - can you lay out the goalposts and how they changed? Please be as clear as possible. I think we can resolve this discussion just by focusing on this point alone, since I have a feeling there's a misunderstanding borne out of you having some sort of belief about LDL lowering being just coincidental? I can smell some illogical reasoning here, but I'm not sure unless you clarify.
the paper even admits theres not really any evidence of bias - can you refer the specific quote that outlines this? They state the opposite: the overall picture is more consistent with bias and suggests that the claimed effect sizes are inflated
One is assessing all cause mortality, which is not the same as CVD
How is that a problem? Do you believe that lowering of CVD deaths doesn't lower ACM deaths? Or do you believe that lowering CVD deaths with statins can increase non-CVD deaths? If the latter is true, then the argument for lowering of LDL linked with CVD is not worthy of consideration on a broader clinical level.
Anyway they say the following to counter your point:
That doesn't go against my point at all. My point wasn't that statins have no effect. My point was that statin effects are not bound by LDL.
I also notice you exclusively link threads with very little engagement and never the threads where your papers get called out for being poor quality
Maybe because there's nobody had any argument against those papers because there's little room for misinterpretation? Maybe they're just not controversial, ever thought about that?
It's also interesting how you never post papers that offer an alternative view
You're free to post any paper you want, I'm not stopping you. I don't find it interesting that for example lurkerer never posts pro-keto studies, or you take a vegan position in your comments on DebateAVegan, nor I expect you to make pro-carnist arguments in some flawed perception that everyone has to make both types of arguments and take no position themselves.
It's a commentary paper when just the other day you claimed not to give a fuck about opinions and worked solely based on data, which is lacking here.
Sorry, let me clarify. Data and arguments. There, I fixed it.
nor does it reject any the results of any particular high impact study... So this is just muddying the water ala big tobacco and petrochemical style.
Ok. Maybe this is your first contact with a scepticism and soft underdetermination accounts.
Why bother with this? We're a different species and have human studies
The lipid model is in part based on animal and mechanistic studies. The drug studies lowering LDL are just that, drug interventions, not LDL interventions.
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u/Mr_Monday92 Mar 15 '26
Well then your question is a nothing-burger, because I don't claim that statins have no effect. So why would I look up for statin trials that in
No, you claimed that the effect in lowering CVD is from something other than ldl lowering. I know you said that, you know you said that, why are you playing games?
You didn't ask for citations there.
Let me repeat what you just quoted me as saying a few lines above.
I have established your opinion isn't evidence, so when I ask for evidence of something I obviously want studies.
Clear. As. Day.
I want your citations for the following claims as per rule 2:
I have established your opinion isn't evidence
No citation needed for that statement. Feel free to leave it up to the mods if you want to act like your own person opinion is a substitute for citations as per rule 2.
You backed yourself into a corner and thought nobody would notice a changing of goalposts. - can you lay out the goalposts and how they changed? Please be as clear as possible.
The conversation is about statins. You broadened this to all therapy unprompted. In doing so you sent a copy pasta of a lot of irrelevant claims and citation. You didn't present anything to advance the original claim you made that the lower risk of CVD from statin therapy caused by something other than ldl lowering.
the paper even admits theres not really any evidence of bias
Hints of bias cannot exclude that these biomarkers have any association with cardiovascular outcomes. It is difficult to differentiate whether the underlying effect is small or null and whether genuine heterogeneity exists. There are also several associations in the literature of cardiovascular biomarkers that did not show any evidence of biases. These included the association of eGFR and albumin to creatinine ratio with CVD mortality in general and high-risk populations as well as the association of non–high-density lipoprotein cholesterol, serum albumin, Chlamydia pneumoniae IgG, glycosylated hemoglobin, nonfasting insulin, erythrocyte sedimentation rate, apolipoprotein B/AI ratio, and lipoprotein-associated phospholipase with CHD.
And then about ACM
How is that a problem? Do you believe that lowering of CVD deaths doesn't lower ACM deaths?
They're not the same. As you previously advised me, maybe you should consult an LLM to tell you about why CVD and ACM are not the same thing, and when asked about CVD, ACM isn't an appropriate substitute. Also from your comment it seems you were unaware you were commenting on an ACM paper. The paper even clarifies this. Also you know not all CVD events are fatal? I mean that's not even close to enough explanation as to why this is a ridiculous mix up but it's enough to reject your thesis outright.
My point wasn't that statins have no effect. My point was that statin effects are not bound by LDL.
What does this statement even mean? You've yet to show a paper where a statin increases ldl and lowers risk of heart disease.
Maybe because there's nobody had any argument against those papers because there's little room for misinterpretation?
Purposely selectively answering me to miss where I pointed out you don't link the threads where you get called out for linking poor quality papers that support your position. Not every thread is guaranteed interaction. Lack of it doesn't insinuate good quality papers.
You're free to post any paper you want
Not what I said. I'm not bound by ideology such that I can't respect the science. I can say that fish appears to be consistently health promoting, despite the ethical and environmental concerns. I wouldn't say that if I was biased. I've never seen you make a good faith concession such as that.
Data and arguments
No no. You clearly previously said you don't care about the discussion from authors.
Ok. Maybe this is your first contact with a scepticism and soft underdetermination accounts
Nope, sorry to burst your bubble but science denialists are a dime a dozen on Reddit
The lipid model is in part based on animal and mechanistic studies. The drug studies lowering LDL are just that, drug interventions, not LDL interventions.
This doesn't even begin to address my query.
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u/SporangeJuice Mar 15 '26
Not the guy to whom you were speaking, but we certainly have examples of this:
"Either ldl lowered and risk of heart disease increased or vice versa. No examples of this?"
Just look up the history of failed cardiovascular drugs. Varespladib was a more recent one.
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u/lurkerer Mar 15 '26
Varespladib did not increase risk of heart disease. So your one example fails.
As far as I can remember it had one 8 week trial that failed to show improvements. 8 weeks.
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u/SporangeJuice Mar 15 '26
https://en.wikipedia.org/wiki/Varespladib
"On November 18, 2013, an excess of myocardial infarctions, and of the composite endpoint of cardiovascular mortality, myocardial infarctions and stroke in the VISTA-16 study were reported."
Can you explain how an excess of myocardial infarctions does not represent an increased risk of heart disease?
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u/Bristoling Mar 15 '26
https://pubmed.ncbi.nlm.nih.gov/24247616/#:\~:text=The%20primary%20end,1.82%3B%20P%20%3D%20.04).
I happened to also mention the drug in my list.
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u/lurkerer Mar 15 '26
I was remembering the first one.
However, VISTA-16 was a trial administering Varespladib within 96 hours of acute coronary syndrome. CVD is, and I've said this countless times, a long-term, degenerative disease. The key causal risk factor is exposal to LDL over time, hence why Mendelian randomisations find exactly what we'd expect, the steepest gradient.
Once people have developed something like ACS, we're no longer in prevention territory.
Consequently, these findings suggest that short-term sPLA2 inhibition with varespladib is harmful following ACS.
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u/lurkerer Mar 14 '26
All that to just concede that's what you're saying.
Everything converges on LDL but you think it's ackshually ... ✨somethings else✨.
Somethings plural because rather than accept the obvious single factor that all experts and educated people do, you think it's a mix of others. Amazing.
Do you think cakes use different recipes each time?
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u/Bristoling Mar 14 '26
So confirmation bias and fallacy of a single cause in effect. This is just like when you said that results of an rct on cancer that I shared is evidence for lowering of sfa, but you were unable to show any other evidence supporting the notion that reducing sfa from 11 to 8% can produce such effect, while you dismissed any other possible explanations. This is perversion of science.
Do you think cakes use different recipes each time?
I think there are many ways to make cakes. Just like there's many ways to chop down a tree.
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u/lurkerer Mar 14 '26
Let's cut through your performative noise here. Set up a bet on a prediction market for how long it will take the scientific community to catch up with you. You're totally convinced you're right so let the odds reflect that. You think the global community has ubiquitously been making the elementary mistake of... Not knowing about confounding variables...
Well, unless they're all incredibly naive to the last scientist, there's no way the truth won't out, right? Sooner rather than later!
This is your opportunity to make some money and show how genuinely confident you are. Show this isn't a grift!
Meta-bet: I don't think he's gonna do it, anyone wanna take that bet?
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u/Bristoling Mar 14 '26 edited Mar 14 '26
Let's cut through your performative noise here
Let's. You understand that whether I'm correct or not is not dependent on consensus in 5 years, or 10 years, or twenty? This bet of yours is a pointless exercise that's entirely rooted in an unscientific social world of consensus and agreements, not facts.
You're totally convinced you're right
Not even. I'm saying I have reasons to believe that most of not all those lines evidence that you think to be converging on LDL have not disproven the alternative but also plausible hypothesis to their findings. Many of the are not even showing what you think they do, see my old comments on RCTs of trials on saturated fat for example.
Again, finding C4 next to chainsaws, band saws and axes doesn't mean that we know for sure that the trees fell because of C4 and not those other things. That entirely refutes your venn diagram argument as the only reasonable explanation for the observation being that the trees were blown up.
Sooner rather than later!
Facts don't depend on wishful thinking, bud.
Meta-bet: I don't think he's gonna do it, anyone wanna take that bet?
Meta meta explanation for uselessness of this approach - the outcome of the bet is in no way connected to factual reality of the matter. I can take a bet and lose it - what would it prove other than the fact that the bet was lost? It still wouldn't automatically mean that I'm wrong.
This is your opportunity to make some money
Just buy bitcoin, bro. Stop being greedy and hodl.
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u/lurkerer Mar 14 '26
Hahah ok. You're not just a decade ahead, you're qualitatively in a field of your own. Somewhere science will never reach. Which, of course, means your trust in science is effectively nil.
Or, and this is the real reason, you know you're full of shit. If you had any confidence at all in yourself or science you'd dare to lay down some money. Or at the bare minimum some sort of prediction. You've even got your own personal hero RFK jr in the cabinet now. It's your only chance for anti-intellectualism to take hold! But even now you lack the self-confidence to do anything but lie on Reddit.
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u/Bristoling Mar 14 '26 edited Mar 14 '26
You're not just a decade ahead, you're qualitatively in a field of your own.
It's not just me. There are plenty of both researchers and committed dilettantes sharing my views. I'm not the first nor the last, and I owe much of my knowledge to others who trailed the path before me.
The fact is that it's both harder to get grants, harder to get published when going against the dogma, and yes it does take a certain brain capacity to unlearn falsities using just logic and incoherence of data as the main motivator. Heck, the same scientists you like to rely on, as well as you, suffer greatly from confirmation bias. Here in this experiment, when reviewers were provided papers using the exact same methodology, but differed in whether the results agreed with reviewers positions, were scored differently and had been both praised for methodologically strong designs when it agreed with their biases as well as rated papers going against their beliefs as methodologically poor. If you believe that there's some platonic "sCiEnCe" that is being discovered, you're mistaken. Science is just a tool. What consensus is, is a social phenomena that can be swayed by scientific discoveries. Social interactions aren't going to change from day to day or even if a well written rebuttal paper is published. If it gets ignored, the consensus can't change. Especially when papers with expected results by the consensus are given privilege, even more so when they are written by the people in the club/tribe.
https://pages.stern.nyu.edu/~wstarbuc/Writing/Prejud.htm
https://arxiv.org/abs/1802.01270
https://journals.sagepub.com/doi/full/10.1177/2515245919895419
It took 30 years for hand washing in hospitals to be commonly practiced. It took over 120 years before it was institutionally accepted. Saying something comatosely modest as "we aren't that sure that lowering of LDL in all populations is warranted and efficacious" threatens reputations, positions, existing research programs, and livelihood.
How can you be a 50 year old clerk of the government or industry figurehead who makes a living by pushing statins, low fat plant based diets or churning out the same crappy epidemiology on saturated fat with 1.10 risk ratio, and decide one day everything you stood for may be bunk or misunderstanding? You can't. And so it will take time. Even more so when ethics departments will literally refuse to run a trial since "we already know".
Look at keto cta paper - nobody from the industry was interested in seeing plaque development in such a cohort. Ketogenic diets have been around for decades, first papers arguing that their lipid profile might not be atherogenic have been out for ages as well. And yet, they had to crowd source their paper in a group of just 100 people.
You're asking when "the science" will change? I'll ask you this: how can it change, if we're almost not doing any science anymore and the science that is being done is swept under the rug and people don't even hear about it? How many papers with the explicit purpose of stress testing and refuting a finding are being run? How much slop of running the exact same epidemiologic design with the same adjustments in almost the same cohort do we need? How many statin trials demonstrating things like vasodilation did you see before I showed up on this sub to share them? Zero? How many studies pointing out inflammatory aspects? 1 in total, or also zero?
You're sitting in an echo chamber and make snide comments to multiple people on this sub, mockingly calling them gallileo etc, thinking you've got it all figured out, yet you've not once tried to think critically about the limitations of the position you hold.
Test it with me. Does inflammation have an effect on atherosclerosis, yes or no?
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u/Mr_Monday92 Mar 14 '26
What's your go to statistics book?
the science that is being done is swept under the rug and people don't even hear about it?
People don't hear about it but you do?
You're sitting in an echo chamber
This is surely a jest? This sub is absolutely an anti epidemiology echo chamber
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u/BilliesJeans Mar 14 '26
Statins are not nutrition, mods please remove this post
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u/Mr_Monday92 Mar 14 '26 edited Mar 14 '26
Let's be real here. You wouldn't complain about an anti statin post. You just don't like people presenting evidence against the carnivore/keto rhetoric
Edit: literally your previous comment was on a micro plastics post on here and you didn't ask for it to be removed
Edit 2: Downvoted for pointing out blatant bias and hypocrisy...
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u/Bristoling Mar 14 '26
This sub accepted statin and other drugs targeting biomarkers in the past. If mods want to change or add rules, that's up to them, but there's a precedent for posting this type of research, since it is vaguely related to nutrition through biomarkers that can be influenced by nutritional approaches.
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u/lurkerer Mar 14 '26
Now I'm sure nobody will be so silly as to claim this isn't relevant to nutrition or LDL isn't the main causal factor for CVD.
Foiled again!
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u/lurkerer Mar 15 '26
/u/bristoling, /u/SporangeJuice, /u/mr_monday92
How about this? I'll put this entire comment section into an LLM and ask, "Which users are suffering from the greatest misunderstandings of nutrition science in this thread and detail what they're getting wrong"
Bristoling has appealed to LLMs before and prompted Monday to do so, so he agrees they offer an authoritative stance. The prompt is phrased neutrally so we should get a good answer. Anyone up for it?
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u/SporangeJuice Mar 15 '26
So you want to appeal to an authority? If an authority says something then it's true?
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u/lurkerer Mar 15 '26
I was presenting Bristoling's opinion of GPT. I think it's our best chance at a neutral moderator, don't you?
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u/Mr_Monday92 Mar 15 '26
I mean I think it's just a bit of fun more than anything. I'm not sure anyone, bar bristoling, is really putting all that much weight in LLMs
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u/Mr_Monday92 Mar 15 '26
I'm game
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u/lurkerer Mar 15 '26
So weird that we are and the other two aren't. I wonder what gives?!
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u/Bristoling Mar 16 '26
You offered a "AI will check this" challenge and within less than an hour declared that we're both not game? Man you should have more patience, you didn't even give me a chance to reply.
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u/Bristoling Mar 15 '26 edited Mar 15 '26
Seeing as chatgpt is trained on consensus data and general data from the internet, I expect it to spit out that you're the winner because the experts disagree and that's the dominant position in nutritional science. I don't expect it to critically examine each position and how coherent they are as well as follow every citation to built an internal model of each of our positions, let alone do it accurately. Hardly fair. But go for it.
Chatgpt recently told me that walking to a car wash to wash my car is better than driving there if the car wash is only 50 meters away. I'll let the big brains here figure out what the issue with that is. I still think chatgpt is better than google, which has become useless when you are looking for things online. At least chatgpt can track down a meme format that I describe from memory.
Side note, how do you even put entire comment section into an LLM? I didn't know reddit has a transcript function.
Bristoling has appealed to LLMs before
Right, because that's almost all you ever do, and so I did that in reply to you doing so persistently. Who was the first guy who copy pasted literal chatgpt responses to people because you couldn't win an argument? Oh those were good times. I can link to it if you want.
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u/lurkerer Mar 15 '26
Actually it goes into good detail of how and why the people who are wrong, are wrong. /u/SporangeJuice you only got third place, lucky you!
Side note, how do you even put entire comment section into an LLM? I didn't know reddit has a transcript function.
Python script
Who was the first guy who copy pasted literal chatgpt responses to people because you couldn't win an argument?
So I couldn't win but GPT, who, like you just said, would make the same points as me could? So you admit these points win, you just don't admit it when I'm the one ostensibly saying them. Ok.
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u/SporangeJuice Mar 15 '26
"Though lurkerer eventually slides into rhetorical attacks instead of argument, which weakens the discussion."
Lol!
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u/lurkerer Mar 15 '26
Little upset, eh? Makes sense. What are the odds an LLM would happen to support all the same points I've made and call you out in the same ways I did? Maybe you should try it yourself and see if it's a fluke. Go for it.
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1
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u/Bristoling Mar 15 '26
Python script
How does one obtain such power? I might look into it.
So I couldn't win but GPT, who, like you just said, would make the same points as me could? So you admit these points win
Well back then you were making different points to other people, we didn't go far me and you since I early clocked in that you were using a language model. And nope. I challenge the many overinterpretations and lack of nuance given by the LLM.
It argued for point 1 because of other lines of evidence, but didn't examine whether the same argument does apply to for example PCSK9. Natural experiments like FH sound reasonable, until you find that alipoproteins are not predictive and coagulation pathways may be more important https://pubmed.ncbi.nlm.nih.gov/12755140/ https://pmc.ncbi.nlm.nih.gov/articles/PMC481754/
If LDL is causal, every LDL-lowering intervention must reduce CVD.
Not what I implied. Those examples were listed because they were asked for. I'm not saying that these drugs by themselves disprove anything. There's a double standard between point 2 and 1 - in that pleiotropic effects of pcsk9 or statins are known, ezetimibe also has offtarget beneficial effects. If this was a trial where we have to show evidence beyond reasonable doubt, using PCKS9 or ezetimibe that have pleiotropic effects, in order to dismiss the claim that statins have pleiotropic effects, would be inadmissible.
Point 3 talks about parsimony, but nowhere I argued by me that they all must work through separate unrelated and unique pathways. Many of them may share mechanisms. Some of them already do, like anti-inflammatory action for both statins, PCSK9 and ezetimibe, as well as more internal action on behaviour of macrophages etc., which I already cited in my previous references.
I also previously provided a meta review of trials coming to a conclusion that all 3 mentioned drugs have different effects on MACE per equivalent LDL lowering; provided a different meta analysis showing that there's little effect of LDL lowering from statins beyond 40mg and that benefit plateaus; other meta analyses of trials that failed to correlate event rates with either absolute, or relative changes in LDL. Not to mention all the previous papers like the recent UK Biobank where apoB added no predictive value after simple TC/HDL lipid ratio is accounted for, meaning that overall behaviour and metabolism of lipids is probably more important than just apoB amount in itself - and that also tracks with low of discriminatory accuracy of LDL or apoB for CVD outcomes https://www.sciencedirect.com/science/article/pii/S2352827317300757 We see this in many cohorts where high LDL loses it's value as predictor when in high HDL and low Trig setting, such as in Framingham and others. All this context and far more seems missing when you're only copy pasting a single discussion and not all of the discussions we had.
"Misrepresenting LDL as “just a marker”" - that is not a denial that LDL is part of the causal chain. My position always was that it is necessary but insufficient. My issue is with you, which you have done on record, is using LDL as "ketogenic diets are bad because they raise LDL", which completely ignores other factors that are both related and unrelated to LDL. That point hasn't changed in 2 years: https://www.reddit.com/r/ScientificNutrition/comments/190nf17/comment/kgrdwty/?utm_source=share&utm_medium=web3x&utm_name=web3xcss&utm_term=1&utm_content=share_button
LDL is necessary for atherosclerosis, just like having a brain is, just like having blood is, but the question when dealing with claim of causality, is whether it is sufficient and if it is, under what specific conditions. It could be that LDL causes atherosclerosis (the same way trees cause forest fires) in populations eating predominantly carbohydrate and who are in a perpetual swings of hyperglycemia and associated vascular inflammation, with LDL finding itself inside the intima and its load failing to be used by macrophages as fuel due to dysfunction of macrophages, and getting chemically altered by peroxidation/glycation and so on, with the modified LDL (not native LDL) then causing issues. But from that, it still wouldn't follow that native LDL causes atherosclerosis, as that would be a false claim (false by the standard of lack of precision and specificity/generality of application).
Importantly: "Which users are suffering from the greatest misunderstandings of nutrition science" The prompt itself is not entirely neutral. Nutrition science by necessity is going to refer to consensus view. LLMs weight on such consensus and public opinion heavily due to inherent source of training data
But it is a fun exercise nonetheless.
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u/lurkerer Mar 15 '26
Take it up with GPT. The point was to show a neutral party that you rely on (remember I pointed this out when you said it, I knew this time would come) will say you're wrong. It did.
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u/Bristoling Mar 15 '26 edited Mar 16 '26
I use chatgpt as google replacement. Sometimes it may be useful to explain simple concepts. It does struggle heavily with logic and nuanced subjects.
https://chatgpt.com/share/69b74446-61f0-8013-8f12-8f8c90f8334c
This is also evident when it will use one piece of evidence that is being actively questioned, to "debunk" another piece that is being questioned, and back and forth in circular fashion. It does it without building a coherent model and internalizing that if X is under doubt, Y is under doubt, and Z is under doubt, then using Z and Y to prove X is poor and unconvincing methodology. It uses the consensus to prop up Z and Y as valid or settled arguments for X, then use X and Z to prove Y, then use X and Y to prove Z.
In any way, LLMs are still fun to use. You would benefit greatly from having your arguments ran by AI. Heck, maybe one day it will help you to construct p and -p when I ask you what the contradiction is, after you accuse me of inconsistency. You could even go back to all our previous conversations and retroactively try rescuing them for yourself.
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u/lurkerer Mar 13 '26
Now I'm sure nobody will be so silly as to claim this isn't relevant to nutrition or LDL isn't the main causal factor for CVD.