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.
Ultimately, what's happening in atherosclerosis is that the inflammatory response is being activated by the accumulation of indigestible waste products, specifically oxidized cholesterol, in macrophages in the artery wall, which turn to foam cells, and generally make cells around them angry. If that didn't happen, if we could get rid of that oxidized cholesterol, then it wouldn't matter at all how strong your inflammatory response was. You would not get atherosclerosis.
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 the best way to deal with this is to find a best of both worlds solution, to let people have the strong inflammatory response that they need in order to be protected well against infections, but to fix the problem of maladaptive activation of the immune response. And what we're kind of doing exactly that, not by changing the inflammatory response itself, but rather by changing the targets.