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.
but the people with the high triglycerides who are at increased risk of heart disease have a higher number of ldl particles and vldl particles it's the particle and when you're measuring the triglyceride you're just measuring a blob of liquid in a bunch of particles and you need to know the number of them
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.
if you increase the concentration of triglyceride and again clinically that's very obvious you measure that in a standard lipid panel we know that risk goes up but the question is through what mechanism well it goes up through apob why because triglycerides like cholesterol are not water soluble they're fat soluble which means they can't be trafficked on their own they can't just freely float through plasma they need a chaperone and the most common chaperone we use to move cholesterol are APO B bearing particles namely the vldl particle which is itself very athrogenic