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What is wrong with the MDMA available today? - v2

How much time has passed between these sessions ?


Interestingly, the polydrug synergy is reduced when meh-MDMA is administered first. This is explicitly mentioned in the meh-MDMA effects profile.


1st few times i took 7-oh-mitragynine it was very euphoric! Over time it became a strong opioid and lost euphoria. Here, 2 years later... same deal regardless of dose or how long its been since i last took it.

Exact same material that i personally made, and i cannot get the euphoric aspect again, but maybe some gremlins snuck in to my bedroom amd replaced it with meh-7-oh? That must be why i dont get euphoria any more...
 
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I also collected some meh-MDMA for comparison on FTIR (which I have an easy access to) but I never detected any differences in their spectra after removing the excipients with solvent extraction
Youre not an analytical chemist obviously.

Im not either, but i run HPLC, GCMS, UHPLC-Q/TOF-MS systems pretty regularily.

Id say send me a sample of your MEH, but i dont recieve drugs in mail especially from strangers.

Regardless i never seen wierd alpha-m analogues EVER in a sample. Meth yes. Caffeiene frequently but only in pills.

I call bullshit on you. Show me the FTIR chromatogram.

I have dozens of MDMA sample GC/MS reports that i can upload, but they get ignored by people like you so why bother. Scroll back, i already put them up. No comments on them, just more rebuttals from ppl like you.

"I gave some meh out and everyone had meh results" --- thats how you sound.

Upload the FTIR results please. We would all love to see them.
 
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chromatogram
yes this would be interesting to me.

i would so love to have my own analyzer. i will it into existence. it is written.

so ot:
maybe its been said.
i am not a connoisseur of mdma. only a few dabbles. i do feel it has a lot to do with source - as with anything these day or ever maybe.

planning a roll or flip soon. I want to be in the midst of others when i do to test the waters and my theories. ;)

yall have a safe one whatever it is

over
 
Exact same material that i personally made, and i cannot get the euphoric aspect again, but maybe some gremlins snuck in to my bedroom amd replaced it with meh-7-oh? That must be why i dont get euphoria any more...
I think this thread has pretty conclusively made the point that the interfacing of MDMA with one's subjective neurochemical landscape is what's actually going on here, but dude I want to get another thread going about these gremlins bc I have had a sheet of acid produce progressively less interesting results recently and I'd rather blame goblins than anything else hahahaha.
 
Interestingly, the polydrug synergy is reduced when meh-MDMA is administered first.
Yeah but the polydrug synergy is reduced when MDMA is administered first. What people call "MehDMA", is what I just think of as shitty ecstasy, and that could be for any of a number of very plausible reasons, all with outcomes too similar to delineate from one another via bioassay. MDMA will trigger the massive release of pre-synaptic serotonin it's known for, in which it primarily acts as a serotonin releasing agent, but it also acts as a serotonin reuptake inhibitor, blocking the serotonin transporter eventually, essentially inhibiting its own action after the initial effects. This, among other reasons, is why it's best to re-dose only once, if at all, early into the experience in case you eased into it… However, this also happens to inhibit other serotonergic drugs, like psychedelics.

Meaning to say: it's quite arbitrary to attempt to establish some would-be threshold of MDM-meh*. It will wind up in circular logic, impossible-to-prove subjective claims, and endless "debate" or "discussion" or whatever on this topic, because, by design, the original post held a loaded question that I honestly think was the result of unconscious confirmation bias. It's hella easy to do, and I'm also willing to admit that I may be under the effects of my own confirmation biases. It's virtually impossible to know now as the relevant samples to test for previous claims of sublime MDMA experiences are locked away in the past.

* ☞ this is my version of the term, which I feel rolls off the tongue more easily; saying "MDMA" starts with a "emm" sound, not a "meh" sound; meanwhile it fits in more nicely with the terminating phonetic "m-ay"

This is explicitly mentioned in the meh-MDMA effects profile.
This "effects profile" post from years ago is certainly well-written, educated grammar and syntax, and it cites other works, too. So it comes across authoritative, official, and rigorously studied, proofed and presented or whatever, but let's keep it real, here. You will not find MDM-meh or any version of same in, say, The Merck Manual or any other respected publishing. So it doesn't matter what anecdotal verbiage was used in the original thread post here; nothing about it is "official" or well established in any scientific or medical community as far as I know, but as always I'm open to being proven wrong by evidence…
 
Yeah but the polydrug synergy is reduced when MDMA is administered first. What people call "MehDMA", is what I just think of as shitty ecstasy, and that could be for any of a number of very plausible reasons, all with outcomes too similar to delineate from one another via bioassay. MDMA will trigger the massive release of pre-synaptic serotonin it's known for, in which it primarily acts as a serotonin releasing agent, but it also acts as a serotonin reuptake inhibitor, blocking the serotonin transporter eventually, essentially inhibiting its own action after the initial effects. This, among other reasons, is why it's best to re-dose only once, if at all, early into the experience in case you eased into it… However, this also happens to inhibit other serotonergic drugs, like psychedelics.
As I've mentioned a long time ago, after taking some shitty MDMA crystal which gave black or purple on Marquis, I've tried to take massive amounts of insufflated 2C-B (30-40 mg) or a normal dose of AL-LAD. The absence of effect was completely different to my own and others experiences using real MDMA with psychedelics (I'm talking in the first 2 hours), Interestingly enough, 3-FEA has exactly the same effect on psychedelics.
 
As I've mentioned a long time ago, after taking some shitty MDMA crystal which gave black or purple on Marquis, I've tried to take massive amounts of insufflated 2C-B (30-40 mg) or a normal dose of AL-LAD. The absence of effect was completely different to my own and others experiences using real MDMA with psychedelics (I'm talking in the first 2 hours), Interestingly enough, 3-FEA has exactly the same effect on psychedelics.
Cool story. And so what's your conclusion from this? All of the world's MDMA is obviously 3-FEA then, right? Is that what you're saying? And I should ignore all of my own personal experiences with what I know to be MDMA, because you've figured it all out, and I'm unable to tell the difference between 3-FEA and 3,4-MDMA? If only I had known that all I had to do was take 2C-B or AL-LAD to figure out that the world's MDMA supply has been magically substituted with 3-FEA and that they both test identically on the Marquis. Welp, mystery solved, guys! I know everyone is as satisfied as I am with that answer. All other data is fake and all other opinions are void now. Because you know, there is NO WAY that both legit MDMA and fake MDMA could be on the market at the same time. That's just not possible. And so, who cares that this thread is predicated on a loaded question? There really MUST BE something wrong with today's "MDMA", and that's the fact that today's MDMA is really 3-FEA. Uh derrrrrrrrrrrp. That's good enough for me, derp derp! Derp out.
 
Cool story. And so what's your conclusion from this? All of the world's MDMA is obviously 3-FEA then, right? Is that what you're saying? And I should ignore all of my own personal experiences with what I know to be MDMA, because you've figured it all out, and I'm unable to tell the difference between 3-FEA and 3,4-MDMA? If only I had known that all I had to do was take 2C-B or AL-LAD to figure out that the world's MDMA supply has been magically substituted with 3-FEA and that they both test identically on the Marquis. Welp, mystery solved, guys! I know everyone is as satisfied as I am with that answer. All other data is fake and all other opinions are void now. Because you know, there is NO WAY that both legit MDMA and fake MDMA could be on the market at the same time. That's just not possible. And so, who cares that this thread is predicated on a loaded question? There really MUST BE something wrong with today's "MDMA", and that's the fact that today's MDMA is really 3-FEA. Uh derrrrrrrrrrrp. That's good enough for me, derp derp! Derp out.
You're putting words in my mouth. I've never said that all that's sold as MDMA is Meh. Nor have I said that it's 3-FEA (it obviously isn't). Obviously it would be easily detected by both Marqus, GCMS and Raman,

All I think we can say is that for a period the amount of Meh-reports increased a lot regarding what was sold as MDMA. I do find the overlap in lack of effects for 3-FEA and the Meh when taking psychedelics is interesting as it points to pure serotonin release being a mechanism shared with what people experience as Meh. The difference from MDMA being 5-HT2A competition without DA/NE counter boost.

Same phenomenon has been reported from MDAI and would probably be true for 2,3-MDMA that is a pure serotonin releaser with subjective effects similar to Meh (- and I don't think nor claim that the Meh is any of those substances).

Anyhow, great that you share your knowledge and skepticism here, though IMO you could take the latter part off steroids sometimes,
 
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You're putting words in my mouth. I've never said that all that's sold as MDMA is Meh. Nor have I said that it's 3-FEA (it obviously isn't).
Were you not implying it? Be honest.

Obviously it would be easily detected by both Marqus, GCMS and Raman,
It's never "detected" with a Marquis test; that's not how reagent testing works fundamentally. GC-MS and RAMAN are on an entirely different level of actual analytics.

All I think we can say is that for a period the amount of Meh-reports increased a lot regarding what was sold as MDMA.
You're just assuming that, which is not how science works. No one has presented real data to back up the claim that "meh-reports increased a lot". This is not demonstrably true, regardless whether it's objectively true. Your own awareness of a thing does not prove that thing is increasing universally, even if that's often been the case. Your subjective experience skews how you perceive the world, by necessity, but we've been blessed with logic, reason, abstract thinking, and intelligence. So while not perfectly possible, try to think as objectively as possible and remember to factor in your subject filter and question your own perceptions enough to see the limits and possible illusions.

I do find the overlap in lack of effects for 3-FEA and the Meh when taking psychedelics is interesting as it points to pure serotonin release being a mechanism shared with what people experience as Meh.
There's no data to support what you're claiming about neurotransmitter affinities here, and it seems pretty unlikely to me, even accounting for people's described lackluster responses. I think maybe you're taking an overly simplistic, reductive, and unrealistic jumping to conclusions approach for what you note as an "interesting overlap of effects". Or is it all just me being too intense about sticking to peer-reviewed science published in respected journals? You know: steroids.

The difference from MDMA being 5-HT2A competition without DA/NE counter boost.
This isn't how MDMA works.

Same phenomenon has been reported from MDAI and would probably be true for 2,3-MDMA that is a pure serotonin releaser with subjective effects similar to Meh (- and I don't think nor claim that the Meh is any of those substances).
Uh huh.

Anyhow, great that you share your knowledge and skepticism here, though IMO you could take the latter part off steroids sometimes,
🙄🔫

Is it necessary for you to try to insult me like this? Have I made you feel so defensive that this becomes your rebuttal disguised as a "IMO" statement? Or am I just tired of arguing with brick wall opinions and people's easily bruised egos, and the frustration is coming across as confrontational and/or argumentative? Look, you and I agree on a huge number of things, and you've mostly replied with perfectly intelligent comments in this discussion indicating you're simpatico with me on the subject and the points I've argued throughout this thread. I respect you and don't mean to sound harsh or overzealous in criticizing faulty logic and reductive thinking.

I'm just OCD about the truth, pharmacodynamic accuracy, biochemical understanding, and ending the drug war with knowledge, wisdom and application. I know this sounds corny, but all of it stems from my love for my fellow humans and desire to eliminate unnecessary suffering and cruelty. And also I've seen the damage mass incarceration from drug prohibition causes to individuals, families and whole communities, firsthand, and I've personally been deeply affected by the disturbing way society handles non-violent, unspectacular drug crimes. If that's too "steroid" intense for anyone's delicate sensitivities, maybe consider voting and supporting bills to decriminalize drug use and possession, increase treatment availability, spread knowledge of how dependency/tolerance works and drug awareness without fear-mongering or "scared straight" attempts, promote responsible use and harm reduction, reject and avoid "drug shaming" and help fight in the effort (peacefully) to end the War on Drugs.

Have a great rest of your week 🙂

EDIT: re-reading my post-before-last, I answered you in way that conveyed a shitty attitude. Sorry. I'm working on being more patient and using kinder speech more likely to kindle a change in thinking. Much can be lost in the transference of ideas to written word. Even with emojis and stylistic emphasis, there is nuance lost that is preserved in the audio of spoken word and the visual communication of body language. Anyway, sorry I'm a little harsh at times, but, like many others on this thread, I like to think we'd get along swimmingly IRL and have a good time hanging out, even if we were just talking on a train; listening to music in my office; or randomly meeting, unplanned, at the same holiday vacation resort (I mean, if we're gonna imagine an encounter, why not something nice? Lol).
 
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The difference from MDMA being 5-HT2A competition without DA/NE counter boost.

Don't forget the MDMA α2-adrenergic MOA. Shulgin reported using BP medication (imidazoline/α2-adrenergic agonists) in his experiments and notes entactogenic qualities reminiscent of MDMA.

Shulgin report from this BL thread:
8.0 mg 2C-B-fly and 2.0 mg of rilmenidine at 12:30 pm; cannabis vapor at 4:00: The result was spectacular. I got a +4 experience from a pure imidazoline blood pressure medication! It is probably the entactogenic core of MDMA.
I believe this capacity for calm contemplation and discussion of painful personal issues is a core feature of the entactogenic state of MDMA, and here I was experiencing it with blood pressure medication.... For me it’s really, astonishingly among the best psychedelic experiences I’ve ever had. Unbelievable. (Shulgin 2016) Pharm 2, p. 26-27

Rilmenidine is an I1-imidazoline selective ligand and α2-adrenergic agonist, while Clonidine (see Shulgins report below) is purely an α2-adrenergic agonist. I think these receptors are too easily dismissed as unrelated or irrelevant to psychedelic & entactogenic effects.

0. 2 mg clonidine and 9.0 mg of 2C-B-fly at noon, cannabis at 3:00 pm: I felt it strongly by 30 minutes. By an hour I was pretty sure that it is more than 2C-B-fly.
I felt the rebirth of my love for my wife, no small thing. I have taken 2C-B-fly several times at various doses, and it was always relatively boring. This was completely different, much more than 2C-B-fly alone. It was spectacular that the primer/probe method worked. Clonidine (unlike 2C-B-fly) is a beautiful psychedelic.
...
I was very present, but not just in the moment. (Shulgin 2016) Pharm 2 , p. 25

Now we know where this "primer/probe method" originated:
Constructing the ecstasy of MDMA from its component mental organs: Proposing the primer/probe method
10.1016/j.mehy.2015.12.018
...the consensus is that the distinctive entactogenic effects [of MDMA] arise from the release of neurotransmitters, primarily serotonin. I propose an alternative hypothesis: The entactogenic mental state is due to the simultaneous direct activation of imidazoline-1 (I1) and serotonin-2 (5-HT2) receptors by MDMA.
I propose the "primer/probe" method to test these hypotheses. A "primer" is a drug that selectively activates 5-HT2 (e.g. DOB or MEM) or serotonin-1 (5-HT1) and 5-HT2 (e.g. DOET or 2C-B-fly). A "probe" is a drug that activates a receptor whose corresponding mental organ we wish to load into consciousness in order to understand its role in the mind.
 
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The Biggest Problem With It Is That We Don’t Have Any Of It.
"We"? … You speaking French or you have a mouse in your pocket? 😉

Don't forget the MDMA α2-adrenergic MOA. Shulgin reported using BP medication (imidazoline/α2-adrenergic agonists) in his experiments and notes entactogenic qualities reminiscent of MDMA.
Great find, thanks for sharing. Interesting to mull over, but I'm a little dubious of this alternative mind organs model, though it's interesting to contemplate nonetheless.
 
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