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.
so this led researchers to ask at a very important question which is when a human being takes ketamine in order to treat their depression and they get some relief from depression is that the consequence of neuroplastic changes in all those nmda glutamate bdnf related circuits that we talked about before or is it the consequence of something happening in the opioid system
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.
it is metabolized to something called hnk which is hydroxy norketamine now I don't expect you to know what hydroxy norketamine is and I don't expect you to care about it until I tell you what I'm about to tell you which is that hydroxy norketamine has an incredible specificity for the MU opioid receptor and maybe that Kappa opioid receptor as well