KempyKolibri

It’s a fair point, I’ve never even thought about that. I think it’s just something that’s awkwardly come about because there was an early broad categorisation of lipoproteins by density, and then there a subsequent need to divide those species even further by density.

I tried to come up with a corollary but the best I have is “jumbo shrimp”. Sigh.

I don’t mind discussing arachidonic acid after this - I’m less woke on the literature on it and am always up for learning something new. When I was referring to no evidence in humans, I meant with regards to the idea of n3:n6 ratios.

If n3 is at sufficient levels, I see no reason to believe the n3:n6 ratio should be of any concern in terms of health risks. All the evidence I’ve seen cited to support the claim that a given n3:n6 ratio raises risks of negative health outcomes has induced “unhealthy” n3:n6 ratios by dropping n3 levels to insufficiency.

It’s on that point that I believe there is no supporting evidence in humans, and the fears of an issue are rooted in speculation. Happy to be proven wrong, though!

Not sure what you’re basing that claim on. There are boatloads of data suggesting that replacing SFA with PUFA leads to a 20-30% reduction in CVD events.

Does added sugar seem to be a risk factor too? Sure.

There are floods of case reports online about vaccines causing autism, but I’d hope you wouldn’t think that it’s obvious there’s a problem there too? Such reports should not be the driver of our reasoning when we have high quality studies on the question.

In what way am I shutting down discussion? I’m just participating in it. There’s a great deal of misinformation on this thread that could lead people to make lifestyle decisions that would put them at risk. Don’t see why there’d be an issue in discussing the evidence behind this misinformation so people can come to their own, hopefully informed, decision instead of a misinformed one.

I’m not interested in poor attempts at mind reading (“this subject makes you desperate to call yourself a specialist”) but I’m happy to discuss the evidence on this subject if you’d like.

That’s an answer to a different question. I don’t disagree that CVD risk is multi factorial - having T2DM massively increases the risk, for example. But this being the case does not serve as evidence that arterial wall injury or an inability to repair damage is required in order for high serum cholesterol to be a risk.

CAC scores (which it sounds like what you’re referring to) only look at calcified plaque, but not soft plaques. So there’s a whole category of risk that is missed by them. People’s CAC only tends to go up when they’re in a very late stage of atherosclerosis, and calcified plaques also tend to be more stable than soft plaques, so if two individuals had the same mass of plaque, but one’s was soft and the other’s one’s hard (sorry for the “carry on cardiology”) then we’d actually expect the individual with the CAC score of zero to be at greater risk of a CVD event.

It’s my interlocutor’s burden to show that arterial wall damage and/or an individual’s inability to repair damage is required for ASCVD to take hold, and so far they’ve yet to meet it. That’s what I’m looking for, basically.

Because Mason’s making a number of flawed assumptions based on a misunderstanding of what drives atherosclerosis risk. The important factor js number of ApoB tagged lipoproteins (ApoB) and not mass of cholesterol within those lipoproteins. There is significant collinearity between these two things, but in ~30% of individuals there is discordance, which can create this illusion of “lbLDL is harmless”.

This is because a given individual with the same amount of lbLDL-c as someone else’s sdLDL-c (that is, mass of cholesterol in both), the person with the same mass of sdLDL-c will have more ApoB tagged lipoproteins and therefore more risk. But when we stop using LDL-c as the measure, and use ApoB, which is what lipidologists now recommend, then the risk from large and small LDL particles is more or less the same. That is, one particle of sdLDL carries about the same risk as one particle of lbLDL.

If you’d like something more consumable, lipidologist William Cromwell covers the topic very well in this video: https://youtu.be/kplh30RmYo8?si=WvDMwG-Z82voxDMp

It’s not hard to make an X account, but ok. I can link to the individual posts so you can have a laugh: Mason said the entirety of the lipid hypothesis was challenged by the fact that those randomised to reduced fat diets had a higher risk of dying in the 2006 WHI RCT: https://x.com/drpaulmason/status/1335411781557075968?s=46

It was pointed out to him that the lipid hypothesis is about P:S ratio, not total fat reduction: https://x.com/avibittmd/status/1335470882987323392?s=46 Avi explained the criteria a study would need to meet to challenge the LH: https://x.com/avibittmd/status/1335475024854192129?s=46 There’s some back and forth, eventually Mason says the rebuttal that WHI failed to significantly reduce serum cholesterol/was a failed intervention because it targeted total fat doesn’t make sense because the intervention arm of the WHI reduced their serum cholesterol by 30%,so clearly the intervention was significant according to the LH: https://x.com/drpaulmason/status/1335488114534481920?s=46 Avi asks him what he’s talking about, the serum cholesterol between intervention and control was basically the same, showing the table in the study: https://x.com/avibittmd/status/1335488453417562112?s=46

Avi suggests he might have confused serum cholesterol with dietary cholesterol: https://x.com/avibittmd/status/1335489121486299138?s=46 They share the table from the study that confirms this: https://x.com/avibittmd/status/1335491375073271808?s=46

And then Paul, previously so headstrong and sure he was nailing everyone on this one, just peaces out from the conversation (or runs away, if you were to be less generous). His entire argument against the lipid argument was based on misreading dietary cholesterol as serum cholesterol. So good. No one should take him seriously, he’s either purposefully deceptive or completely incompetent at reading the evidence. Don’t see why anyone interested in reaching the truth should be interested in his arguments in either case.

Where was human behaviour discounted in my argument?

They are related, dietary cholesterol does affect serum cholesterol: https://pubmed.ncbi.nlm.nih.gov/30596814/

The problem with the “lbLDL is harmless” argument is that, while it was an interesting theory ten years ago, we have very strong evidence this is not the case now. I could go through exactly why people thought this is the case, and why the hypothesis turned out to be wrong, but this paper does a better job than I could: https://pmc.ncbi.nlm.nih.gov/articles/PMC7369156

Paul Mason is a renowned spreader of misinformation on this topic (and many others). My favourite moment of his is when he tried to teach a clinical research scientist that the lipid hypothesis was false, and in doing so revealed that his entire argument against the lipid hypothesis was based on an undergraduate-level misreading of a study, after which he just ran away from the conversation instead of admitting he was wrong. Absolute chef’s kiss moment, enjoy: https://x.com/avibittmd/status/1335491375073271808?s=46

I’d say the evidence on LDL and atherosclerosis is even clearer than the SFA evidence. The EAS consensus paper is really good, I’d recommend giving it a read: https://academic.oup.com/eurheartj/article/38/32/2459/374510...

The evidence overwhelmingly shows that replacing SFA with PUFA leads to a 20-30% reduction in cardiovascular disease incidence. Considering this is one of the top killers in the western world, this is massive.

I’m not sure how you’re determining that it’s otherwise?

The argument is probabilistic, it’s not required that food seeking behaviours are entirely genetic for it to go through. As long as food seeking behaviours and/or preferences are to some degree genetically determined, then the argument is sound and valid.

Why would we care about mechanistic speculation from in vitro models when we have evidence from higher up the evidence hierarchy showing direct benefits on human health outcomes when PUFA is substituted for SFA?

It’s like someone providing evidence that exercises decreases mortality risk in humans and countering with “but exercise induces oxidative stress at a cellular level so we shouldn’t do it.”

It’s just turning the evidence hierarchy on its head. I’m curious why you would interpret evidence in this way - why are mechanistic studies with incredibly low internal validity more convincing than RCTs and prospective cohort studies to you?

I hate this Crichton quote so much. It gets thrown around all the time and no one thinks about how demonstrably false it is. Science obviously has plenty to do with consensus.

When an evolutionary scientist publishes a paper, do they have to reference or recapitulate the theory of evolution? No, because that position is scientific consensus. Ditto for the hypothesis that smoking increases cancer risk.

Consensus doesn’t mean “impossible to change”, it just means it is generally agreed upon. If some evidence about smoking and cancer comes out down the line, the consensus can change. It’s still the consensus, though.

If you’re discounting a rigorous and well-referenced critique solely because it’s on a “spamtaculous” cite, then my intuition is that either you’re a motivated reasoner and nothing would push you off your position, or your epistemic framework for deciding what is credible and what isn’t is so wild that trying to discuss this issue with you would be like trying to teach French to a dolphin.

Just read the critique, ignore whatever “spamtaculous” things you’re seeing on the site. The content of the review is what we should care about. Happy to discuss that.

This is just mechanistic speculation based on animal studies. There is no good evidence that I’m aware of showing harms from high n6 consumption in humans, outside of their contribution to caloric excess.

The n3:n6 ratio was a hypothesis that never panned out. If you look at the studies that “support” it, the “bad ratio” is brought about by reducing n3 levels below sufficiency, not by keeping n3 levels at the RDA or higher and then boosting n6 further.

So it’s no more evidence that n6 is harmful than taking a cohort of people, reducing half of the group’s iron intake to a minuscule amount and claiming that because that group’s “iron:magnesium” ratio is wrong, then consuming more magnesium is clearly harmful. It just doesn’t add up.

The control group is modelled from the different quintiles of consumption, so it’s false to say there’s no control group.

What differences in goals and methodologies have you identified that you believe renders them so different that they cannot be summated?

Not sure what you mean by “no indications how balanced and what components where in diets”, you’ll have to clarify.

Honestly, your steadfast insistence that you couldn’t possibly be wrong on this is fascinating to me. I’m happy to admit I made a mistake if I’m misreading the data, so walk me through what you think I’m getting wrong.

Please be specific: name the event subtypes you’re looking at, give specific references to the table numbers etc. If I’m wrong about this, I want to know.

In what way was the certainty used to refute the findings? The point Yoder was making was that Teicholz made an inference that was incompatible with the study used to support it.

Ok, so you have an issue with the certainty that Yoder used in his discussion of that particular issue. Does expressing certainty when the author of the referenced study uses less certain terms make something a joke?

If so, I have some wonderful things to show you from Teicholz that will have you rolling on the floor with laughter compared to Yoder’s stuff.

In what sense is nutrition science a joke?

There have now been several intervention trials investigating whether HDL-raising meds improve health outcomes (there’s no evidence to show they do) and MRs looking at genetically determined HDL-c and various health measures (no evidence of effect either). We don’t actually have any evidence that HDL is anything other than a proxy for other factors, and no evidence that it directly affects anything.

Yes, there are no known issues. You can speculate that there might be, but we could equally speculate that they’re actually superfoods and we don’t know it yet. At the end of the day, speculation is all it is so I believe it’s most sensible to apply the principle of indifference and look only at what we do know. That is, margarine is a sensible replacement for butter on the current evidence.

Because of antagonistic pleiotropy, we can actually make an a priori argument that given two foods that are equally health promoting within the reproductive window (I.e. it’s not killing or neutering people before the age of ~50), then probability holds that the food to which we are least adapted is actually more likely to promote longevity than the ancestral food.

Because adaptations are on net more likely to be antagonistically pleiotropic than not, foods to which we are most adapted are more likely than not making a trade off in favour of reproductive success over longevity. Since we don’t have these adaptations to novel foods, this concern does not apply to them.

Therefore, given butter and margarine are both similar in their effects on reproductive success, with no further information at all we should favour margarine. The fact there are studies confirming this is just icing on the cake.

Why? Evolution doesn’t select for longevity, it selects for reproductive fitness. We have no reason to believe ancestral foods are more longevity promoting than novel ones, and antagonistic pleiotropy would suggest that all else held equal, ancestral foods are less healthy.

Heck, water treatment plants are novel compared to the pathogen-laced water we’ve been ancestrally consuming, but I doubt you eschew tap water for puddle water.

Ok, then if you have no idea then clearly there’s room for heterogeneity in studies that pool those different types. So there’s no contradiction in the studies I posted, which is the original claim you made.

Between subgroups is not significant, but the replacement with PUFA is significant in itself.

As I’ve already pointed out to you, that’s not a contradiction when the studies are looking at CHO as a whole and not disambiguating between whole grain and refined carbohydrates.

If you think a 21% reduction in one of the largest killers in the western world is a tiny effect, then that’s genuinely laugh-out-loud funny.

If you misread data in the way you appear to, that doesn’t surprise me. I can’t imagine you think many studies’ conclusions appear to follow from their results.

It’s just that you’re blaming the studies, rather than your comprehension.

What’s your reading of that study and how does it disagree with the inference I’m making?

Yes.

It’s literally in the reference given. Just read it yourself and all will be revealed:

Biss, K., Ho, K.-J., Mikkelson, B., Lewis, L. & Taylor, C. B. Some Unique Biologic Characteristics of the Masai of East Africa. N. Engl. J. Med. 284, 694–699 (1971).

Literally all of them now (in the US and UK at least). Trans fats in industrially produced foods are banned.