^Interesting post. I just checked the link you provided and it seems I've missed a portion of conversation/debate in the aMT thread over the last few weeks.
Anyhow, I'd like to point out a few things from that post if I may, because it seems like we're interpreting the data differently:
The first point is about aMT's ability to inhibit the increase of 5-HT due to iproniazid. Iproniazid is an irreversible non-selective MAOI; irreversible MAOIs can be inhibited and prevented from covalently bonding to the MAO enzyme by other MAOIs if they are administered within a certain time window. The point about aMT being able to exert this inhibition of an irreversible MAOI is demonstrating the affinity aMT has for the MAO enzyme; i.e. that it has a similar affinity as harmaline.
In relation to your above analogy about "tastiness", this could be re-phrased as "MAO finds aMT as tasty as harmaline when it has it's mouth full of something else".
Secondly, about the figures graphically relating the effectiveness of various MAOIs on the increase of endogenous 5-HT:
In the first graph you can see that, up to about 8 hours, aMT is taking the lead so to peak, but then it levels off into a plateau after which harmaline catches up and overtakes it at around 21 hours. Clearly harmaline is stickier and is bound to MAO for longer. The difference between them at 21 hours is ~130% with aMT and 160% with harmaline. That's not really very far behind, and equates to harmaline being roughly
1.2x as effective as aMT at increasing endogenous 5-HT until aMT starts losing it's grip. Maybe this is is because of the way that aMT binds to the enzyme; from your post and from wiki "because the methyl screws up MAO by getting in the way and taking up its time". Nevertheless, whilst the enzyme is inactive, it is almost as useless as it would be if harmaline were bound to it.
Also, about aMT being a serotonin releaser and it's comparisons to MDMA. I still have huge doubts about whether it can be a serotonin releaser on the scale of MDMA. That
study you linked to doesn't really tell me anything. All it says is that they gave rats
8 huge massive doses of
aET and killed them after a wekk, and found that their brains were depleted of serotonin. Umm, wut? Well of course they are going to be depleted, but in the abstract there are no numbers to show how this compares to other similar drugs such as MDMA. The data collection part of the study was in vitro, not in vivo.
Moreover, I haven't seen any evidence of MDMA being an MAOI of the same degree as the above study shows aMT to be. And it couldn't be, if it was simultaneously a potent serotonin releaser. You can take an SSRI with MDMA - I have done it many times myself - but you could not get away with doing that on aMT without risking serotonin syndrome.
I find it difficult to accept that you could take a drug - which is apparently 0.8x as effective as harmaline at boosting 5-HT via MAO inhibition and a strong serotonin releaser like MDMA - and survive. I find it much more likely that it's serotonin releasing properties are slight (still enough to cause depletion if given 8 mega doses in a week before being slaughtered, but slight in it's acute effects), and that it is the MAOI action combined with small serotonin release/SSRI effect which gives rise to the intense euphoria and empathogenesis.
And regardless, it still wouldn't be correct to assume that it is safe to combine aMT with SSRIs or other serotonergic agents. With what little we know of MAOIs, it would be foolhardy to jump to the assertion that aMT is not an MAOI worth considering. I have personally taken aMT a day after stopping 5-HTP, and it was verging on more than I could handle; it felt like I had to constantly battle to not pass out. It definitely is an MAOI worth taking into consideration when dosing other compounds.
As you said yourself, the discrepancy between figures 4 and 5 cannot be explained without more in-depth knowledge of the matter. The above graphs are confusing enough, but there is enough information in those studies to indicate that aMT is definitely more powerful an MAOI than dexamphetamine, and according to the data, only very slightly behind harmaline in it's ability to increase endogenous 5-HT as per figure 1.
Until a psychopharmacologist comes on here to interpret the data better, it will continue to be a matter of confusion and speculation.