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@pmiguel You’re mixing up LDL-P and LDL-C. this review is disputing the proposed causal link between LDL-C (amount of cholesterol contained in LDL particles) and CVD. Ron Krauss as you correctly said was talking about the proposed causal relationship between LDL-P (number of LDL particles) and CVD which is widely supported among experts.
While much is made of cases where someone has borderline hign LDL-C but a low LDL-P, cases where someone has sky-high LDL-C will almost always have high LDL-P.
And, whether expert or not, there are plenty of people out there who would dismiss LDL-P as a risk factor for CVD.
@pmiguel Actually LDL-C and LDL-P are discordant quite often and increasingly so as people get closer to a profile of metabolic disease.
You can also see from this scatter plot that you are incorrect. The amount of people with high LDL-C and low LDL-P is small but not clinically insignificant. It should be considered.
Name a serious lipidologist/cardiologist who disputes the link between LDL-P and CVD…
I’d also like to point out that in your original comment you said
“At this point my main reason for believing the cholesterol (or apoB) hypothesis”
This is incorrect. They are not the same hypothesis. The cholesterol hypothesis is the hypothesis that cholesterol is causative in atherosclerotic disease. The apoB hypothesis is that apoB proteins (which are structural features of lipoproteins) are the causative agent. This paper is trying to show that the cholesterol hypothesis is incorrect. Everything you mentioned in your original comment is evidence against the cholesterol hypothesis but supports the apoB hypothesis.
Also, again. This study is disputing that there is a CAUSAL link between LDL-C and CVD. There is certainly an ASSOCIATION between LDL-C and CVD but that is not the same thing. All the people you are referencing (Peter Attia, Tom Dayspring, Ron Krauss) would AGREE with this paper.
@ManyLives I’ll just cede the point to you.
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