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 seems that LP little-a has a pretty Giller affinity for going there and inducing bone forming proteins to create calcifications and when that valve loses its suppleness and it becomes calcified you get basically a blockage of that valve called the stenosis
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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.
these um oxidized phospholipid can have a signaling effect uh in the uh in the aortic valve and that might be totally uh independent from from from ldl so so we don't know i'm i'm only speculating here but there's some signaling effects of uh of oxidized phospholipids that i think are very important and they act they um they activate a lot of of different inflammatory processes uh and also uh osteoblastic uh processes
now we had known for a few years that lpa was present in the valve and in the valve it actually co-localizes with oxidized phospholipids so so we we we knew this but that that study was really i think a game changer for our understanding of of aortic valve stenosis