The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
what there's good evidence that in states of insulin resistance LDL is enriched in a possi 3 which is a molecule that makes it a little stickier it's a at a 4 lipoprotein that goes into the membrane of LDL and then the proteoglycan layer in the intima also looks like it could be getting stickier more charged and maybe more retaining of that LDL on the intima layer
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
but I think at a very basic level at a very broad strokes level what we see clearly is that insulin resistance is the determiner you know insulin resistance is the switch there and something about LDL something about the internal space changes when people become insulin resistance and it's maybe it's coming from both the endothelial side and the arteriole you know the base of his arm side and it's kind of getting stuck in that little layer