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.
I wonder if there's a clue to a very vexing question which is why is it that some people with high LP little-a do not go on to get premature heart disease many do most do a significant number do not and it appears completely uncoupled from the level of their LP little-a which makes me wonder are there virulent and non virulent phenotypes that at the level of expression by number or molecular weight aren't captured
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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.
why wouldn't the LP little a phenotype or the LP a gene flatline after 80 in other words I understand why see tap VV is protective I don't understand why LP little a should concentrate
and in the families where the alpha literally is very elevated but nobody's having any events into their 80s maybe you don't need to be as aggressive