Is this observed with purely monomeric-targeting 5HT2AR agonists though? Because the psychedelics exert their strong perceptual effects and I believe some other effects by binding to those in an oligomer with mGluR2,to disinhibit glutamate activity, though I think there had been challenges to that idea recently. Either way there would be something more to the effects of psychedelics at 5HT2ARs because those like lisuride that bind to the monomeric form only don’t induce the same kind of effects, though I may be missing something.

I would wager there are poorly documented or culturally roped off (in the sense that western society just isn’t privy to the knowledge of yet) psychedelics used all throughout those regions. The size of traditional medical and shamanistic systems in Africa and Asia are immense and no less complex than were the ones in Europe, the MENA region, and the Americas. It’s just not open to the western mind fully yet. I believe ibogaine is from the medicinal arsenal of Central African Pygmy (would love to know if there’s a better collective word for these peoples as this is clearly an outdated term still being used) peoples like the Mbuti and Mbenga who have quite a distinct lifestyle and background compared to surrounding Africans who likely have their own equivalents too.

I contracted COVID multiple times from family members and haven’t been vaccinated yet due to a mix of some medical conditions I have that I’m fearful of potential interaction with but also just every time I intended to do it something happened that made it impossible then I’d catch covid again and have to wait and etc.

I never lost my sense of smell or taste even during active infection, or got very sick (also a reason I didn’t necessarily prioritize vaccination despite being adamant my at high risk family members should get it) and I kind of want to attribute it to some of the medications I’m on. I take a lot of medicine to treat a messy combination of a genetic condition, neuropsych conditions, GI and immunological issues I have including some unconventional stuff. Two that I feel could’ve helped were famotidine which I take in supratherapeutic doses with approval from a doctor and memantine, which is potently neuroprotective.

My point is I think I preserved smell and taste throughout because of these drugs. I’m curious to see if long COVID and it’s brain fog type symptoms are responsive to any of these kinds of agents that induce neurogenesis.

I mean, you can argue x causes y for a lot of comorbidities in psychiatry and you may not be wrong. I don't think it limits the utility of the diagnosis. I also have a hunch the poor awareness and understanding of dissociative disorders and dissociation itself really is probably a strong reason it seems like it is only existing as a comorbid type of psychopathology to others like depressive episodes. Someone suffering from chronic dissociation as the main and only substantial issue may just never present to psychiatric care due to the still somewhat vague nature of how dissociation is described and how recent of an entry the word is in casual use. People can piece together more what anxiety or depression are and are more likely to end up in treatment for them because its often routinely screened for, they're not recent entries into common use in the english language so people have more of a name to put to their feelings, and they've been extensively defined over and over due to their prominence.

On the flipside, something like dissociation is probably going unnamed in many suffering from it even to the point of having psychosocial impairment to some degree, and in other cases is probably, due to difficulty in naming and describing it especially amongst middle aged and elderly segments of the population for whom its a pretty foreign concept. I think more bipolar individuals would get a hunch regarding manic episodes if those were, similarly but less so, something the general public knew how to describe. If mania didn't commonly co-occur with depressive episodes as in BD then I would wager most people with some degree of mania would never even present to psychiatrists for diagnosis for this reason, and I think that may be the case with dissociative conditions.

I’ve always conceptualized dissociation (not in terms of identity as that’s obviously a more severe and post traumatic etiology) as simply parallel to anxiety or panic in my understanding and thus not really ever understood why depersonalization disorder is not more commonly diagnosed especially as concurrent to anxiety disorders or another affective disorder like depression here. Then again there aren’t even diagnostically separate parallel working concepts that handle irritability (unless you want to count the rather narrow relatively speaking IED) and apathy as separate from depression/anxiety or unipolar mania being restored as a diagnosis so I dunno why I would expect anything that makes sense from the current framework and way of defining psychopathological symptom domains.

I was under the impression that milder cases of depression may not be that responsive to SSRIs but with more severity a benefit becomes apparent.