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.
by medical established literature at this point in particularly of of diagnosis it is a phenotype as in — your for example for a while there the criteria it may have changed since is that once you reach a certain level of LDL it you're automatically FH and I think it was at 190 and above
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.
and then there's also polygenetic FH right yep and polygenetic FH gets the what you were talking about outside of monogenetic so poly is now we're actually getting a whole bunch of different types of ways by which LDL levels can be influenced and because of these larger genetic studies these gwas studies and so forth they're getting to where even granular levels like there's just a very small Divergence of LDL um that can then get added to this clustering of others and that's why it's poly it's multiples for which they can see so for example you may know somebody who doesn't have monogenetic FH one of those big four but they might have poly gentic FH and the poly part actually brings them up to an LDL of say 190 or something
so you can never use LDL alone as a hundred percent certain marker for your normal UF heterozygous FH or UF homozygous of age