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How long after AMT until its safe to use other drugs?

jess046

Bluelighter
Joined
Nov 14, 2012
Messages
217
I tried AMT a week ago and didn't realise it had MAOI properties...!

And so on the same weekend I used meth and mda and on the saturday after using AMT (used on thursday) I ended up getting serotonin syndrome, although I have also summised that this may have been a result of the combination of meth and mda in too high doses.

But I'm also curious as to whether my AMT use (20mg) also had an impact...

Which has led me to do some research and my first question is how soon after AMT is it safe to use a serotonin antagonist?

While I'm here it might also be worth asking those more experienced than I, what the best dose for AMT is to produce the MDMA high without the visuals. I have some friends who aren't big into psychedelics, but want to try some AMT as an alt to MDMA, but I'm worried about them not handling the psychedelic aspect.


Cheers, guys
 
Hi !
long time lover of aMT here :)

I do believe the serotonin syndrome is caused by the mix of MDA and meth. aMT is a MAOI but a not so powerful one and also not lasting longer than the main effects. I don't know about the chemistry or pharmacology but that's how it feels to me.

I may be jumping to conclusions here but do you perhaps mean serotonin agonist ? When I mix aMT with low dose mushrooms I am affected more by the mushrooms, so there is definetly some interaction, but I would be surprised if it lasts longer than 15 hours (low dose aMT) or 24 hours (higher dose aMT)

About the dose for your friends, it's all personal but:

I use 3-7mg as a "day enhancer". It lastst 15hours for me. 3hours of comeup, 8-9hours of plateau, and 2-3hours of comedown. Nobody notices and I'm in a very good mood ;)
10-25mg is very empathogenic without too much visual distractions. But since it's a tryptamine there will always be brighter lights, some trails, shifting of colors.
25-40mg has some more visual effects. Same sort, but more pronounced. I rarely "see" things on aMT.

Did you experience strong visual effects on 20mg ?
 
lol, yes I mean agonist.

At 20mg I had some notable visual distortions during the comeup, first couple of hours. After that it more so became a speedy, mdma buzz.

So I guess 10-15mg would be a good estimate for the mdma high without the visual stuff- but it was nothing like an acid trip for me, more just that psychedelic vibe.
 
It seems to me like there is more than one batch of aMT around and they seem to have surprisingly varied doses.

I believe I have the weaker, cream-coloured batch. 40mg was a very mild trip for me, neither particularly psychedelic or very MDMA-like.

I honestly don't think you could replace MDMA with aMT unless you were happy to have the psychedelia too. It's a very different drug and that's just part of its nature.

Although aMT is a competitive MAOI it does not appear to be a particularly strong one and I would think it's far more likely that the MDA/meth combination was responsible for your SS.
 
aMT felt nothing like MDMA, for me..

I doubt the aMT had anything to do with it.. It has very very weak (if any at all) MAOI properties.
 
aMT felt nothing like MDMA, for me..

I doubt the aMT had anything to do with it.. It has very very weak (if any at all) MAOI properties.

Not true guys, and I keep having to bust this misconception over and over and over again. aMT has comparable MAOI strength to harmaline. See this post, which contains the links and relevant quotes you need: http://www.bluelight.ru/vb/threads/651978-amt-mdma-combo?p=11066546&viewfull=1#post11066546 .

That having been said, it is also a short acting MAOI, and the citation link is in one of my posts somewhere but I don't have time right now to dig it out. Meaning, that MAOI effects shouldn't last much longer than the main effects of the drug itself, although you need to consider the half-life and that of aMT's metabolites which could also potentially be MAOIs. This is similar to harmaline, in that once an ayahuasca trip is over, you are pretty much in the clear in terms of dietary restrictions and drug combos.
 
I also have some brick orange powder that seems below par.

does it also have a very strong smell? this sounds like my batch.

Fucking gagged on that stuff when snorting it, but it wasn't as painful as 2cb...now that was nasty to ingest in powder form. :/
 
My batch was bought over a year ago. It started off a moderate tan colour and has now become orange. It still works though, and is very potent.
 
The MAOI matter confuses me. Is it possible for a drug to be dangerous as a MAOI when combined with monoamine releasers but not potent enough as MAOI to activate oral DMT ? It is, right?
 
That's a good question. Maybe someone with greater biological knowledge can chime in. You would think, though, that if there is enough MAO in the body to destroy DMT before it reaches the brain to produce a threshold effect, then there must be enough to metabolize any extra serotonin, norepinephrine, and dopamine released as a result of the consumption of a monoamine releasing drug.

Do you ask this question because you have tried to activate oral DMT with aMT?
 
No it's more because people sometimes seem to equate MAO inhibition potential either with the potential to activate tryptamines and/or the potential to render concurrent use of monoamine releasers dangerous. OR the general potential as a MAO substrate. This may then become somewhat of a two-dimensional oversimplification.

I guess this is what triggered me:
Yes really survived.

As Murple points out all tryptamines are MAOIs. Even DMT. That doesn't mean when you take DMT by itself it provides an MAOI action otherwise you wouldn't have to take an MAOI to activate it. Y'follow?

Since tryptamines may be considered MAOIs or not by different criteria, it rubbed me the wrong way. Some tryptamine may be a MAOI as a MAO substrate but not in its potential to fuck with any MDMA you may ingest. Or, it may be dangerous together with other drugs but still not activate DMT.

Part of this may be because they are not all equally selective for MAO-A or MAO-B.

All these are matters that add up to the safety of a drug as a MAOI, and that only makes for a certain 'chance' that combination with other drugs will mess you up.
 
I'm no expert, but I'm pretty sure different compounds have different levels of susceptibility to MAO due the number and kind of functional groups in their structure that MAO finds tasty (and so that tastiness, I think, varies from "ravenously delicious" to "bland but passable" between compounds). We're talking about billions of molecules in a dose of most drugs, so the amount of a dose that gets broken down by MAO is better understood by probability and proportion rather than "MAO destroys it or not". Thus, MAOIs are weak or strong based on how strongly "appetizing" they are to MAO, and because DMT is highly susceptible to being broken down by MAO, it requires a compound that is very attractive to MAO (but is resistant to being broken down by MAO itself [keeps its molecular mouth full like gum]) to keep MAO away from it.

A very similar conversation from aMT's Big and Dandy thread that speculatively elaborates on the dangers.
 
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^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:

NSFW:
bripharmchem00065-0169.tif

bripharmchem00065-0171.tif


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.
 
Has anyone actually been able to activate DMT with AMT? Surely it would be the ultimate activator by also adding to the trip. I've always assumed no-one uses it because it has fuck-all effect - much like that other "MAOI" St.Johns Wort. Is there any reason why you wouldn't use AMT to activate DMT if was an MAOI?
 
I assumed that too, but I think one of the most infuriating things is that it will be very difficult to tell if the aMT has activated an oral dose or if it is just a placebo effect. How does one objectively measure activation?
 
Until a psychopharmacologist comes on here to interpret the data better, it will continue to be a matter of confusion and speculation.
Agreed, and perhaps it will remain somewhat ambiguous even then. We are using mostly just abstracts based on rats or pieces of rats to make guesses about humans. No doubt there are factors at play that we haven't even considered. A quick search pulled this ADD thread related to the matter.

I've personally titrated aMT in conjuction with MDAI up to 80 mg MDAI and there was no sign of danger as I would suspect there would be if it was an MAOI on par with harmaline. I also used aMT with 4-FA (20 mg aMT intramuscularly and 80 mg 4-FA rectally), and though it was way more than the some of its parts empathogenically (probably stronger than any MDMA experience I've ever had, and far stronger than any 4-FA) there was again no subjective sign of danger at that dose (however I feel aMT/4-FA is nevertheless a very dangerous combo and that dose was getting close to problems). I've also used aMT (15 mg IM) with ~350 mg propylhexadrine (a.k.a. hexahydromethamphetamine - which drug bank reports is a triple releaser), and mephedrone, a number of times with no issues.

All of these confirmed or strongly suspected triple releasers feel as though they share something fundamental with each other and with aMT to me, and if aMT was a harmaline-strong MAOI I should probably be dead or at least have experienced something more undesirable than feeling hot and sweaty with these combos. There's also a report of combining substantial doses of aMT with MDMA late during the aMT trip on Erowid by Scotto, who reports 6 others also did the combo without negative consequences. Again, these combos and doses are quite likely right on the edge of disasters, but the fact that their not coroner reports suggest aMT is not as strong an MAOI as harmaline (or PMA). Reports of brain zaps after single doses (personally experienced) or a low number of successive doses (see Xorkoth) of aMT also suggests strong rather than weak serotonin release to me, as these sorts of reports also pop up among people who have used MDMA and MDAI (see Jamshyd) in similar ways. The uncertain generalizability of the scientific data in conjunction with personal experience and what anecdotes indirectly suggest still makes me think aMT is a strong serotonin releaser in humans and a significant but not nearly "harmaline strong" MAOI. This suggests the dose of aMT needed for "aMT-huasca" would be prohibitively large.

Transform said:
I assumed that too, but I think one of the most infuriating things is that it will be very difficult to tell if the aMT has activated an oral dose or if it is just a placebo effect. How does one objectively measure activation?
You can't really, but you could have an aMT party with experienced users where half of the people willing to attempt aMT huasca get capsules of DMT and others get a placebo (tell them half are getting placebo and that aMT huasca may not work too to help avoid placebo effect). I've used synthetic DMT intramuscularly with aMT and the before and after difference is stark. You'll know if it works. BTW the combo isn't all that great. It was like IM DMT with mescaline cacti in that the DMT was too harsh a contrast. However, ayahuasca with mescaline cacti is one of the greatest things ever if you can keep it down (and of course ayahuasca and aMT is likely deadly). I assume the qualitative difference owes to the rate DMT gets to the brain.
 
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