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.
another rare condition are people who lack lcat genetically and as you might maybe expect from what I just said people who lack lcat who can't do that process of esterifying the cholesterol have extremely low levels of HDL not quite as low as Tanger disease but very low and simply can't form the mature HDL particles that we see in most people
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.
so lcat rides on the HDL particle on that nascent particle it takes a fatty acid from one of the phospholipids on the particle and it transfers that fatty acid to the cholesterol and creates the cholesterol Ester remember that cholesterol Ester is more oily it actually then moves to sort of the center of the particle because it wants to be by itself and not interacting with the water and it starts to form the core of the HDL particle so the core of the mature what I'll call the mature HCL particle is basically cholesterol Esters that are entirely dependent on lcat for their formation