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.
i think that you don't even need elevated ldl to get accelerated atherosclerosis if you have insulin resistance driven by an exceeding um driven by you know moving past the ceiling of your personal fat threshold in this situation of a genetic mutation causing an inability to store fat in the subcutaneous adipose
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.
i think that's fascinating that you don't even need elevated ldl to get accelerated atherosclerosis if you have insulin resistance driven by an exceeding um driven by you know moving past the ceiling of your personal fat threshold
If you cannot expand your fat mass, if your fat cells are broken, either because of a mutation in the LMNA gene, like the monogenic form of familial hyperlipodystrophy, Dunnigan type, or because you've broken your fat cells by what you eat, and I'll get to that now, you will become insulin resistant. You will become hypertensive. You will get atherosclerosis.