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Under title Research: Change - A 2014 review of the safety and efficacy of MDMA as a treatment for various disorders, particularly PTSD, indicated that MDMA has therapeutic efficacy in some patients;[62] however, it emphasized that issues regarding the controlability of MDMA-induced experiences and neurochemical recovery must be addressed.[62] The author noted that oxytocin and d-cycloserine are potentially safer co-drugs in PTSD treatment, albeit with limited evidence of efficacy.[62] This review and a second corroborating review by a different author both concluded that, because of MDMA's demonstrated potential to cause lasting harm in humans (e.g., serotonergic neurotoxicity and persistent memory impairment), "considerably more research must be performed" on its efficacy in PTSD treatment to determine if the potential treatment benefits outweigh its potential to harm to a patient.[14][62]

To: A Systematic Review and Meta-Analysis published in May 2021.

{https://www.cureus.com/articles/58217-the-efficacy-of-mdma-34-methylenedioxymethamphetamine-for-post-traumatic-stress-disorder-in-humans-a-systematic-review-and-meta-analysis#references} Findings show promising evidence for the potential therapeutic use of MDMA alongside psychotherapy in the treatment of PTSD. The pharmacological profile of MDMA may provide direction for future drug developments to treat patients with treatment-resistant psychiatric disorders.

Studies have shown the potential benefits in clinical trials for post-traumatic stress disorder (PTSD). A larger amount of data has been provided for the push in support of MDMA-assisted psychotherapy in these patients.

Studies on psychiatric treatments for mental illness have shown that there is a general dose-dependent benefit of MDMA in assisted psychotherapy, where the Clinician-Administered PTSD Scale (CAPS) total scores at the primary endpoint showed changes proportional to the dosage amount { https://dx.doi.org/10.1177/0269881118806297?utm_medium=email&utm_source=transaction} There are, however, adverse health effects with recreational use due to overdosing, such as hypertension, faintness, panic attacks, and, in severe cases, loss of consciousness and seizures [1]. There is still much to be learned about MDMA’s therapeutic dosing effect and its support with psychotherapy treatment of PTSD.

When patients are exposed to occurrences that trigger traumatic events while under the therapeutic treatment, this enables them to reactivate their fear response and work on separating these traumatic triggers from the conditioned response [2]. MDMA-assisted psychotherapy theoretically targets both the memory reconsolidation and fear extinction processes [3]. The term “memory reconsolidation” describes a type of neuroplasticity that involves the process of an established memory being reactivated, destabilized, and then modified or updated with additional information [4]. Hypothetically, when trauma memories are retrieved while under the influence of MDMA during therapy, a strong prediction error is generated by the unique internal state of MDMA-stimulated elevation of neurochemicals, hormones, and the supportive therapeutic setting [5]. This mismatch of experiences, such as recall of memory with strong fear/anxiety versus recall with emotions such as love or empathy, would allow for an update of the information through molecular mechanisms [https://www.drugabuse.gov/publications/research-reports/mdma-ecstasy-abuse/what-are-effects-mdma?utm_medium=email&utm_source=transaction ]. MDMA increases the release of dopamine (DA) in the striatum and midbrain. Dopamine positively correlates with prediction error, and therefore, MDMA-stimulated DA efflux may amplify and drive a prediction error related to the traumatic memory [6].

Clinicians have found that MDMA can be purified and used to facilitate the above-mentioned therapeutic effects [7]. MDMA promotes the release of dopamine, serotonin, and norepinephrine in the mesolimbocortical circuitry of the brain, as well as the neurohormonal signaling of oxytocin, cortisol, prolactin, and vasopressin [8]. The comprehensive effect of these neurochemicals has been shown to enhance therapeutic success as well as decrease nonresponse and dropout rates [9]. Long-lasting PTSD remission and a reduction in symptoms have been reported after only two to three MDMA-assisted therapy sessions [10].

The Meta Analysis dated 2014 to be removed. To replace with the information sourced from the meta analysis dated May 2021. the current data is redundant and contrary to more recent findings which clarifies all of the uncertainty and misinformation. Fredrickaltchwiezenbeurg (talk) 07:57, 25 September 2021 (UTC)[reply]

 Not done: Seems like a dubious journal, since it isn't included in MEDLINE ([11]) and has a very low impact factor (just above 1, which for medicine doesn't seem too convincing). Please see WP:MEDRS, this is unambiguously within the scope of that. RandomCanadian (talk / contribs) 12:23, 25 September 2021 (UTC)[reply]

Also, D-Cycloserine? The drug that's a second line tuberculosis treatment because of all the nasty neurological side effect is supposedly safer than MDMA? Do they wait until all the side effects kick in, then yell, "see? doesn't this make your previous problems seem so minor?" Although I guess alcoholism tends to follow PTSD around like a dog that just rolled in something foul and D-Cycloserine tends to cause seizures in alcoholics... usually the resultant disrupted thought patterns and constant memory gaps after a good ol' round of seizures makes you unable to focus on anything that was bothering you (or that you care about) for very long stretches of time after it's all said and done. Take it from me. Given the choice I'd have picked the MDMA and preferred that they started me off on the medications that weren't waking nightmares. At least they're not suggesting antipsychotics or large doses of ciprofloxacin, although I'm sure I just gave some federally sponsored lab the idea to feed both to a chimp then claim whatever happened was caused by the E. :P --A Shortfall Of Gravitas (talk) 04:30, 16 June 2022 (UTC)[reply]

The intro section says: | MDMA is illegal in most countries[15][22] and, as of 2018, has no approved medical uses.

That's true. But there are approved medical uses in Canada in 2022.

1. https://globalnews.ca/video/8497644/psychedelics-approved-for-medical-use-in-canada
2. https://www.canada.ca/en/health-canada/services/health-concerns/controlled-substances-precursor-chemicals/policy-regulations/policy-documents/subsection-56-1-class-exemption-conducting-activities-psilocybin-mdma-special-access-program-authorization.html

Bobagem (talk) 20:15, 8 January 2022 (UTC)[reply]

@Bobagem: Thank you. I updated the lead with your information (diff). The body of the article still needs to be updated, if you might be able to do that. ;^) Mark D Worthen PsyD (talk) [he/him] 16:28, 20 February 2022 (UTC)[reply]

Edit: I think the first study is badly mistaken (especially regarding SERT binding) and untrustworthy. 1A agonism is known to show biphasic activity where 1A autoreceptors can effectively counteract increased serotonin levels up to a certain point. MDMA's presumed ability to massively increase serotonin levels via mass reverse transport of serotonin as a 5-HT tranporter substrate compared to it's reputation of being ineffective at low doses (perhaps ~<50mg) or the relatively mild activity of SSRI inhibitors may be demonstrative of this biphasic relationship. MDMA is solidly linked to serotonin syndrome with MAOIs but not SSRIs and user reports of SSRIs rendering MDMA essentially impotent (presumably by binding to similar transporter locations and preventing reverse transport) further suggest this to be the case. /end — Preceding unsigned comment added by CloudBoy9001 (talk • contribs) 01:17, 20 July 2022 (UTC)[reply]

I'll let other editors evaluate the following first in case I'm mistaken but it appears to me that the mental effects of this drug are almost entirely a product of 5-HT2B agonism rather than SERT, 2A, 2C, etc binding.

From https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009019: "It is also useful to present the npKi data of Fig. S2 in numerical format. In the listing below, the npKi values for each drug are arranged in decreasing order. A value of 0.00 means that the Ki value was measured as >10,000 nm. “ND” indicates that the data is not available. The 5-HT2A and 5-HT2C receptors are also highlighted in bold font for easier location. npKi values below about 2.0 should be imperceptible, while values above about 2.0 should be perceptible, and the higher the npKi value, the more perceptible a receptor should be ... MDMA: 4.00 Imidazoline1, 3.64 5ht2b, 3.26 Ca+Channel, 3.21 Alpha2C, 3.09 Alpha2B, 3.07 M3, 2.94 Alpha2A, 2.54 M5, 2.43 M4; 0.00: 5ht2c, 5ht1d, D2, 5ht1e, 5ht1a, 5ht2a, Alpha1A, Alpha1B, 5ht5a, 5ht6, 5ht7, D1, Beta2, SERT, DAT, NET, 5ht1b, H1, H2, D3, KOR, Beta1, M1, M2, D5, D4, CB1, NMDA, MOR; ND: DOR, Sigma2, CB2, Sigma1"

As well, knockout mice without functional 2B receptors demonstrated no MDMA induced hyperlocomotion and WT had MDMA induced locomotion abolished via a 2B antagonist: "Subsequent activation of postsynaptic 5-HT receptors by released 5-HT has been shown to be critical for the unique psychostimulatory effects of MDMA. In contrast, the effects of direct activation of presynaptic and/or postsynaptic receptors by MDMA have received far less attention, despite the agonist actions of the drug itself at 5-HT2 receptors, in particular the 5-HT2B receptor. Here we show that acute pharmacological inhibition or genetic ablation of the 5-HT2B receptor in mice completely abolishes MDMA-induced hyperlocomotion and 5-HT release in nucleus accumbens and ventral tegmental area. Furthermore, the 5-HT2B receptor dependence of MDMA-stimulated release of endogenous 5-HT from superfused midbrain synaptosomes suggests that 5-HT2B receptors act, unlike any other 5-HT receptor, presynaptically to affect MDMA-stimulated 5-HT release. Thus, our findings reveal a novel regulatory component in the actions of MDMA and represent the first demonstration that 5-HT2B receptors play an important role in the brain, i.e., modulation of 5-HT release." (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6670669/). CloudBoy9001 (talk) 23:45, 17 July 2022 (UTC)[reply]

A small (260 people) 2007 study in Atlanta seems to show increased aggression in heavy users. Is this confirmed by other studies? (Reid, Elifson & Sterk, Violence & Victims Vol 21: Issue 1, quoted by the US DoJ.) — Preceding unsigned comment added by 36.11.225.146 (talk) 05:15, 18 July 2022 (UTC)[reply]

Greetings, I would like to propose adding a subsection for non-human animals to MDMA#Research and describe the effects of MDMA on octopuses (see e.g. this study). Any objections or further suggestions? Plasmastate (talk) 18:04, 21 July 2022 (UTC)[reply]

The lead sentence says "crystal form (molly or mandy)". This is correct, these are the most popular terms for the crystallized version of MDMA.

However, "Molly" is U.S. English, whilst "Mandy" is U.K. English. This was also made clear in the edit, however it is not clear in the article for the reader.

It should be made clear that "Molly" is the U.S. term, and "Mandy" is the U.K. term. Maybe with a footnote or similar? 89.8.217.46 (talk) 15:24, 28 August 2022 (UTC)[reply]

I agree that this sort of detail is appropriate for the article, but not sure about it being in the WP:LEDE. The second sentence of § Forms has it. DMacks (talk) 16:25, 28 August 2022 (UTC)[reply]