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MDMA and Naltrexone after MDMA and SSRIs

kailinu

Bluelighter
Joined
Jul 29, 2008
Messages
117
Location
under my umbrella
Hi,

I quickly UedFSE and saw nothing relevant to my experience. My bad if it was too quick. :\

So I have been on SSRIs before and tried to roll while on them and like everyone said, the roll is so dimmed that it's not worth it. I could feel some light amphetamine-like activation (boring) and that was it. Add the frustration and you wished you hadn't tried at all.

But every one knows that nowadays, esp. around here. Bear with me!

I stopped taking any kind of SSRIs 3 months ago. And I had a weird way to use them: I would take them when the depression would be too heavy for me: I would take them for two days then stop, then take them again for two days when the next depressive episode would come upon me, and so forth. You must think this is so weird since A/D only work their charm after at least a couple of weeks. Not so in my case: I take one SSRI pill and two hours later I can feel my mood is totally flattened, like I don't care about anything anymore (and cannot be bothered to work either). So two days here and two days there was working for me. Kinda.

I saw a new Pdoc 6 weeks ago who thinks that the serotonin imbalance theory of depression is Big Pharma BS and would only prescribe them to patients who are adamant they need to stay on them. Actually quite a few... So that new Pdoc believes in the therapeutic value of NMDA antagonists (and the mother of all of them: ketamine) but not as a first-line treatment since it is hard to get patients embarked on the experimental ketamine protocol programs). His first-line treatment are kappa opioid receptor antagonists and in my case Naltrexone. Anecdotally it seems to work quite well in my case. Might be a placebo effect maybe not. My depression comes in waves and it is very possible that I haven't had any "wave" in the last four weeks.

But let's get to the point: what is rolling (or at least trying to roll) when you are taking naltrexone (50 mg / day, brand name Revia). So I scored some Molly today and wanted to test it at home before going to a club with friends (the guy was a new connection and he could have ripped me off with some light brown sugar). I tested a tiny crumb of the light brown powder (it's not actually a powder, it looks like flakes) with the Marquis and it did turn a very dark purple. Things were looking good. I tasted a bit of the powder and the stuff was absolutely acrid on my tongue, but bitter is bitter and doesn't mean all that much). I was really impatient so took 120 mg sharp of the powder and parachuted it as soon as I got home. I got a little stimulated right away but I always get that and attribute it to the anticipation: you cannot feel the effect within minutes of having taken it). Half an hour later however things became really interesting: First the light became brighter, my pupils became dilated and then boom I got crazy eye wiggling. Like I never had before. Or at least that I can remind of. Oddly there was no surge of energy. I had to lay down, and due to the eye wiggling that was the best thing to do anyways. And there was a tiny bit of euphoria but nothing major. And very little empathogenic effects either. The experience lasted 4 to 4 and a half hour only and I came down smoothly and went to sleep half an hour later. I'm feeling OK today I guess, no harsh feelings but no afterglow either.

Now on to what I think may have contributed to this muted experience. AFAIK, naltrexone is a full opiod antagonist (on the µ, delta and kappa receptors). But opioid antagonism probably does not play any kind of role here. Indeed naltrexone is also used as an agent to curb alcohol consumption in alcoholics as well as meth consumption in meth-heads because it makes alcohol and methamphetamine consumption much less rewarding. I can attest to the effect on alcohol consumption: a couple of weeks ago I bought a bottle of red wine with the intent to drink it all in the evening and surprisingly I only drank half of it: this is so not me. There was no reward and there was no interest in drinking more. Weird. The rationale behind that is that naltrexone blocks the dopamine surge in the reward center (nucleus accumbens) which makes using alcohol or meth much less rewarding. This has now been confirmed in multiple studies on lab rats but also clinically on people using alcohol and methamphetamine.

So what I think happened yesterday is that I had a huge serotonergic surge (and therefore huge serotonergic effects : the eye wiggles, the bright lights, the feeling of content and overwhelming serenity) but that the naltrexone blocked the dopaminergic surge hence no magic, no energy, no real euphoria to speak of. All in all an OK experience that left me a tiny bit frustrated and lacking in oomph as opposed to using MDMA combined with SSRIs which is just a waste of money, time and good MDMA.

I'd be interested to have the input of guys who also have tested the combo or people chiming in on whether the lack of dopamine surge played a role in the muted effects or whether other parameters could come into the equation. I'd also be interested to know if the theory of MDMA neurotoxicity induced by dopamine recapture by serotonergic neurons is still the object of a consensus as of 2016 and if so, does it mean that the naltrexone actually protected my serotonergic neurons.

Sorry for the long post BLers! :!
 
I personally think dopamine plays a very important role in MDMA intoxication - people argue that serotonin is the generator of the high (mostly because they like to think that mdma is very different than primary dopaminergics like cocaine IMO) but it's been shown that all of the dopamine release is via serotonin.

Dopamine uptake into the serotonin nerve terminal is for many reasons still the leading theory, though MDMA metabolites are playing some role as well. Regarding whether opoid antagonists are protective or not - they could be if they reduced dopamine globally but I suppose there is a chance that most of the protection is region specific, for example the nucleus accumbens where there are a lot of opoid receptors might have received the brunt of the dopamine reduction.
 
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