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.
I think the other thing where insulin especially hyperinsulinemia is playing a role is with endothelial dysfunction so again if you take a step back and ask the question what is the Cascade of events that leads to ascvd uh endothelial dysfunction is an important risk factor why because if the endothelium is not working the APO B particles have an easier time getting through the gaps and into the sub-endothelial space
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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.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
but uh I I think there's reasonable evidence that that endothelial dysfunction is also a manner through which hyperinsulinemia impacts the risk of scbd
well insulin itself seems to um drive this endothelial dysfunction now this is a much harder thing to demonstrate because we don't really have great clinical commercial assays for endothelial function we have a bunch of indirect things but if you do look at cultured endothelial cells and you alter insulin concentration you're going to see signaling Pathways in the endothelium that suggest that they are becoming less functional