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.
it's really this histologic examination that makes a very clear unmistakable case that it's not the cholesterol in the membrane that's doing this it's this trafficked cholesterol that ultimately becomes a foam cell through the macrophages ingestion of the lipoprotein that is the insult
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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.
no i think histologically we know it's foam cells and where do foam cells get their sterol content from ingesting oxidized lipoproteins carrying cholesterol is the vase of a sorum which supplies the arterial intimate with blood cells dumping red blood cells in there that are contributing cholesterol maybe a few molecules but i don't think we have any evidence that's the driver of cholesterol that's resulting in arterial wall pathology
histologically we know it's foam cells and where do foam cells get their sterol content from ingesting oxidized lipoproteins carrying cholesterol is the vase of a sorum which supplies the arterial intimate with blood cells dumping red blood cells in there that are contributing cholesterol maybe a few molecules but i don't think we have any evidence that's the driver of cholesterol that's resulting in arterial wall pathology