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Not sure what to think of this. At this point my main reason for believing the cholesterol (or apoB) hypothesis are the genetic results showing 88% reduction of CVD rates among pcsk9- people (or actually, they would be pcsk9-/+ heterozygotes, given how rare the allele is) in the ARIC study:
https://www.ncbi.nlm.nih.gov/pubmed/24518357
That, if I’m being honest, and Thomas Dayspring’s anecdote about the terrible MI epidemic he dealt with as a resident (or was he an intern?) and the dramatic decline in such events after the advent of statins. He regaled us with this story during Peter Attia’s “Week of Dayspring” Drive Podcast:
https://peterattiamd.com/tomdayspring1/
And, I suppose @rhonda either your podcast or Attia’s podcast interview of Ron Krauss: https://www.foundmyfitness.com/episodes/ronald-krauss https://peterattiamd.com/ronkrauss/
Where Krauss mentions almost off-hand being an author on a review paper pointing out the CHD effects of higher LCL-P levels and saying “which I would not have thought necessary” – meaning the case had been so thoroughly proven there was little point even undertaking the task.
@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.
https://peterattiamd.com/wp-content/uploads/2012/05/MESA-LDL-P-vs-LDL-C.jpg
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.
I think the anecdote could be a complete coincidence. Who is to say we didn’t get better at screening and surgical treatment? Or that in that particular hospital there was just a coincidental amount of cases? No offense to the person who said that, it’s just that it is easy to see correlation when we are looking at things strictly through our own perspective.
Additionally I think the issue is so complicated that we are still just beginning to scratch the surface. What if statin treatment works really well for some people and not so well for others? It could also be possible that statin treatment causes other effects that are unintended and reduce risk of CVD.
Personally I think at this point all we really know is that in most people dietary fat is not the culprit, and sugar is. Even though in my master’s nutrition program they are still preaching a low fat diet -_-