The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
if the LDL is if there's inflammation and insulin resistance then the LDL will come into the arterial wall but in the absence of inflammation in the absence of insulin resistance doesn't matter how much LDL you have in your arteries it won't come in your arteries
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.
They don't have inflammation, they don't have insulin resistance, they make nitric oxide on demand. You know, they have healthy endothelial glycocalyx, those LDL particles are just zipping on by, you know, kind of like a maglev train, you know, the the glycocalyx is negatively charged, the outside of your red blood cells and the lipoproteins are negatively charged, negative repels negative.
Well, you got to know who, you know, is likely not to. They don't have inflammation, they don't have insulin resistance, they make nitric oxide on demand. You know, they have healthy endothelial glycocalyx, those LDL particles are just zipping on by, you know, kind of like a maglev train, you know, the the glycocalyx is negatively charged, the
they don't have inflammation they don't have insulin resistance they make nitric oxide on demand you know they have healthy endothelial calyx those LL particles are just zipping on by