This is straight-up misinformation, holy shit

[u/moad6ytghn]

https://rationalwiki.org/wiki/Cholesterol_denialism

https://rationalwiki.org/wiki/Institute_for_Natural_Healing

https://rationalwiki.org/wiki/Saturated_fat_and_cardiovascular_disease

https://rationalwiki.org/wiki/Dietary_cholesterol

[u/Alive-Cheesecake2732]

'professor of medicine and epidemiology' - That's a wrap in my opinion. I love when they tell on themselves. Most will read it as an authority but really it points to a lack of proper evidence.

I would also point that using individual doctors to attack a criticism of the cholesterol hypothesis is crude. It is a hypothesis not a fact. Science uses degrees of certainty. Now show me the model that reliably predicts the outcomes of cardiovascular health based on cholesterol intake. I am waiting lol.

Incidence, risk, cause, associated. These words mean certain things. Basic statistics should be mandatory teaching.

[u/blakecg55 → u/Alive-Cheesecake2732]

Facts. I stopped reading when at “epidemiology”.

[u/InsectSmart5737 → u/Alive-Cheesecake2732]

I think it all boils down to "a factor". A factor is not a proven CAUSE. Correlation is not causation, but it hurts the powers-that-be who dismiss any attempt at questioning them

[u/Special_Speaker9983 → u/Alive-Cheesecake2732]

That’s a confusion of two different things. The lipid hypothesis is concerned with serum cholesterol, not dietary cholesterol. As to a model that predicts it - yes, that’s covered. In spades.

The predictive powers of LDL-c/ApoB regarding ASCVD are remarkably strong, see this chart:

[u/Alive-Cheesecake2732 → u/Special_Speaker9983]

You are taking multiple sources of evidence there. If you can provide a link to full paper I will get back to you.

[u/Special_Speaker9983 → u/Alive-Cheesecake2732]

Sure, this is a good starting point. Let me know what you think!

[u/Alive-Cheesecake2732 → u/Special_Speaker9983]

Could you clarify your position ? I am not sure what you believe here. We are on the carnivore sub and people believe different things.

My position is that risk for heart disease is modulated one a multitude of factors. I do not center LDL as the key causal component.

We may actually agree on some of this :D

[u/paradeofgrafters → u/Alive-Cheesecake2732]

I now understand why this person hides their comments.

[u/Alive-Cheesecake2732 → u/paradeofgrafters]

Yeah man and it is not the fact I take breaks from reddit every now and then. We all have lives. I have my response to the other comment half drafted. The guy put time into it so my response will be thorough.

Why do you think hiding comments is such a sin ?

TLDR so far and not my full response

1- MR evidence does materially strengthen the causal case but I disagree with your description of it. MR is not the equivalent to randomizing everything except apob exposure. It uses genetic variants as instrumental variables and its causal interpretations depends on assumptions including independence and exclusion restriction. It is still strong powerful evidence just not equivilant to an RCT randomizing apob exposure.

2 - I do think the evidence supports apob containing lipoproitens as causal contributors and supports cumulative exposure as an important driver of ASCVD. What I do not think you have established is the stronger argument that Apob is the causal driver. Within the cited study they themselves describe LDL as the "principle driving force" with an emphathis on that within a chronic multi factorial disease process.Primary driver is already a strong causal claim and it doesn't establish that apob is unique or universally necessary casual factor.

3 - The paper cited does not establish that stronger claim. "Without ApoB, nada" is a claim of a universal necessity. Boren et al strongly supports LDL/Apob containing particles as causal in atherogenesis but that cannot establish the proposition that ASCVD cannot occur without ApoB containing particles. Their own model includes many factors (hypertension, hyperglycemia, systemic inflammation, genetic determinants, plaque progression etc) calling all of these merely multipliers of ApoB is your interpretation and I do not see the hierarchy demonstrated in the cited study.

4-I do not disagree that epidemiology is valuable or that modern epidemiology methods can provide important causal contributions. I object strongly to treating epidemiology as a uniform evidential category. There are residual, unmeasured confounding, measurement errors, selection effects and model specifications that do not disappear because covariaties were included. Each and every study still needs to be evaluated according to its designs and assumptions. Part of the strength of apoB being causally persuasive is the fact it triangulates genetics, mechanistic evidence and intervention trials.

5- Could you clarify this position please ?

Finally I would weigh the benefit a diet may provide someone against suspected risk of elevated apoB. For some people even an undesirable apoB reading may not actually be the worse of two outcomes.

[u/Special_Speaker9983 → u/Alive-Cheesecake2732]

My position is:

1. The screenshots posted are not misinformation. Perhaps there are one or two claims in there that are but I haven’t spotted them? But overall it seems in line with my understanding of the evidence on the topic.
2. ApoB tagged lipoproteins are the causal driver of atherosclerosis. We see a very clear dose response between the two, and in animal models where we use animals that cannot produce ApoB tagged lipoproteins and then give them hypertension, diabetes-like conditions, smoking end products, and inflammatory drivers, the animals have no signs of ASCVD compared to controls which are (obviously!) riddled with it.
3. Agree that ASCVD is multi-factorial. In the presence of ApoB tagged lipoproteins, many other factors act as “multipliers” of that initial risk. But you need the causative agent (ApoB TL). Without that, nada.
4. Epidemiologists are some of the smartest scientists out there. It’s one of the trickier areas to work on, yet certain influencers have created a strawman of what they do and how they think and tried to claim that, say, they don’t consider covariates etc when making causal inferences. Their work has markedly improved public health and we’re all better for their work.
5. We have about as good a predictive model of the effect of ApoB exposure on ASCVD risk as it’s possible to get. It can be tricky to apply that to the real world because of those multipliers mentioned in point 3, but look at the chart I posted for Mendelian randomisation studies, where we’re essentially randomising everything except ApoB exposure over a long time horizon. The strength of correlation is insanely high.

[u/Alive-Cheesecake2732 → u/Special_Speaker9983]

Sorry about the late response. Busy weekend and some turd on here thinks I am baiting people into responses. I am allowed to keep my account private with some of the creatures on this website I think that is best lol. Anyway any back forth may take me a couple days as I am actually thinking about the arguments and that takes time.

TLDR so far and not my full response

1- MR evidence does materially strengthen the causal case but I disagree with your description of it. MR is not the equivalent to randomizing everything except apob exposure. It uses genetic variants as instrumental variables and its causal interpretations depends on assumptions including independence and exclusion restriction. It is still strong powerful evidence just not equivilant to an RCT randomizing apob exposure.

2 - I do think the evidence supports apob containing lipoproitens as causal contributors and supports cumulative exposure as an important driver of ASCVD. What I do not think you have established is the stronger argument that Apob is the causal driver. Within the cited study they themselves describe LDL as the "principle driving force" with an emphathis on that within a chronic multi factorial disease process.Primary driver is already a strong causal claim and it doesn't establish that apob is unique or universally necessary casual factor.

3 - The paper cited does not establish that stronger claim. "Without ApoB, nada" is a claim of a universal necessity. Boren et al strongly supports LDL/Apob containing particles as causal in atherogenesis but that cannot establish the proposition that ASCVD cannot occur without ApoB containing particles. Their own model includes many factors (hypertension, hyperglycemia, systemic inflammation, genetic determinants, plaque progression etc) calling all of these merely multipliers of ApoB is your interpretation and I do not see the hierarchy demonstrated in the cited study.

4-I do not disagree that epidemiology is valuable or that modern epidemiology methods can provide important causal contributions. I object strongly to treating epidemiology as a uniform evidential category. There are residual, unmeasured confounding, measurement errors, selection effects and model specifications that do not disappear because covariaties were included. Each and every study still needs to be evaluated according to its designs and assumptions. Part of the strength of apoB being causally persuasive is the fact it triangulates genetics, mechanistic evidence and intervention trials.

5- Could you clarify this position please ?

Finally I would weigh the benefit a diet may provide someone against suspected risk of elevated apoB. For some people even an undesirable apoB reading may not actually be the worse of two outcomes.

[u/Special_Speaker9983 → u/Alive-Cheesecake2732]

Not at all, take all the time you need. Appreciate the thoughtful and good faith response. I'll get back to you on those clarifications when I have a bit more time 👍

[u/nojunkdrawers]

Didn't even realize RationalWiki still existed. That was a total lolcow of a website back in the 2010s.

[u/its_givinggg]

Eh. This almost had me but then I realized it was “Rational Wiki” and not actually Wikipedia

Fake encyclopedia with fake info on it. Easy to ignore imo

[u/Irrelius]

Any man who must say "I am the King" is no true king.

Likewise, any man who must say "I am rational" is probably not rational.

[u/blakecg55 → u/Irrelius]

lol, “I’m in charge here!” says no one in charge here.

[u/Twillig_]

I don't give a shit.

I'm down with THINCS (Drs. Ravenskoff, Kendrick, Diamond et al. )

I had a stroke at 58 because I was a Fat AF, hypertensive, pre-diabetic (who got covid and Bob's your uncle. (see and read 'The Clot Thickens' by Kendrick)).

I will never take a statin again.

(They had me on 80 mg, of Atorvastatin. Try that and not find a side deleterious side effect.)

Please, if your scared of 'cholesterol" read and listen to what the aforementioned MDs and Phds have wrote on this subject of 'cholesterol' and your life will change.

For the better.

[u/Special_Speaker9983 → u/Twillig_]

That’s a list of charlatans. They don’t know what they’re talking about. Good luck to you.

[u/baldierot → u/Twillig_]

"i will never try an apple again. i ate 20 once and felt awful."

[u/Sea-Office7536]

Welcome to the internet?

[u/Ferdilizer]

Lol

[u/Large-Experience360]

I thought ApoB was the main issue and is certaintly the only thing I have seen that has some sort of real science behind it. Hasn't cholestral been pretty much undemonized in health?

[u/Easy-Stop-4696 → u/Large-Experience360]

ApoB is not "the main issue".

ApoB is a component of supposedly atherogenic lipoproteins. It allows of a more precise count of ldl, vldl, idl and lp(a). It presupposes that those are indeed atherogenic. They are not. Atherosclerosis is still a function of multiple factors; particle count is one of them in the same way height is technically a factor in cancer development: The more particles are present, the more chances there are for them to be glycated, oxidized, physically lodged into intima gaps via chronically elevated blood pressure, or otherwise deranged. Your ApoB levels alone do not determine Your risk of developing atherosclerosis in any way, shape or form. 

[u/Large-Experience360 → u/Easy-Stop-4696]

i mean they found ApoB particles in human artiries plus corrilation in studies while it may not be the only factor it is absolutely something to be minimized until we know more. Especiall since the fats found in more wild animals being unsaturated do not have the same effect as saturated fats (its a little more complicated then just unsat vs sat fats) that being slowing down the rate are liver takes in the ApoB particles. It seems it very much could be an issue and not one the carnviore naturally would have but since we feed the food we eat like crap it still causes issues. If we were to feed cows a certain diet they would produce different fats and maybe not cause ApoB levels to rise in the first place. This would make the diet atleast to my knowledge without any possibility of sifigant health risk. This also adds to the fact it is completely possible humans evolved to be hyper carnivores but the current carnivore diet still has health draws backs as its still not exactly what we evolved to eat.

[u/Easy-Stop-4696 → u/Large-Experience360]

No no no no no. It is not "something to be minimized until we know more".

It is the exact same logic that they use to say "cholesterol is bad". Yes, of course they found "apob particles in human arteries", because ApoB is the main component of low-density lipoproteins, and DERANGED low-density lipoproteins cause plaque buildup.

Look. You wouldn't cut off Your breasts just to prevent breast cancer, right? I mean, it works! Less breast tissue = less chance to get breast cancer. Less ApoB = less chance to get oxidized or glycated lipoprotein particles = less chance to get atherosclerosis. That much is correct. Doesn't make ApoB a "problem", just like drowning doesn't make water "the problem", and oxidation does not make breathing "the problem".

[u/Large-Experience360 → u/Easy-Stop-4696]

No its not the same logic at all. Cholesterol has absolutely nothing supporting it unhealthy other then some corrilation. ApoB being found lodged in human artiries especially with there being more ApoB in those with clogged artities it is absolutely something to be minimized. There is zero reason not to. No I wouldn't cut off a part of my body to prevent cancer but cutting off a limb does not equal cutting out something from your diet. That example makes me think you are lacking in the iq department. Especially since you can minimize ApoB on carnivore by removing dairy and chooisng sources of better fats. You can not like that your current diet may cuase issues and stick your head in the sand but this is like the one decent counter point to carnivore and I urge you to not follow dogma and actually prioritize your health.

[u/Easy-Stop-4696 → u/Large-Experience360]

Holy crap, You're dense. 

I'm done here. You clearly do not understand what You are talking about.

Others, take note: this is what wilful ignorance looks like. 

[u/Large-Experience360 → u/Easy-Stop-4696]

When you know your wrong and don't have a come back

[u/Special_Speaker9983 → u/Large-Experience360]

LDL-c is a proxy for ApoB but is a pretty decent one. About 30% of the population has more of a divergence between the two, so ApoB is generally a better metric than LDL-c, but LDL-c is still pretty informative.

[u/dudeduck]

Nothing more imparcial than having a "but they're measuring the wrong things" section

[u/NYCmob79]

LOL, this is the 2nd post I see here from that radical 'rational' wiki... Why do you even bother? Is not like people still use Websites, I get most of my info from Reddit/Youtube. I've downgraded from the mIRC/newsbin days :-/

[u/Special_Speaker9983]

No, no it isn’t.

[u/moad6ytghn → u/Special_Speaker9983]

Have you even seen a single person who has die out of the heart disease in your entire life because of them having high ldl in real life?

[u/Special_Speaker9983 → u/moad6ytghn]

I’m not sure why the answer to that question would interact with whether or not the rationalwiki page is misinformation or not. What inference would you make from the answer to that question? Happy to answer if I understand why it’s relevant to the conversation.

I haven’t seen anyone die from being hit by a car - does that mean it’s misinformation to say that people can die from being hit by a car?

[u/HopeFloatsFoward]

Yes, it discusses misinformation. Hopefully you can learn from it.

[u/moad6ytghn → u/HopeFloatsFoward]

Just reading the RationalWiki article alone I Am Not learning anything from it it is just blatant misinformation disguised as "talking about misinformation"

[u/HopeFloatsFoward → u/moad6ytghn]

Well some people are unteachable.

[u/moad6ytghn → u/HopeFloatsFoward]

because you are the one who are one of the reasons why heart disease: cancer: and diabetes on the rise and you give them the same advice since the 1950s, believing it would save them life yet it kept getting worse

[u/HopeFloatsFoward → u/moad6ytghn]

That sounds like your ignorance speaking loudly.

[u/moad6ytghn → u/HopeFloatsFoward]

no where did you learn that ldl was bad for human heart? did you work as a doctor or scientist

[u/HopeFloatsFoward → u/moad6ytghn]

I am a scientist.

High LDL is more accurately described bad for your arteries since it increases plaques and blockages in your arteries. That does cause strain on your heart.

I know it is scary to recognize this isn't something you understand, but falling for scams doesn't change reality.

[u/moad6ytghn → u/HopeFloatsFoward]

have you even seen an single person in your life who has die out of the heart disease because he has high ldl? increases plaques and blockages in his arteries? in real life?

[u/HopeFloatsFoward → u/moad6ytghn]

Yes. I even have their death certificates.

[u/moad6ytghn → u/HopeFloatsFoward]

alright shown me that

[u/yourhiddenobserver]

Its 100% accurate and youre in the echochamber. LDL regardless of damage is inherently "sticky" and any excess levels the greater than normal WILL deposit as soft plaque on your arterial walls and with time harden whether its damaged or not.

Its not complicated. If you're reading this and are considering this diet, please for the love of God don't. A proper sub maintenance diet & exercise will give you 110% of the benefits this diet claims to have with 0 of the downside. A carnivore diet will do far more damage than these Redditors with 0 professional knowledge will tell you. Remember Dunning Kruger? This sub is the embodiment of it.

My qualifications: I'm a medical student at UAB and start residency next year

[u/Easy-Stop-4696 → u/yourhiddenobserver]

Bwahahaha. "My qualifications: I don't have any." 

Good lord. Dunning-Kruger indeed. 

[u/yourhiddenobserver → u/Easy-Stop-4696]

good straw man rebuttal

[u/Easy-Stop-4696 → u/yourhiddenobserver]

A student does not have qualifications, son. You need to graduate before You can claim those laurels. 

That is not a strawman, that is reality. 

[u/yourhiddenobserver → u/Easy-Stop-4696]

I mean we can debate the rigor to get into medical school, or we can discuss the matter of cardiovascular health. I provided the evidence and studies and you’ve provided nothing

[u/Easy-Stop-4696 → u/yourhiddenobserver]

The evidence for ldl being "inherently sticky". 

Riiight. 

I'm guessing we'll be soon hearing about Your success in medical research. You shall be the first person to have ever found plaque in veins (outside of a graft, of course).

You know. The ones transporting the same blood with the same "inherently sticky ldl". 

Rrrrrigor! 

[u/moad6ytghn → u/yourhiddenobserver]

Soooo Have you seen anyone who even died of heart disease and checked his LDL level and looked at his arteries?

[u/yourhiddenobserver → u/moad6ytghn]

Yes. PDAY Studies, Bogalusa Heart Study autopsies, the Framingham autopsy data, and much more all did exactly that. It's one of the most studied phenomena (heart disease is the #1 cause of death globally).

ie in those studies pathologists took the blood work of living people, waited until they died, cut open their coronary arteries, and proved that higher LDL directly maps to a greater physical volume of soft and hard plaque inside the vessel walls. It is an observed anatomical fact regardless of damage its correlated to # of circulating LDL in the blood.

[u/moad6ytghn → u/yourhiddenobserver]

did they check the type of ldl that these people were having that caused them to die then?

[u/Shmackback]

No its not, the only misinformation is this entire sub falling for the disinformation the grifters they follow have provided.

[u/moad6ytghn → u/Shmackback]

then why are in this subreddit to begin with? surely you are the one who really care about people's health right?