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.
the primary Phoenix that's seen in these individuals who do or don't have what we call the risk variants is food intake I mean if you measure their food intake very carefully in a lab you can see that the individuals with the variance will eat slightly more they actually may have a slight preference for fatty or for higher fat foods than individuals who don't
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.
so even though our ancestors would have had these genes the reason or never mind our ancestors even though a hundred years ago or 50 years ago this gene still existed probably at the same prevalence you didn't have the food environment to pour fuel on that fire
because the effect size of this genetic variation is not on or off it just widens I think the or increases the susceptibility to whatever it is in the environment that's doing this