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 you take people with a pcsk 9 uh uh loss of function mutation run around the LDL 15 their entire lives even if they're obese and smokers and hypertensive one have you their chance of having anything autostrotic is incredibly low
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.
their mirror opposites were discovered several years earlier which had a hyperfunctioning pcsk9 gene or hyper fun a gene that produced a hyper functioning protein and these people had sky high LDL cholesterol they were a subset of the uh familial hyper cholesterolemia syndromes and these people weren't and what was interesting to note uh is that they just didn't develop cardiovascular disease