With Ayahuasca the MAOI and DMT are taken together at the same time so how is there enough time for the MAOs in the stomach to be inhibited? Shouldn't the MAOs in the stomach process the DMT and the MAOIs in the stomach together meaning that the DMT is completely processed before the MAOs are inhibited to the point they should be by the MAOIs. How are the MAOs completely inhibited by the MAOIs if the DMT is taken at the same time as the MAOIs? Wouldn't this cause much of the DMT to be processed by the MAOs as the MAOs have not been sufficiently inhibited by the MAOIs at the time the DMT was processed?

it appears that the effects of the betacarbolines upon glutamate is the primary cause of potentiation. This makes a lot of sense when you review aya additives and discover that their effect upon glutamic acid is a common theme.

However, it seems to really work best if harmalas are both previously taken, and also taken with the dmt.

Could you please elaborate on this or supply some references that you draw this conclusions from? It sounds a rather interesting area and i think other members would be interested as well.

I've been looking into the action of a lot of alkaloids, including caffeine, various PEAs and Tryptamines and other medicinal and psychoactive agents
something that I am learning for the first time is the significance of GABA, glutamate, NMDA receptors, and seratonin.

I recently read an article stating that blocking glutamate receptor activity attenuated the effects of LSD, I also read that Ibogaine was a NMDA antagonist, interestingly enough so is caffeine.

Quote:

We next tested its efficacy in both wild type animals and in an ALS animal model of disease and demonstrated that harmine effectively increased GLT-1 protein and glutamate transporter activity in vivo.

Harmine, a natural beta-carboline alkaloid, upregulates astroglial glutamate transporter expression.
Li Y, Sattler R, Yang EJ, Nunes A, Ayukawa Y, Akhtar S, Ji G, Zhang PW, Rothstein JD.
Source

Department of Neurology, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.

there has been a lot of speculation about MAOI effects being involved in the pharmacology of various traditional ethnobotanicals, however there has been very little if any evidence to support this notion, however there is a very strong indication that the effects involved involve NMDA and glutamate and it is interesting to learn that very recently harmine was shown to affect this.

looking at the list of NMDA antagonists (from wiki) a pattern begins to emerge:
ketamine (K),
dextromethorphan (DXM),
phencyclidine (PCP),
nitrous oxide (N2O)

when you consider that NMDA is a glutamate receptor, and that harmine affects this, the pharmacological action of harmine in traditional ethnobotanical applications becomes explainable in terms of the effects it has upon the glutamate receptor pathway, as opposed to MAOI activity


scanning through the NMDA antagonist list we find Rhynchophylline, this interesting alkaloid is found in some Uncariaspecies, which are known additives to ayahuasca!

it is interesting that caffeine is known to stimulate glutamate release and is also found in plants added to ayahuasca, such as Ilex guayusa

then you can look at nicotiana species and see that not only do they play a major role in traditional use of things like ayahuasca, nicotine also stimulates glutamate release!

I find it interesting to note that nicotine containing species are also used in a traditional setting in conjunction with both peyote and san pedro cacti.