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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:


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:


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.

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    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 -_-