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.
there's a strong case to be said that's not the case that can't be the case for many reasons these LDL molecules may be part of an a thorough sclerotic plaque but they are probably almost certainly not the inciting event they are not the the catastrophe and Dave's analogy they are not the proximate event
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
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.
it's completely almost completely implausible for LDL to be causal in heart disease if you actually look at the pathology if you slice open people who have died in accidental deaths and look at their arteries the plaques form prior to the deposition of lipids
looks like probably heart disease is related to insulin resistance inflammation maybe even autoimmune in nature which is pretty fascinating damage to the arterial wall there are all sorts of interesting ideas you know the amount of LDL in your blood is constant and plaques only form at certain places suggesting there's something that is initiating the injury whether it's turbulence causing arterial wall injury I know David diamond feels like there is potentially damage to the vazaha Zoram which is a series of blood vessels that supply the artery wall so the actual arteries have a blood supply to the artery and if that becomes occluded the artery can become necrosis of the artery and perhaps that's the initiation of an a thorough sclerotic plaque but that is not directly a result of an LDL particle