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Low Dose Daily AMT as an Anti-Depressant - Safe?

PepperSocks

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Hi there, I did a search using titles only function for "AMT" but nothing specific about this came up.

I am starting a regimen of taking a low dose of AMT every morning for depression, anxiety, and general nootropic effects.

On Friday I took 5mg but once I got to work it felt like a very rough come-up and I was starting to go down. I had cold sweats, a lot of tension, etc. I took my xanax prescription with me just in case and I was glad I did.

On Saturday I tried again at 3mg; What an amazing day :D

It took a couple hours to get going and the come-up had some tension and anxiety but nothing serious. I peaked about T+7 and felt amazing. Also aphrodisiac effects were out of this world. I wasn't having visuals or anything but I did have a very nice stimulated euphoria characteristic of monoamine release.

Today (Sunday) I feel a little bit drained; I am not surprised by this considering how I felt yesterday. I only took 2mg today because I saw how 3mg affected me and I don't want it to be strong like that; just a little lift is all I want in a daily anti-depressant.

I also suspect I will become tolerant and higher doses will be required. This is good in a way because the body effects will be diminished. The 2mg dose today didn't do much; but that could just be because I feel drained from yesterday.

I am going to take another 2mg tomorrow. I know with other psychedelic tryptamines that they absolutely will not work if dosed in a daily manner. They produce a strong tolerance and nearly completely lose function. Is this likely to happen with AMT?

Before I go too far into this; what kind of risk am I running using a low dose monoamine releaser such as AMT as a daily stimulant/anti-depressant?

I know it has been used as the pharmaceutical anti-depressant Indopan in the Soviet Union so it must have at least some amount of safety and effectiveness.

Thanks for your expertise.
 
I tried it for 2 weeks, started at 5 mg and went up to 10mg. Only side effect was some gastric discomfort. Gonna try it in higher doses soon.
I did take a 2 day break in my experiment.

Didnt feel any negative effects after i stopped taking it.
 
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although it has not been proven AFIK, based on the studies of aET it would seem likely aMT exerts some degree of serotonergic neurotoxicity - i have never been sure how much exactly (less than MA?) but if it was my brain i would not take the risk regardless of efficacy. if you do decide to continue experimentation supplement with plenty of NAC, ALA, melatonin, ascorbic acid etc.
 
I take Cod Liver oil and multi-vitamin daily. I take tryptophan if I feel fried or need sleep. I took some about an hour ago and am going to hit the hay soon.

I know the signs of serotonin depletion and will be looking out for them (like they're hard to look for; they tend to be kind "in your face" ;)) and taking appropriate action if I feel it going downhill. I have experience with MDMA and know how to minimize it's side effects and harm from serotonergic toxicity.

What does NAC stand for?
 
although it has not been proven AFIK, based on the studies of aET it would seem likely aMT exerts some degree of serotonergic neurotoxicity - i have never been sure how much exactly (less than MA?) but if it was my brain i would not take the risk regardless of efficacy. if you do decide to continue experimentation supplement with plenty of NAC, ALA, melatonin, ascorbic acid etc.

Id say the chance of it being neurotoxic would be unlikely in low doses.
 
Wouldn't 5ht2b agonism and the heart issues it's associated with in the long term be a concern with daily use of pretty much any serotonergic psych?
 
In mice, there appears to be a direct relationship between the concentration of serotonin in the brain, spleen, and lungs and resitance to influenza virus.
http://www.ncbi.nlm.nih.gov/pubmed/919502

Something to bear in mind, in the light of the recent swine flu pandemic.

Actually that was a thought of mine. I did read about being more susceptible to influenza with a higher serotonin concentration.

I also haven't gotten the vaccine and am on the fence about getting it.
 
Wouldn't 5ht2b agonism and the heart issues it's associated with in the long term be a concern with daily use of pretty much any serotonergic psych?

Apperantly this wasnt an issue in the USSR.
 
^^^
how do you know, have you examined the heart valves of the people who used it? the idea that a drug is safe because it was prescribed in russia half a century ago is utterly ridiculous. shulgin had to have his aortic valve replaced - i was told by shulgin's assistant that his condition was unrelated to the 5ht2b agonist effect of psychedelics/empathogens, but i did not probe as to why he was sure of this...ie i doubt they could be sure (unless shulgin has a family history of aortic valve malfunction which is possible)

I love aMT - there was a time two years ago when i used it with relative frequency (probably 4 times total) but i would be worried about neurotoxic effects even at low doses. MDMA is toxic at low dose, although low dose=low damage presumably
 
alpha-ethyl-tryptamine was also sold as Monase in the US, don't forget. Given that the US has generally led the way in research, I'd be far more interested in what US researchers were finding about a closely related drug than what Communist-era Russian researchers were finding about the exact drug.

I'm certain that American post-approval research was much better. Who knows how closely the russians looked for agranulocytosis.
 
They would have noted it considering how widely Indopan was prescribed in the 60s-80s period. It's withdraewl from use was probably due to misuse - about 10-125 years to find a drug has addictive problemns seems about right for drugs in the UK, well other than obviously abusable ones like amphetamine - as no report of long term toxicological symptoms has ever been published (I got my ex other half to check courtesy of the poisons international database - well the Russian equiv of toxbase)
 
Would they though? The occurance of agranulocytosis was extremely small, but the postmarketed surveys for that sort of thing are pretty intense. I doubt that for communist russia for some reason.
 
I've been google scholar'ing AET and all I seem to come up with is a bunch of studies where they give massive doses and look for anything to make psychedelic drugs look bad. :\

Same deal with AMT.
 
Would they though? The occurance of agranulocytosis was extremely small, but the postmarketed surveys for that sort of thing are pretty intense. I doubt that for communist russia for some reason.

I have mailed http://www.vnihfi.ru/ (research institute who made indopan avaliable as a antidepressant therapy in USSR) about information on toxicity, maybe they will provide it.
 
I've been google scholar'ing AET and all I seem to come up with is a bunch of studies where they give massive doses and look for anything to make psychedelic drugs look bad. :\

Same deal with AMT.

the most important study done on AET toxicity was proformed by DE Nichols who, if you aren't aware, does NOT have an antipsychedelic agenda - some things really are toxic.
 
^Is this the one you're referring to? They were using a pretty intense dosing regime, which I think is what PepperSocks was complaining about.

There's an informative table in this paper, which shows aMT's monoamine releasing power in rat synaptosomes is somewhat comparable or even greater (for serotonin) than MDMA and meth's. I personally treat it like MDMA in how I use it, and would not take it daily even in low doses. It demands the successful user take breaks more than most psychedelics. I recall that Xorkoth reported worrisome symptoms after a week of daily psychedelic dosing. I doubt daily low dosing would result in anything so subjectively alarming as what he mentioned, but not that substantial damage could accumulate in the long term, esp. without taking breaks.
 
The first link was the one I was talking about. 8x30mg/kg; that's one heck of a dosing regimen even though I know it's different for rats.

Thanks for that second link. It pretty much shows AMT is one of the strongest inhibitors of monoamine re-uptake and one of the strongest releasers of monoamines.

Of course strength is all dependent on what dose you take.

I'm only taking 2mg per day at the moment and I feel fine. I don't feel high at all, I just feel like I'm being directed into a more positive state.
 
Of course strength is all dependent on what dose you take.
Yeah, plus the synaptosomes were submerged directly in a solution of the different chemicals for 5 minutes or 30 minutes. I'm no expert, but, if I'm reading correctly, those concentrations correspond to the respective chemical's half maximal effective concentrations (the concentration of drug needed to have the same releasing effect as half the maximally effective releasing concentration of tyramine, I think). I have no idea what human doses of aMT that might translate to (could be light, common, or extreme overdose), or how the rate at which aMT enters the brain, gets distributed and metabolized plays a role, though. Perhaps someone more familiar with this type of research can say more.
 
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I'm only taking 2mg per day at the moment and I feel fine. I don't feel high at all, I just feel like I'm being directed into a more positive state.

Well the soviets used 5-10mg/day, so that seems about right in terms of response
 
What does NAC stand for?

Just because it looks like no one addressed that question, I assume he was abbreviating N-Acetyl Cysteine, which primarily benefits heavy smokers and drinkers, and can be your liver's greatest ally ;)

In fact, I think there are some "hangover pills" being sold today that are basically just overpriced NAC in a cap...

-

And as for daily use of threshold entheo/entacto's, I've been keeping a steady routine of MDAI intake ~2-3 doses a day ~4 days a week for nearly 2 months now and haven't noticed any decrease in effectiveness.

Perhaps AMT would follow a similar course?

Makes me wonder about all these reports you hear from people "if you take serotonin-releasing compounds frequently, you will gradually dilute your native 5HT receptor density, experience an increase in depression symptoms, etc etc".

Hasn't been remotely the case for me.

Perhaps one cannot rationally apply this rule of thumb to all serotonin releasing compounds?

Each different 5HT-releasing drug will affect a different spread of neurological regions. Is it not possible there exists a compound (AMT? MDAI? MDMAI? etc.) which binds to just the right nuclei ripe with, say, Glial cells that are complex enough to modulate the health/functionality of the Reward System neurons, such that they may safely endure a permanent state of empathogenic toxicosis =D

Although my personal experience with frequent use of MDAI has so far been favorable, I also take daily doses of Bacopa Monnieri and Rhodiola Rosea extract, which are both known to affect a great deal of elements in a person's 5HT system, including but not limited to cell density.

DMT, also, has a fair pile of data suggesting it changes one's native 5HT system dramatically over time, and this is good era for anyone really interested in becoming a regular DMT voyager to have that chance without much difficulty (myself included ;) ).

What a veritable cauldron of competing (stewing?) cognitive alterations some of our brains are, eh?
 
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