We can't find evidence that holds up here. Proponents are reasoning from mechanism or analogy rather than direct human data, and the most credible skeptics raise objections we can't dismiss.
that that notion is perhaps the biggest differentiating factor in the way that that I and I believe you think about LDL and the way that the rest of the world thinks about LDL I think most of it ologist believe to be directly targeted to the endothelium yeah which i think is integral to the response to retention hypothesis that mainstream lipid ology espouses yeah
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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if you don't have inflammation or damage the endothelium and your arteries are inherently healthy pipes then the LDL is to say falls away to irrelevance
what do you know after a sclerosis gets worse it's not all about LDL in fact it's not at all about LDL
is there any solid data really pointing really indicting ldl and a b containing particles as directly injuring the endothelium i believe there's not