The real question is, can you take DMT
orally after aMT and have an aMThuasca experience? Going by the articles I've linked to before regarding aMT's MAOI potency, I would think there must be potential here. It's just a case of whether anyone with access to both compounds is going to try it.
As it pertains to combining MAOIs with aMT, I just want to throw this little wrench in to the works for you all to mull over:
Take a look at this paper -
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2043998/?page=1
We know from the papers I have previously cited
that aMT is indeed a worthy MAOI, measuring as effective in it's inhibition and competitive ability as harmaline. But there is scant evidence of it being a serotonin-releaser. In fact, I've searched through pages of pubmed, and have yet to come up with any evidence whatsoever of it's serotonin releasing properties. (Please point me in the right direction if there is an explanation out there.) This is not to say it isn't, because it may very well be the case that it is. [I'm aware of the paper cited by wikipedia, but it doesn't give any explanation in the abstract about the methodology used for the experiment, although I assume from what I read that it involves studying fractions of dead rat synaptosomes prepared from cortex material, and not the
in vivo electrochemical method used in the above study.]
But, since MAOIs are contraindicated with MDMA due to serotonin syndrome, don't you find it strange that both these mechanisms could be present in aMT to the same degree as it's comparative counterparts MDMA and harmaline whilst at the same time people are taking it day in day out and not freaking out/dying.
I would think that if serotonin release happens from aMT to the same degree as MDMA, and if it is also an MAOI comparable to harmaline in strength, then taking a dose would be instant serotonin syndrome by default. It cannot be a strong MAOI
and a strong serotonin releaser, it doesn't make any sense. Surely it's much more likely that it's more one than the other. Maybe its serotonin releasing properties are actually very slight (if at all) and as such are amplified greatly by the MAOI properties of the drug. Or that both properties happen in a reduced enough intensity at "normal" doses.
If, as the paper suggests, the drug is actually a mild SSRI (rather than a serotonin releaser) with simultanous MAOI properties, then this would also explain it. And it may also explain why aMT lacks the crash of MDMA, and why similarly "rolly" drugs like 5-MeO-MiPT work the way they do.
I'm not saying any of this with conviction for any particular explanation, but it's a curiosity worth considering.