Paul Saladino· MD
and we know that insulin resistance can cause more a possi 3 which is one of the lipoproteins on an LDL particle that is more sticky and insulin resistance can cause more of these proteoglycans in the sub and athelia space
Loading…
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.
and we know that insulin resistance can cause more a possi 3 which is one of the lipoproteins on an LDL particle that is more sticky and insulin resistance can cause more of these proteoglycans in the sub and athelia space
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 don't think there is robust enough evidence to implicate LDL as directly toxic to the endothelium I think that instead what we see is that states of metabolic syndrome and insulin resistance this would be metabolic dyslexia are really what is causing this sub endothelial proteoglycan layer to become more sticky
do these diabetic states do these uh insulin resistant States create the deposition of more proteoglycans in the subintimal space making LDL more likely to get stuck there and if your LDL is more likely to get oxidized this to me con starts to begin at least suggesting a hypothesis by which we could connect um directly things like metabolic dysfunction and the progression of atherosclerosis
insulin resistance could induce higher amounts of protog glyp in this subintimal space essentially making the subintimal space more sticky