Harmaline + 5-MAPB

[dopamimetic]

Might it be possible to carefully titrate a combination of these two, to avoid serotonin depletion in attempt to recreate the 4,4'-dimethylaminorex experience?

Does serotonin syndrome come with a warning so you could snort an antagonist of choice or would it hit too fast? I've asked for reports about suspected serotonin toxicity in BDD, sorry for kinda cross posting.

As it is possible to safely titrate even stimulants on irreversible MAOIs, where the danger lies in hypertensive crisis which to me sounds equally bad if not even worse than serotonin syndrome, I wonder why nobody attempted this yet.

I wouldn't consider such a combo if I hadn't so glowing experiences with 4,4'-dmar (hell, even with some remaining venlafaxine in my system) which later turned out to be a SNDRA+MAOA-I.
Too I did extensively combine venlafaxine + DXM (pretty nice) as well as moclobemide + d-amphetamine (not recommended, 2mg required an acute administeration of clonidine and had no recreational effects whatsoever) and have been on SNRI for half my life which probably fucked my serotonin system and both originates my problems as well as makes me consider and maybe tolerate such extreme measures.

Of course it'd be better to do this first in a clinical setting but guess I'm out of luck here. Other possibility would be a mild SSRI + harmaline but guess this will primarily hit the autoreceptors.

In the end tobacco smoke contains afaik at least one MAOI and nobody gets serotonin syndrome from smoking on XTC. I talk about ridiculously low amounts, not unlike ultra low dose naltrexone! Just enough for a little boost. I urgently need something against my crippling social anxiety and low self esteem. Opioids, stims, booze, gabapentinoids, benzos failed, dissos are unpredictable and socially awkward from time to time and mess with memory.

Finally another possibility would be just harmaline as I have read that high doses of it are psychoactive on its own, just my trial of moclobemide 600mg/d made me loose hope in reversible MAOA-I alone. Maybe a threshold dose of tranylcypromine but I don't see myself maintaining a rigid diet, even right now I need to watch out for not to drift into malnourishment. And bleeding out of your eyeballs doesn't exactly sound like fun.

I remember once having very mild signs of serotonin syndrome from DXM + releaser (sweating, headache, possibly temperature) which wasn't pretty but faded away by itself. As I would do it while resting in a cooled room I guess hypertensive crisis might be worse? Would have a benzo handy for intranasal administration, unfortunately no serotonin antagonist.

Any thoughts?

 

[polymath]

There's this article, for instance, but better start with a really low dose when trying that...

https://www.researchgate.net/publication/8172064_Combining_stimulants_with_monoamine_oxidase_inhibitors_A_review_of_uses_and_one_possible_additional_indication

 

[dopamimetic]

Things are complex indeed.

MDMA lowers the SERT density. This is what SSRIs do while they are in effect (downstream the SERT will upregulate and the 5HT autoreceptors downregulate, leading to the initial delay). Ok, I think to know that MDMA toxicity stems rather from 5HT producing cells dying out (which makes an acute crash and depression on the long term) so maybe the SERT change is even regulatory but I guess the these scientists will have considered this before.

Now, DXM inhibits this change - it is a reuptake inhibitor, makes sense for it to diminish 5HT release. Just that they attribute it to anti-inflammatory properties of the drug, which might come from NADPH oxidase inhibition. This, or whatever mechanism, indeed aids with comedowns and rebounds, dissociatives are good in amoreliating alcohol, opioid and stimulant rebound, SSRI withdrawal and so on. They protect against seizures by excessive electrical discharge (you can't do a ECT on ketamine for example. I don't buy ECT altogether but that's not the topic for here & now) and hypoxia. But might cause their own toxicity (which isn't established yet afaik and might be a problemacy of excessive rebound NMDA activation[?]).

My gut feeling was that combining MDMAoids with DXM would amplify side effects because DXM is a pretty strong stimulant on its own, strong enough to cause full blown panic attacks at some hundred mg. Also literature tells there's the danger of serotonin syndrome even when these two agents should compete for SERT and if DXM being a SNRI would win over the SNRA, we'd be left with a headache and crash but it seems like this might be a wrong assumption. They didn't interrogate the monkeys about levels of euphoria though.

So, does DXM or even memantine make a worthy complement to rolling? People confirmed that K erases the come down but I need to know if you just don't feel it while dissociated or if there's really less toxicity happening.

I know that my intention sounds like a ticket to desaster but I am desperate. I want to live, not vegetate.
A shame that no selective serotonin releasing agent like 5-AI is available currently. Also that one had afaik been found to be non-toxic on its own but to induce similar changes like MDMA when combined with a stim.

So in theory low 5-AI + low harmaline + high memantine (DA agonist, NMDA antagonist) sounds like fun. Or medium MDMA + low DXM + low clonidine + maybe even ultra low harmaline after tachyphylaxis sets in. And emoxypine against the dopamine oxidation - this works well with stims. Possible or bullshit?

 

[polymath]

If some obscure RC stimulant were to metabolize to something that inhibits MAO-A and/or B, it could cause problems for people who are sensitive to a combination of those effects. Another reason to be suspicious of untested drugs.

 

[dopamimetic]

Yeah but theoretically, assuming we had selective agents. Harmaline isnt exactly a RC, neither is MDMA nor DXM*, memantine or clonidine. The APBs and 5-AI, purity implied, are afaik assayed.

Could these combos work?

* Granted, there might be some lacking and/or conflicting data but the odds of it being a MAOI are pretty low.