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.
you know last I checked there were probably more than 2500 different genetic mutations that produce that phenotype so this is an interesting point that there's still value in looking in other words just having that phenotype how many of the genetic drivers of FH do we know and contribute to that very interesting point you made which is identifying that specific genetic driver carries with an even greater risk than is embedded within the LDL
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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 do send them they're willing for genetic testing you know trying to discern whether they have the monogenic FH from a mutation in the LDL receptor or apop or pcsk9
but if they have the genetic mutation you know having the monogenic mutation their increased risk is even greater than their LDL value so that's why genetic testing is really helpful not only for Cascade effects for determining the risk of their first degree relatives and their offspring but also because they have a greater risk even beyond their absolute LDL value