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.
Well, these particles that are secreted, as I mentioned, will get smaller and smaller. LPS produced through this infectious inflammatory signal does bind to these particles. Their binding to VLDL and LDL is partly, I think, a protective mechanism to sequester the LPS. Again, this is somewhat hypothetical, but it's a plausible scenario, which requires a lot more study to really get the molecular basis of this interaction understood.
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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.
as inflammation goes up, VLDL production is increased. And, at least in a couple of studies that I've read in literature, it seems to be implied the reason for that is that inflammation increases the release of endotoxin, which is a lipopolysaccharide from, you know, bacterial cell walls in the gut that gets released, and it binds to lipoproteins, to all lipoproteins, and it's sort of like an adaptive response to make sure we don't get sepsis or some sort of a toxic infection.