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| {{decree|type=notice|message=This article is in the 'Talk' namespace because it is an unfinished draft. This section is used to host drafts for unpublished articles as well as discussions for published ones. If you'd like to use this area to discuss this draft, please do so in the 'Discussion' section at the very bottom of the page. This notice will be removed once this draft has been approved for publication by an administrator.}}
| | '''''Nymphaea nouchali'' var. ''caerulea''''' (Commonly known as '''Blue Lotus''') is a water lily found throughout most of the eastern half of Africa.{{SubstanceBox |
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| {{SubstanceBox/BlueLotus}}
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| '''3,4-<u>M</u>ethylene<u>d</u>ioxy<u>m</u>eth<u>a</u>mphetamine''' (also known as '''ecstasy''', '''E''', '''XTC''', '''emma''', '''molly''', '''mandy''', and '''MDMA''') is a classical [[Psychoactive class::entactogen]] substance of the [[chemical class::amphetamine]] class.
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| MDMA is considered to be the parent compound of the [[entactogens]], a diverse group that includes [[MDA]], [[methylone]], [[mephedrone]], and [[6-APB]]. It produces its psychoactive effects by promoting the release of [[neurotransmitters]] [[serotonin]], [[dopamine]], and [[norepinephrine]] in the brain.
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| MDMA was first developed in 1912 by the pharmaceutical company [[wikipedia:Merck Group|Merck]].<ref name="FreudenmannOxlerBrennschneider-Reif2006">{{cite journal|last1=Freudenmann|first1=Roland W.|last2=Öxler|first2=Florian|last3=Bernschneider-Reif|first3=Sabine|title=The origin of MDMA (ecstasy) revisited:the true story reconstructed from the original documents|journal=Addiction|volume=101|issue=9|year=2006|pages=1241-1245|issn=1360-0443|doi=10.1111/j.1360-0443.2006.01511.x}}</ref> However, there is no documentation of human use prior to the 1970s, when it became known in underground psychotherapy circles in the United States.<ref name="shulgin1991">{{cite book|last1=Shulgin|first1=Alexander|author-link1=Alexander Shulgin|last2=Shulgin|first2=Ann|author-link2=Ann Shulgin|date=1991|title=[[PiHKAL|PiHKAL: A Chemical Love Story]]|volume=Part 1|publisher=Transform Press|chapter=Chapter 12|pages=66-74|isbn=0963009605}}</ref>
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| In the early 1980s, MDMA spread into nightlife and rave culture, eventually leading to its federal scheduling in 1985.<ref>Pharmaceutical company unravels drug's chequered past | http://www.mdma.net/merck/history-ecstasy.html</ref>
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| By 2014, MDMA was estimated to be one of the most popular recreational drugs in the world, alongside [[cocaine]] and [[cannabis]].<ref>Global drug survey: 2014. | https://www.globaldrugsurvey.com/past-findings/the-global-drug-survey-2014-findings/</ref> Recreational MDMA use is popularly associated with dance parties, electronic dance music, and the club and rave scene.<ref>World Health Organization (2004). Neuroscience of Psychoactive Substance Use and Dependence. World Health Organization. pp. 97–. ISBN 978-92-4-156235-5. Archived from the original on 28 April 2016.</ref> Researchers are currently investigating whether MDMA may assist in treatment-resistant post-traumatic stress disorder (PTSD), social [[anxiety]] in autistic adults,<ref>ClinicalTrials. (n.d.). MDMA-assisted Therapy for Social Anxiety in Autistic Adults - Full Text View - ClinicalTrials.gov. Retrieved from https://www.clinicaltrials.gov/ct2/show/NCT02008396?term=mdma+social+anxiety&rank=1</ref> and anxiety in those with life-threatening illness.<ref>Multidisciplinary Association for Psychedelic Studies. (n.d.). MAPS - MDMA-Assisted Psychotherapy for Anxiety Associated with Life-Threatening Illness. Retrieved from http://www.maps.org/research/mdma/anxiety/life-threatening-illness</ref><ref name="meyer">3,4-methylenedioxymethamphetamine (MDMA): current perspectives - Jerrold S Meyer | https://www.dovepress.com/34-methylenedioxymethamphetamine-mdma-current-perspectives-peer-reviewed-article-SAR</ref><ref name="Parrott">The potential dangers of using MDMA for psychotherapy - Parrott AC | https://www.ncbi.nlm.nih.gov/pubmed/24830184</ref>
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| [[Subjective effects]] include [[stimulation]] or [[sedation]], [[anxiety suppression|anxiety suppression]], [[disinhibition]], [[Empathy, affection, and sociability enhancement|enhanced empathy and sociability]], [[muscle relaxation|relaxation]], and [[euphoria]].
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| MDMA is classified as an entactogen due to how it facilitates feelings of closeness with one's self and others.
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| Tolerance to MDMA builds unusually quickly and many users report that it dramatically loses its effectiveness if used on a frequent basis. It is commonly recommended to wait one to three months between each use to give the brain adequate time to restore serotonin levels and avoid toxicity. Additionally, using excessively high doses and multiple redosing is highly discouraged as these are thought to significantly increase toxicity.
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| Acute adverse effects of MDMA are usually the result of high or multiple doses, although single dose toxicity can occur in susceptible individuals.<ref>Meyer JS (2013). "3,4-methylenedioxymethamphetamine (MDMA): current perspectives". Subst Abuse Rehabil. 4: 83–99. doi:10.2147/SAR.S37258. PMC 3931692 Freely accessible. PMID 24648791.</ref> The most serious short-term physical health risks of MDMA are [[overheating]] and [[dehydration]], which has resulted in deaths.<ref>Greene SL, Kerr F, Braitberg G (October 2008). "Review article: amphetamines and related drugs of abuse". Emerg. Med. Australas. 20 (5): 391–402. doi:10.1111/j.1742-6723.2008.01114.x. PMID 18973636</ref> MDMA has also been shown to be neurotoxic at high doses;<ref>Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 375. ISBN 9780071481274.</ref> however, it is unclear how much this risk applies to typical recreational usage.<ref>Gouzoulis-Mayfrank, E; Daumann, J (2009). "Neurotoxicity of drugs of abuse—the case of methylenedioxyamphetamines (MDMA, ecstasy), and amphetamines". Dialogues Clin Neurosci. 11 (3): 305–17. PMC 3181923 Freely accessible. PMID 19877498.</ref> MDMA has moderate to high abuse potential and can produce psychological dependence in some users.
| | <!-- Combination --> |
| It is highly advised to use [[harm reduction practices]] if using this substance.
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| ==History and culture== | | |CombinationImage2_Caption= |
| [[File:MDMA_Patent.jpg|thumb|left|200px|Patent Certificate for Merck's synthesis of MDMA, dated 1912]]
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| MDMA was first synthesized in 1912 by the German chemist Dr. Anton Köllisch while employed at the pharmaceutical company Merck. Köllisch was in the process of developing agents that would help manage excess bleeding and was interested in MDMA synthesis because it was an intermediate in the production of methylhydrastinin, the methylated analogue of the hemostatic agent hydrastinine. There are no indications of interest in MDMA as an active agent itself.<ref name="FreudenmannOxlerBrennschneider-Reif2006" />
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| MDMA was not mentioned again until 1927, when Dr. Max Oberlin conducted the first proven pharmalogical tests at Merck while searching for compounds with a similar action spectrum to adrenaline or ephetonine. Despite promising results, research was halted due to rising substance prices.<ref name="FreudenmannOxlerBrennschneider-Reif2006"></ref>
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| In 1965, the American chemist [[Alexander Shulgin]] synthesized MDMA as an academic exercise but did not test it for psychoactivity.<ref name="Karch2011">{{cite journal|last1=Karch|first1=Steven|title=A Historical Review of MDMA|journal=The Open Forensic Science Journal|volume=4|year=2011|pages=20-24|issn=1874-4028 |doi=10.2174/1874402801104010020}}</ref><ref name="shulgin1991"></ref>
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| Shulgin claims to have first heard about the effects of MDMA in 1967 from a student and decided to experiment with it himself. He was impressed with the effects of the substance and believed it could have therapeutic utility. He advertised it to therapists and psychiatrists which led it to gain some popularity as an adjunct treatment for various psychological disorders.<ref name="shulgin1991"></ref> During this period, psychotherapist Dr. Leo Zeff came out of retirement and subsequently introduced the then-legal MDMA to over 4,000 patients. From the mid-1970s to the mid-1980s there was a growth of clinicians using MDMA (then known as "Adam") in California.<ref name="Sessa">Sessa, B. (2017). The experience and the drugs. In The Psychedelic Renaissance: Reassessing the Role of Psychedelic Drugs in 21st Century Psychiatry and Society (2nd ed., p. 60). London: Muswell Hill Press.</ref>
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| Recreational use of MDMA became popular at around the same time, particularly in nightclubs, eventually catching the attention of the Drug Enforcement Administration (DEA). After several hearings, a US Federal Administrative Law Judge recommended that MDMA should be made a Schedule III controlled substance so that it could be used in the medical field. Despite this, the director of the DEA overruled this recommendation and classified MDMA as a Schedule I controlled substance.<ref> {{cite web|url=https://maps.org/research-archive/dea-mdma/pdf/0112.PDF|title=In The Matter Of MDMA Scheduling: Opinion And Recommended Ruling, Findings Of Fact, Conclusions Of Law And Decision Of Administrative Law Judge On Issues Two Through Seven|last=Young|first=Francis L.|date=May 22, 1968|website=maps.org|publisher=Multidisciplinary Association for Psychedelic Studies|access-date=November 14, 2019}}</ref><ref name="Karch2011" />
| | <!-- Nomenclature --> |
| | |NameCommon=[[Blue Lotus]], [[Nymphaea nouchali var. caerulea]], [[Lotus]] |
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| In the United Kingdom, the 1971 Misuse of Drugs Act, which had already been altered in 1977 to include all ring-substituted amphetamines like MDMA, was further amended in 1985 to refer specifically to Ecstasy, placing it in the Class A category.<ref name="Sessa" />
| | <!-- Class Membership --> |
| | |EffectClass=[[Sedative]] |
| | |ChemicalClass=[[Morphinans]] |
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| ==Chemistry==
| | <!-- Dosage/Duration per ROA --> |
| MDMA, or 3,4-methylenedioxy-N-methylamphetamine, is a synthetic molecule of the [[substituted amphetamine]] class. Molecules of the amphetamine class all contain a [[phenethylamine]] core comprised of a phenyl ring bound to an amino (NH2) group through an ethyl chain, with an additional methyl substitution at R<sub>α</sub>. In addition to this, MDMA contains a methyl substitution on R<sub>N</sub>, a feature it shares with [[methamphetamine]]. Critically, the MDMA molecule also contains substitutions at R<sub>3</sub> and R<sub>4</sub> of the phenyl ring with oxygen groups -- these oxygen groups are incorporated into a methylenedioxy ring through a methylene bridge. MDMA shares this methylenedioxy ring with other [[entactogens]] and [[stimulants]] like [[MDA]], [[MDEA]] and [[MDAI]].
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| ==Pharmacology== | | |SmokedROA=true |
| MDMA acts primarily as a [[releasing agent]] of the three principal [[monoamine neurotransmitters]] [[serotonin]], [[norepinephrine]], and [[dopamine]] through its action at trace amine-associated receptor 1 (TAAR1) and vesicular monoamine transporter 2 (VMAT2).<ref>"3,4-Methylenedioxymethamphetamine". Hazardous Substances Data Bank. National Library of Medicine. 28 August 2008. Retrieved 22 August 2014.</ref><ref name="Miller">Miller, G. M. (2011). The emerging role of trace amine‐associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. ''Journal of Neurochemistry'', 116(2), 164-176. https://doi.10.1111/j.1471-4159.2010.07109.x</ref><ref name="E Weihe">Eiden LE, Weihe E. VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Ann. N. Y. Acad. Sci. 1216(1)1. 86–98. January 2011. https://doi.org/10.1111/j.1749-6632.2010.05906.x</ref>
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| MDMA is a monoamine transporter substrate (i.e. a substrate for the transporters for dopamine ('''DAT'''), norepinephrine ('''NET'''), and serotonin ('''SERT''')), enabling it to enter monoaminergic [[neurons]] via these neuronal membrane transport proteins.<ref name="Miller" /> By acting as a monoamine transporter substrate, MDMA produces competitive [[reuptake inhibition]] at the neuronal membrane transporters, competing for endogenous monoamines for reuptake.<ref name="Miller" /><ref name="pmid1982265">Fitzgerald JL, Reid JJ. Effects of methylenedioxymethamphetamine on the release of monoamines from rat brain slices. ''European Journal of Pharmacology.'' 191(2). 217–20. 1990. https://doi.org/10.1016/0014-2999(90)94150-V}}</ref>
| | |SmokedROA_Caption= |
| | |SmokedROA_Bioavailability= |
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| | |SmokedROA_Threshold=[[Smoked threshold dose::0.5]] - [[Smoked dose units::g]] |
| | |SmokedROA_Light=[[Smoked min light dose::0.75]] - [[Smoked max light dose::1]] g |
| | |SmokedROA_Common=[[Smoked min common dose::1.25]] - [[Smoked max common dose::2]] g |
| | |SmokedROA_Strong=[[Smoked min strong dose::2.5]] - [[Smoked max strong dose::3]] g |
| | |SmokedROA_Heavy=[[Smoked heavy dose::5]] g + |
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| | |SmokedROA_Duration=[[Oral min total time::6]] - [[Oral max total time::8]] [[Oral total time units::hours]] |
| | |SmokedROA_Onset=[[Oral min onset time::10]] - [[Oral max onset time::60]] [[Oral onset time units::seconds]] |
| | |SmokedROA_Comeup=[[Oral min comeup time::5]] - [[Oral max comeup time::10]] [[Oral comeup time units::minutes]] |
| | |SmokedROA_Peak=[[Oral min peak time::1]] - [[Oral max peak time::2]] [[Oral peak time units::hours]] |
| | |SmokedROA_Offset=[[Oral min offset time::2]] - [[Oral max offset time::2.5]] [[Oral offset time units::hours]] |
| | |SmokedROA_Aftereffects=[[Oral min afterglow time::6]] - [[Oral max afterglow time::8]] [[Oral afterglow time units::hours]] |
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| MDMA inhibits both vesicular monoamine transporters (VMATs), the second of which (VMAT2) is highly expressed within monoamine [[neurons]] vesicular membranes.<ref name="E Weihe" /> Once inside a monoamine neuron, MDMA acts as a VMAT2 inhibitor and a TAAR1 agonist.<ref name="Miller" /><ref name="E Weihe2">Eiden LE, Weihe E (January 2011). "VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse". Ann. N. Y. Acad. Sci. 1216 (1): 86–98. http://doi.org/10.1111/j.1749-6632.2010.05906.x.</ref> The inhibition of VMAT2 by MDMA results in increased concentrations of the aforementioned monoamine neurotransmitters in the cytosol of the neuron.<ref name="E Weihe" /><ref name="pmid12742084">Bogen IL, Haug KH, Myhre O, Fonnum F. Short- and long-term effects of MDMA ("ecstasy") on synaptosomal and vesicular uptake of neurotransmitters in vitro and ex vivo. ''Neurochemistry International''. 43. 4–5. 393–400. 2003 https://doi.org/10.1016/S0197-0186(03)00027-5</ref> Activation of TAAR1 by MDMA triggers protein kinase signaling events which then phosphorylates the associated monoamine transporters of the neuron.<ref name="Miller" />
| | |SublingualROA=false |
| | |SublingualROA_Collapsed=true |
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| | |SublingualROA_Light=[[Sublingual min light dose::x]] - [[Sublingual max light dose::y]] mg |
| | |SublingualROA_Common=[[Sublingual min common dose::x]] - [[Sublingual max common dose::y]] mg |
| | |SublingualROA_Strong=[[Sublingual min strong dose::x]] - [[Sublingual max strong dose::y]] mg |
| | |SublingualROA_Heavy=[[Sublingual heavy dose::x]] mg + |
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| | |SublingualROA_Duration=[[Sublingual min total time::a]] - [[Sublingual max total time::b]] [[Sublingual total time units::hours]] |
| | |SublingualROA_Onset=[[Sublingual min onset time::a]] - [[Sublingual max onset time::b]] [[Sublingual onset time units::minutes]] |
| | |SublingualROA_Comeup=[[Sublingual min comeup time::a]] - [[Sublingual max comeup time::b]] [[Sublingual comeup time units::minutes]] |
| | |SublingualROA_Peak=[[Sublingual min peak time::a]] - [[Sublingual max peak time::b]] [[Sublingual peak time units::hours]] |
| | |SublingualROA_Offset=[[Sublingual min offset time::a]] - [[Sublingual max offset time::b]] [[Sublingual offset time units::hours]] |
| | |SublingualROA_Aftereffects=[[Sublingual min afterglow time::a]] - [[Sublingual max afterglow time::b]] [[Sublingual afterglow time units::hours]] |
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| Subsequently, these phosphorylated monoamine transporters either reverse transport direction – i.e. move neurotransmitters from inside the cell to the [[synaptic cleft]] – or withdraw into the neuron, respectively producing the inflow of neurotransmitters and noncompetitive [[reuptake inhibition]] at the neuronal membrane transporters.<ref name="Miller" /> MDMA has ten times more affinity for uptake at serotonin transporters compared to dopamine and norepinephrine transporters and consequently has mainly serotonergic effects.<ref name="Goldfrank 2011">Nelson, Lewis S.; Lewin, Neal A.; Howland, Mary Ann; Hoffman, Robert S.; Goldfrank, Lewis R.; Flomenbaum, Neal E. (2011). Goldfrank's toxicologic emergencies (9th ed.). New York: McGraw-Hill Medical. ISBN 978-0071605939.</ref>
| | |BuccalROA=false |
| | |BuccalROA_Collapsed=True |
| | |BuccalROA_Caption= |
| | |BuccalROA_Bioavailability=[[Buccal min bioavailability::x]]% - [[Buccal max bioavailability::y]]%<ref>APA formatted citation</ref> |
| | |BuccalROA_Microdose= |
| | |BuccalROA_Threshold=[[Buccal threshold dose::x]] - [[Buccal dose units::mg]] |
| | |BuccalROA_Light=[[Buccal min light dose::x]] - [[Buccal max light dose::y]] mg |
| | |BuccalROA_Common=[[Buccal min common dose::x]] - [[Buccal max common dose::y]] mg |
| | |BuccalROA_Strong=[[Buccal min strong dose::x]] - [[Buccal max strong dose::y]] mg |
| | |BuccalROA_Heavy=[[Buccal heavy dose::x]] mg + |
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| | |BuccalROA_TimelineWidth= |
| | |BuccalROA_Duration=[[Buccal min total time::x]] - [[Buccal max total time::y]] [[Buccal total time units::hours]] |
| | |BuccalROA_Onset=[[Buccal min onset time::x]] - [[Buccal max onset time::y]] [[Buccal onset time units::minutes]] |
| | |BuccalROA_Comeup=[[Buccal min comeup time::x]] - [[Buccal max comeup time::y]] [[Buccal comeup time units::minutes]] |
| | |BuccalROA_Peak=[[Buccal min peak time::x]] - [[Buccal max peak time::y]] [[Buccal peak time units::hours]] |
| | |BuccalROA_Offset=[[Buccal min offset time::x]] - [[Buccal max offset time::y]] [[Buccal offset time units::hours]] |
| | |BuccalROA_Aftereffects=[[Buccal min afterglow time::x]] - [[Buccal max afterglow time::y]] [[Buccal afterglow time units::hours]] |
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| MDMA also has weak agonist activity at postsynaptic serotonin receptors 5-HT<sub>1</sub> and 5-HT<sub>2</sub> receptors, and its more efficacious metabolite [[MDA]] likely augments this action.<ref name="pmid2899513">Battaglia G, Brooks BP, Kulsakdinun C, De Souza EB. Pharmacologic profile of MDMA (3,4-methylenedioxymethamphetamine) at various brain recognition sites.''European Journal of Pharmacology''. 149(1–2)1. 59–63. (1988).https://doi.org/10.1016/0014-2999(88)90056-8</ref><ref name="pmid2871581">Lyon RA, Glennon RA, Titeler M . (1986) 3,4-Methylenedioxymethamphetamine (MDMA): stereoselective interactions at brain 5-HT1 and 5-HT2 receptors. ''Psychopharmacology''. 88(4). 525–6. https://doi.org/10.1007/BF00178519</ref><ref name="pmid7824160">Nash JF, Roth BL, Brodkin JD, Nichols DE, Gudelsky GA. Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidylinositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors. ''Neuroscience Letters''. 177(1–2). 111–5 . (1994). https//doi.org/10.1016/0304-3940(94)90057-4</ref><ref name="pmid12761331">Setola V, Hufeisen SJ, Grande-Allen KJ, Vesely I, Glennon RA, Blough B, Rothman RB, Roth BL. 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro. ''Molecular Pharmacology''. 63(6). 1223–9 (2003). https://doi.org/10.1124/mol.63.6.1223</ref> Cortisol, prolactin, and oxytocin quantities in serum are increased by MDMA.<ref name="Betzler2017">Betzler, Felix; Viohl, Leonard; Romanczuk-Seiferth, Nina; Foxe, John (January 2017). "Decision-making in chronic ecstasy users: a systematic review." European Journal of Neuroscience. 45 (1): 34–44. https://doi:10.1111/ejn.13480...the addictive potential of MDMA itself is relatively small.</ref>
| | |InsufflatedROA=false |
| | |InsufflatedROA_Collapsed=True |
| | |InsufflatedROA_Caption= |
| | |InsufflatedROA_Bioavailability=[[Insufflated min bioavailability::x]]% - [[Insufflated max bioavailability::y]]%<ref>APA formatted citation</ref> |
| | |InsufflatedROA_Microdose= |
| | |InsufflatedROA_Threshold=[[Insufflated threshold dose::x]] - [[Insufflated dose units::mg]] |
| | |InsufflatedROA_Light=[[Insufflated min light dose::x]] - [[Insufflated max light dose::y]] mg |
| | |InsufflatedROA_Common=[[Insufflated min common dose::x]] - [[Insufflated max common dose::y]] mg |
| | |InsufflatedROA_Strong=[[Insufflated min strong dose::x]] - [[Insufflated max strong dose::y]] mg |
| | |InsufflatedROA_Heavy=[[Insufflated heavy dose::x]] mg + |
| | |InsufflatedROA_TimelineFile= |
| | |InsufflatedROA_TimelineWidth= |
| | |InsufflatedROA_Duration=[[Insufflated min total time::x]] - [[Insufflated max total time::y]] [[Insufflated total time units::hours]] |
| | |InsufflatedROA_Onset=[[Insufflated min onset time::x]] - [[Insufflated max onset time::y]] [[Insufflated onset time units::minutes]] |
| | |InsufflatedROA_Comeup=[[Insufflated min comeup time::x]] - [[Insufflated max comeup time::y]] [[Insufflated comeup time units::minutes]] |
| | |InsufflatedROA_Peak=[[Insufflated min peak time::x]] - [[Insufflated max peak time::y]] [[Insufflated peak time units::hours]] |
| | |InsufflatedROA_Offset=[[Insufflated min offset time::x]] - [[Insufflated max offset time::y]] [[Insufflated offset time units::hours]] |
| | |InsufflatedROA_Aftereffects=[[Insufflated min afterglow time::x]] - [[Insufflated max afterglow time::y]] [[Insufflated afterglow time units::hours]] |
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| Additionally, MDMA is a ligand at both sigma receptor subtypes, though its efficacies at these receptors and the role that they play have yet to be elucidated.<ref name="Sigma">Matsumoto RR. Targeting Sigma Receptors: Novel Medication Development for Drug Abuse and Addiction. ''Expert Rev Clin Pharmacology''. 2(4), 351–8. July 2009. https://doi.org/10.1586/ecp.09.18</ref>
| | |RectalROA=false |
| | |RectalROA_Collapsed=True |
| | |RectalROA_Caption= |
| | |RectalROA_Bioavailability=[[Rectal min bioavailability::x]]% - [[Rectal max bioavailability::y]] |
| | |RectalROA_Microdose= |
| | |RectalROA_Threshold=[[Rectal threshold dose::x]] - [[Rectal dose units::mg]] |
| | |RectalROA_Light=[[Rectal min light dose::x]] - [[Rectal max light dose::y]] mg |
| | |RectalROA_Common=[[Rectal min common dose::x]] - [[Rectal max common dose::y]] mg |
| | |RectalROA_Strong=[[Rectal min strong dose::x]] - [[Rectal max strong dose::y]] mg |
| | |RectalROA_Heavy=[[Rectal heavy dose::x]] mg + |
| | |RectalROA_TimelineFile= |
| | |RectalROA_TimelineWidth= |
| | |RectalROA_Duration=[[Rectal min total time::x]] - [[Rectal max total time::y]] [[Rectal total time units::hours]] |
| | |RectalROA_Onset=[[Rectal min onset time::x]] - [[Rectal max onset time::y]] [[Rectal onset time units::minutes]] |
| | |RectalROA_Comeup=[[Rectal min comeup time::x]] - [[Rectal max comeup time::y]] [[Rectal comeup time units::minutes]] |
| | |RectalROA_Peak=[[Rectal min peak time::x]] - [[Rectal max peak time::y]] [[Rectal peak time units::hours]] |
| | |RectalROA_Offset=[[Rectal min offset time::x]] - [[Rectal max offset time::y]] [[Rectal offset time units::hours]] |
| | |RectalROA_Aftereffects=[[Rectal min afterglow time::x]] - [[Rectal max afterglow time::y]] [[Rectal afterglow time units::hours]] |
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| ==Subjective effects== | | |TransdermalROA=false |
| {{Preamble/SubjectiveEffects}}
| | |TransdermalROA_Collapsed=True |
| | |TransdermalROA_Caption= |
| | |TransdermalROA_Bioavailability=[[Transdermal min bioavailability::x]]% - [[Transdermal max bioavailability::y]]%<ref>APA formatted citation</ref> |
| | |TransdermalROA_Microdose= |
| | |TransdermalROA_Threshold=[[Transdermal threshold dose::x]] - [[Transdermal dose units::mg]] |
| | |TransdermalROA_Light=[[Transdermal min light dose::x]] - [[Transdermal max light dose::y]] mg |
| | |TransdermalROA_Common=[[Transdermal min common dose::x]] - [[Transdermal max common dose::y]] mg |
| | |TransdermalROA_Strong=[[Transdermal min strong dose::x]] - [[Transdermal max strong dose::y]] mg |
| | |TransdermalROA_Heavy=[[Transdermal heavy dose::x]] mg + |
| | |TransdermalROA_TimelineFile= |
| | |TransdermalROA_TimelineWidth= |
| | |TransdermalROA_Duration=[[Transdermal min total time::x]] - [[Transdermal max total time::y]] [[Transdermal total time units::hours]] |
| | |TransdermalROA_Onset=[[Transdermal min onset time::x]] - [[Transdermal max onset time::y]] [[Transdermal onset time units::minutes]] |
| | |TransdermalROA_Comeup=[[Transdermal min comeup time::x]] - [[Transdermal max comeup time::y]] [[Transdermal comeup time units::minutes]] |
| | |TransdermalROA_Peak=[[Transdermal min peak time::x]] - [[Transdermal max peak time::y]] [[Transdermal peak time units::hours]] |
| | |TransdermalROA_Offset=[[Transdermal min offset time::x]] - [[Transdermal max offset time::y]] [[Transdermal offset time units::hours]] |
| | |TransdermalROA_Aftereffects=[[Transdermal min afterglow time::x]] - [[Transdermal max afterglow time::y]] [[Transdermal afterglow time units::hours]] |
|
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|
| {{effects/base
| | |SubcutaneousROA=false |
| | |SubcutaneousROA_Collapsed=True |
| | |SubcutaneousROA_Caption= |
| | |SubcutaneousROA_Bioavailability=[[Subcutaneous min bioavailability::x]]% - [[Subcutaneous max bioavailability::y]]%<ref>APA formatted citation</ref> |
| | |SubcutaneousROA_Microdose= |
| | |SubcutaneousROA_Threshold=[[Subcutaneous threshold dose::x]] - [[Subcutaneous dose units::mg]] |
| | |SubcutaneousROA_Light=[[Subcutaneous min light dose::x]] - [[Subcutaneous max light dose::y]] mg |
| | |SubcutaneousROA_Common=[[Subcutaneous min common dose::x]] - [[Subcutaneous max common dose::y]] mg |
| | |SubcutaneousROA_Strong=[[Subcutaneous min strong dose::x]] - [[Subcutaneous max strong dose::y]] mg |
| | |SubcutaneousROA_Heavy=[[Subcutaneous heavy dose::x]] mg + |
| | |SubcutaneousROA_TimelineFile= |
| | |SubcutaneousROA_TimelineWidth= |
| | |SubcutaneousROA_Duration=[[Subcutaneous min total time::x]] - [[Subcutaneous max total time::y]] [[Subcutaneous total time units::hours]] |
| | |SubcutaneousROA_Onset=[[Subcutaneous min onset time::x]] - [[Subcutaneous max onset time::y]] [[Subcutaneous onset time units::minutes]] |
| | |SubcutaneousROA_Comeup=[[Subcutaneous min comeup time::x]] - [[Subcutaneous max comeup time::y]] [[Subcutaneous comeup time units::minutes]] |
| | |SubcutaneousROA_Peak=[[Subcutaneous min peak time::x]] - [[Subcutaneous max peak time::y]] [[Subcutaneous peak time units::hours]] |
| | |SubcutaneousROA_Offset=[[Subcutaneous min offset time::x]] - [[Subcutaneous max offset time::y]] [[Subcutaneous offset time units::hours]] |
| | |SubcutaneousROA_Aftereffects=[[Subcutaneous min afterglow time::x]] - [[Subcutaneous max afterglow time::y]] [[Subcutaneous afterglow time units::hours]] |
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|
| |{{effects/physical| | | |IntramuscularROA=false |
| | |IntramuscularROA_Collapsed=true |
| | |IntramuscularROA_Caption= |
| | |IntramuscularROA_Bioavailability=[[Intramuscular min bioavailability::x]]% - [[Intramuscular max bioavailability::y]]%<ref>APA formatted citation</ref> |
| | |IntramuscularROA_Microdose= |
| | |IntramuscularROA_Threshold=[[Intramuscular threshold dose::x]] - [[Intramuscular dose units::mg]] |
| | |IntramuscularROA_Light=[[Intramuscular min light dose::x]] - [[Intramuscular max light dose::y]] mg |
| | |IntramuscularROA_Common=[[Intramuscular min common dose::x]] - [[Intramuscular max common dose::y]] mg |
| | |IntramuscularROA_Strong=[[Intramuscular min strong dose::x]] - [[Intramuscular max strong dose::y]] mg |
| | |IntramuscularROA_Heavy=[[Intramuscular heavy dose::x]] mg + |
| | |IntramuscularROA_TimelineFile= |
| | |IntramuscularROA_TimelineWidth= |
| | |IntramuscularROA_Duration=[[Intramuscular min total time::x]] - [[Intramuscular max total time::y]] [[Intramuscular total time units::hours]] |
| | |IntramuscularROA_Onset=[[Intramuscular min onset time::x]] - [[Intramuscular max onset time::y]] [[Intramuscular onset time units::minutes]] |
| | |IntramuscularROA_Comeup=[[Intramuscular min comeup time::x]] - [[Intramuscular max comeup time::y]] [[Intramuscular comeup time units::minutes]] |
| | |IntramuscularROA_Peak=[[Intramuscular min peak time::x]] - [[Intramuscular max peak time::y]] [[Intramuscular peak time units::hours]] |
| | |IntramuscularROA_Offset=[[Intramuscular min offset time::x]] - [[Intramuscular max offset time::y]] [[Intramuscular offset time units::hours]] |
| | |IntramuscularROA_Aftereffects=[[Intramuscular min afterglow time::x]] - [[Intramuscular max afterglow time::y]] [[Intramuscular afterglow time units::hours]] |
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| *'''[[Effect::Sedation]]'''
| | |IntravenousROA=false |
| *'''[[Effect::Spontaneous bodily sensations]]''' - The "body high" of MDMA can be characterized as a moderate to extreme euphoric tingling sensation that encompasses the entire body. This sensation maintains a consistent presence that steadily rises with the onset and hits its limit once the peak has been reached.
| | |IntravenousROA_Collapsed=true |
| **'''[[Effect::Physical euphoria]]''' - Some users report physical sensations such as a pleasant bodily warmth.
| | |IntravenousROA_Caption= |
| *'''[[Effect::Perception of bodily lightness]]'''
| | |IntravenousROA_Bioavailability=[[Intravenous min bioavailability::x]]% - [[Intravenous max bioavailability::y]]%<ref>APA formatted citation</ref> |
| *'''[[Effect::Stamina enhancement]]'''
| | |IntravenousROA_Microdose= |
| *'''[[Effect::Bronchodilation]]'''{{citation needed}}
| | |IntravenousROA_Threshold=[[Intravenous threshold dose::x]] - [[Intravenous dose units::mg]] |
| *'''[[Effect::Abnormal heartbeat]]'''{{citation needed}}
| | |IntravenousROA_Light=[[Intravenous min light dose::x]] - [[Intravenous max light dose::y]] mg |
| *'''[[Effect::Increased blood pressure]]'''<ref>The pharmacology and toxicology of “ecstasy” (MDMA) and related drugs | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC81503/</ref><ref>Effects of MDMA, MDA and MDEA on blood pressure, heart rate, locomotor activity and body temperature in the rat involve a-adrenoceptors - Sotiria Bexis & James R. Docherty | http://onlinelibrary.wiley.com/doi/10.1038/sj.bjp.0706688/full</ref>
| | |IntravenousROA_Common=[[Intravenous min common dose::x]] - [[Intravenous max common dose::y]] mg |
| *'''[[Effect::Increased heart rate]]'''<ref>The pharmacology and toxicology of “ecstasy” (MDMA) and related drugs | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC81503/</ref>
| | |IntravenousROA_Strong=[[Intravenous min strong dose::x]] - [[Intravenous max strong dose::y]] mg |
| *'''[[Effect::Temperature regulation suppression]]'''
| | |IntravenousROA_Heavy=[[Intravenous heavy dose::x]] mg + |
| *'''[[Effect::Increased bodily temperature]]'''<ref>Effects of MDMA on body temperature in humans - Matthias E Liechti | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008716/</ref> - As MDMA is a [[serotonin]] releasing agent, a rise in core body temperature tends to be a significant and consistent part of the experience. Caution must be taken as too high of a dose in a dangerously hot environment can result in serotonin toxicity, which can be fatal if left untreated.
| | |IntravenousROA_TimelineFile= |
| *'''[[Effect::Muscle contractions]]'''
| | |IntravenousROA_TimelineWidth= |
| *'''[[Effect::Increased perspiration]]'''<ref>3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) and Driving Impairment - Logan, BK & Couper, FJ | https://www.astm.org/DIGITAL_LIBRARY/JOURNALS/FORENSIC/PAGES/JFS15166J.htm</ref>
| | |IntravenousROA_Duration=[[Intravenous min total time::x]] - [[Intravenous max total time::y]] [[Intravenous total time units::hours]] |
| *'''[[Effect::Dehydration]]''' - Users may experience signs of dehydration such as dry mouth and sweating while dancing or in a hot environment. However, MDMA causes water retention and dilution of electrolytes. Consequently, overhydration has caused death from water intoxication<ref>Brvar M, Kozelj G, Osredkar J, Mozina M, Gricar M, Bunc M. Polydipsia as another mechanism of hyponatremia after 'ecstasy' (3,4 methyldioxymethamphetamine) ingestion. Eur J Emerg Med. 2004 Oct;11(5):302-4. | https://www.ncbi.nlm.nih.gov/pubmed/15359208</ref>. It is advised that users have hydration available, drink to thirst and never over-drink.{{citation needed}}
| | |IntravenousROA_Onset=[[Intravenous min onset time::x]] - [[Intravenous max onset time::y]] [[Intravenous onset time units::minutes]] |
| *'''[[Effect::Dry mouth]]'''
| | |IntravenousROA_Comeup=[[Intravenous min comeup time::x]] - [[Intravenous max comeup time::y]] [[Intravenous comeup time units::minutes]] |
| *'''[[Effect::Difficulty urinating]]'''{{citation needed}} - Higher doses of MDMA result in an overall difficulty when it comes to urination. This is caused by MDMA’s promotion of the release of anti-diuretic hormone (ADH); ADH is responsible for regulating urination. This effect can be lessened by relaxing, but can also be relieved by placing a hot flannel over the genitals to encourage blood flow.<ref>Bora F, Yılmaz F, Bora T. Ecstasy (MDMA) and its effects on kidneys and their treatment: a review. Iranian Journal of Basic Medical Sciences. 2016;19(11):1151-1158. | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5126214/</ref><ref>Inman, D. S., & Greene, D. (2003). ‘The agony and the ecstasy’: acute urinary retention after MDMA abuse. BJU international, 91(1), 123-123.</ref>
| | |IntravenousROA_Peak=[[Intravenous min peak time::x]] - [[Intravenous max peak time::y]] [[Intravenous peak time units::hours]] |
| *'''[[Effect::Vibrating vision]]''' - At high doses, a person's eyeballs may begin to spontaneously wiggle back and forth in a rapid motion, causing the vision to become blurry and temporarily out of focus. This is a condition known as [http://en.wikipedia.org/wiki/Nystagmus nystagmus].
| | |IntravenousROA_Offset=[[Intravenous min offset time::x]] - [[Intravenous max offset time::y]] [[Intravenous offset time units::hours]] |
| *'''[[Effect::Nausea]]''' - This effect is most commonly present during the [[come up]] phase of the experience, and at higher doses, but has been reported to occur spontaneously in those who seem to be susceptible to it.
| | |IntravenousROA_Aftereffects=[[Intravenous min afterglow time::x]] - [[Intravenous max afterglow time::y]] [[Intravenous afterglow time units::hours]] |
| *'''[[Effect::Appetite suppression]]'''
| |
| *'''[[Effect::Pain relief]]''' - This effect is generally not as powerful as it is with [[opioids]].<ref>http://www.idmu.co.uk/therapeutic-uses-of-ecstasy.htm</ref><ref>A method of conducting therapeutic sessions with MDMA. - Greer GR, Tolbert R. | https://www.ncbi.nlm.nih.gov/pubmed/9924843</ref><ref>http://www.maps.org/mdma-cancer/5523-a-dose-response-human-pilot-study-–-safety-and-efficacy-of-mdma-in-modification-of-physical-pain-and-psychological-distress-in-end-stage-cancer-patients</ref>
| |
| *'''[[Effect::Excessive yawning]]''' - Excessive yawning is thought to occur as a result of serotonergic activity (similar to [[psilocybin mushrooms]]) and is more likely to occur with higher doses or pure MDMA. It is sometimes used as an indicator of a batch's quality.
| |
| *'''[[Effect::Pupil dilation]]'''
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| *'''[[Effect::Orgasm suppression]]'''
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| *'''[[Effect::Temporary erectile dysfunction]]''' - As a stimulant MDMA is capable of slowing blood flow around the body, possibly contributing to difficulty maintaining an erection.
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| *'''[[Effect::Vasoconstriction]]'''
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| *'''[[Effect::Teeth grinding]]'''<ref>Bruxism after 3,4-methylenedioxymethamphetamine (ecstasy) abuse - Bruxism and ecstasy Ricardo Jorge Dinis-Oliveira et al. | http://www.tandfonline.com/doi/abs/10.3109/15563650.2010.489903</ref> - This effect when experienced alongside the cognitive and physical [[euphoria]] can often lead to users mildly or intensely clenching their jaw muscles, sometimes even to the point where the individual’s facial expression begins to change. This is sometimes colloquially called “gurning”<ref>Urban Dictionary page on "gurning" http://www.urbandictionary.com/define.php?term=gurning</ref> and is typically only experienced in moderate to high dosages.
| |
| *'''[[Effect::Seizure]]''' - Seizures are rare but may occur in those who are susceptible to them, especially when taking higher doses or redosing while in physically taxing conditions such as being dehydrated, fatigued, undernourished, or overheated.{{citation needed}}
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| }} | | }} |
| {{effects/visual|
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| The visual effects of MDMA occur more selectively and less consistently than any of the traditional [[psychedelics]]. This has resulted in many people disregarding the [[psychedelic]] aspects of MDMA as a myth or rumor, despite a large body of anecdotal reports suggesting otherwise. The effects can not be guaranteed to manifest themselves, but are the most likely to occur with chemically pure MDMA at high doses, towards the end of the experience and particularly if the user has been smoking [[cannabis]]. They also seem more likely to occur if the user has prior experience with [[psychedelics]]. | | The flower has been used for over 2000 years in teas, herbal blends and in perfumes. |
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| ====Enhancements====
| | Like other species in the genus, the plant contains the psychoactive alkaloid [[aporphine]] which is thought to be the main constituent causing the effects of the flower, however, it is more likely a group of aporphine alkaloids are working in conjunction to create the various effects as opposed to just aporphine. High potent extracts when ingested or smoked in high doses are reported to produce [[euphoria]] and [[Hallucination|hallucinations]]. |
| MDMA presents an array of visual enhancements which are mild in comparison to traditional psychedelics, but still distinctly present. These generally include:
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| *'''[[Effect::Colour enhancement]]'''
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| *'''[[Effect::Pattern recognition enhancement]]'''
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| ====Suppressions==== | | ==History and culture== |
| *'''[[Effect::Double vision]]'''
| | Blue Lotus is thought to be the primary for the fruit of the lotus tree eaten by the mythical Lotophagi (Lotus Eaters) in Homer's ''Odyssey.'' The Lotus Eaters were a race of people living on an island dominated by the lotus tree, after they ate the lotus, they would forget their home and loved ones and long only to stay with their fellow lotus-eaters, falling into a infinite euphoric stupor. Those who ate the plant never cared to report or return. |
| | |
| ====Distortions====
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| *'''[[Effect::Tracers]]'''
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| *'''[[Effect::Symmetrical texture repetition]]'''
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| ====[[Effect::Geometry]]====
| | This lotus has been used to produce perfumes since egyptian times. According to a 2023 preprint study, traces of ''[[Peganum harmala]]'', and Blue Lotus were identified in an Egyptian ritual Bes-vase, of the 2nd century BCE |
| The visual geometry produced by MDMA can be characterized as more similar in appearance to that of [[psilocin]] than [[LSD]]. It can be comprehensively described through its [[Visual_effects:_Geometry#Variations|variations]] as primarily intricate in complexity, abstract in form, organic in style, structured in organization, dimly lit in lighting, mostly monotone in colour with blues and greys, glossy in shading, sharp in edges, small in size, fast in speed, smooth in motion, equal in round and angular corners, non-immersive in-depth and consistent in intensity. At higher doses, they are significantly more likely to give rise to states of [[Effect::8A Geometry|level 8A]] visual geometry over [[8B Geometry|level 8B]]. Many users report that MDMA geometry presents itself with dark and menacing emotional vibes with a synthetic and nerve-racking feel to them.
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| ====Hallucinatory states====
| | The plant and flower are very prominent and frequent in Ancient Egyptian art, cuisine and perfumes. Blue Lotus flowers have been depicted in numerous stone carvings and paintings, including the walls of the temple of Karnak, and may be associated with rites pertaining to the afterlife. At Heliopolis, the origin of the world was taught to have been when the sun god Ra emerged from a lotus flower growing in "primordial waters". At night, he was believed to retreat into the flower again. |
| MDMA is capable of producing a unique range of low and high-level hallucinatory states in a fashion that is significantly less consistent and reproducible than that of most other commonly used [[psychedelics]]. These effects are far more common during either the very peak or [[Duration#Offset|offset]] of the experience and commonly include:
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| *'''[[Effect::External hallucination]]''' (''[[effect::autonomous entities]]''; ''[[effect::settings, sceneries, and landscapes]]''; ''[[effect::perspective hallucinations]]'' and ''[[effect::scenarios and plots]]'') - This effect shares many similarities to those produced by [[deliriant]] substances, but does not manifest itself consistently and usually happens only at heavy, likely toxic doses. It can be comprehensively described through its [[Visual_effects:_External_hallucinations#Variations|variations]] as delirious in believability, autonomous in controllability and solid in style. They usually follow themes of memory replays and semi-realistic or expected events. For example, people could be casually holding objects or performing actions which one would expect them to be in real life before disappearing and dissolving under further inspection. Common examples of this include seeing people wearing glasses, or hats when they are not and mistaking objects for human beings or animals.
| | ==Chemistry== |
| *'''[[Effect:: Internal hallucinations]]''' - The internal hallucinations which MDMA induces are only present as spontaneous breakthroughs at extremely high doses.{{citation needed}} This effect's [[Visual_effects:_Internal_hallucinations#Variations|variations]] are delirious in believability, interactive in style, new experiences in content, autonomous in controllability and solid in appearance. The most common way in which they manifest themselves is through [[hypnagogic]] scenarios which the user may experience as they are drifting off to sleep after a night of use; these can usually be described as memory replay from the previous several hours. These are brief and fleeting, but frequent and completely believable and convincing as they happen. In terms of the theme, they often are in the form of conversations with people or instead manifest as bizarre and extremely nonsensical plots.
| | The plant has been found to contain [[aporphine]] and similar alkaloids as well as Nuciferine. The effects of Blue Lotus are thought to be down to these compounds but other various Quinoline alkaloids could play a role. |
| *'''[[Effect::Peripheral information misinterpretation]]{{citation needed}}
| | [[File:Lotuscomponents.jpg|thumb|center|The two main active components in Blue Lotus.]] |
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| }}
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| |{{effects/cognitive|
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| The general head space of MDMA is described by many as one of pronounced mental stimulation, feelings of love, empathy, openness and a pronounced sense of rejuvenation and euphoria. It is capable of producing a large number of cognitive effects that are typically associated with [[entactogens]] and [[stimulants]].
| | ==Pharmacology== |
| | [[aporphine]], thought to be the main active component, dopamine receptor agonist targeting the D1 and D2 receptors. Nuciferine, also a prominent alkaloid, is an antagonist at [[5-HT2A receptor|5-HT<sub>2A</sub>]], 5-HT<sub>2C</sub>, and 5-HT<sub>2B</sub> receptors, but is also a partial agonist at D2, D5, and 5-HT<sub>6</sub> receptors, and an [[agonist]] at 5-HT<sub>1A</sub> and D4 receptors. Additionally, it inhibits the dopamine transporter (DAT). |
| | The group of alkaloids known as Aporphines cause the effects of Blue Lotus. This group contains many Dopamine agonists, a wide range of Serotonin antagonists and Agonists and various reuptake inhibitors. |
| | [[Apomorphine]], the active metabolite of Aporphine, has a catechol structure similar to that of dopamine. |
| | [[File:Aporphines.png|frame|center|The group of alkaloids which create the effects of Blue Lotus.]] |
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| The most prominent of these effects include:
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| *'''[[Effect::Empathy, affection, and sociability enhancement]]'''
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| *'''[[Effect::Thought deceleration]]'''
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| *'''[[Effect::Analysis suppression]]'''
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| *'''[[Effect::Focus suppression]]'''
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| *'''[[Effect::Emotion suppression]]'''
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| *'''[[Effect::Language suppression]]'''
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| *'''[[Effect::Enhancement and suppression cycles]]'''
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| *'''[[Effect::Dream potentiation]]'''
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| }}
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| {{effects/auditory|
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| *'''[[Effect::Auditory enhancement|Enhancements]]'''
| | ==Subjective effects== |
| *'''[[Effect::Auditory hallucinations|Hallucinations]]'''
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| *'''[[Effect::Auditory distortion|Distortions]]'''
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| *'''[[Effect::Tinnitus]]''' - Tinnitus is rarely reported, but typically manifests as a muffled roaring in the ears, affected by whether the user is upright or laying down. It is most commonly reported when using in conjunction with other substances but can manifest on its own at higher doses. This may be accompanied by partial or total, yet highly temporary (on the order of a minute), hearing loss, especially when standing. Some users have reported acquiring permanent tinnitus after abuse.
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| }}
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| {{effects/transpersonal|
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| *'''[[Effect::Existential self-realization]]''' - Although present, this effect is not quite as pronounced or as consistent when compared to [[hallucinogens]] such as [[mescaline]], [[psilocybin]], [[LSD]] or [[MXE]]. This component is unique to MDMA in that it almost always comes about in the form of self-affirmation and a personal appreciation for one’s self as well as others.
| | {{effects/base |
| *'''[[Effect::Unity and interconnectedness]]''' - Experiences of lower-level unity and interconnectedness are commonly produced by MDMA. This component most consistently manifests itself within large crowds at raves and musical events in the form of "becoming one with the crowd." Music is said to consistently intensify this effect as well.
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| | |{{effects/physical| |
| {{effects/aftereffects| | | Blue Lotus most potent effects are the sedation and muscle relaxation it causes. This leads many to use it as a sleep aid or lucid dreaming aid. |
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| The effects which occur during the [[offset]] of an [[entactogen]] or [[stimulant]] experience generally feel negative and uncomfortable in comparison to the effects which occurred during its [[peak]]. This is often referred to as a "come down" and is thought to occur because of [[neurotransmitter]] depletion. Its effects commonly include:
| | You may select physical effects to add below [[Subjective effect index#Physical effects|here]]. |
| *'''[[Effect::Anxiety]]'''
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| *'''[[Effect::Appetite suppression]]'''
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| *'''[[Effect::Brain zaps]]'''
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| *'''[[Effect::Cognitive fatigue]]'''
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| *'''[[Effect::Depression]]'''
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| *'''[[Effect::Derealization]]'''
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| *'''[[Effect::Dream suppression]]''' ''or'' '''[[Effect::Dream potentiation]]''' - Although this substance have been known to suppress dreaming, some users note extremely strange and sometimes scary dreams for several nights after taking large doses of MDMA.
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| *'''[[Sleep paralysis]]''' - Some users report a higher incidence of experiencing sleep paralysis after consuming MDMA.
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| *'''[[Effect::Irritability]]'''
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| *'''[[Effect::Motivation suppression]]'''
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| *'''[[Effect::Thought deceleration]]'''
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| *'''[[Effect::Thought disorganization]]'''
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| *'''[[Effect::Suicidal ideation]]'''
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| *'''[[Effect::Wakefulness]]'''
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| }}
| | *'''[[Effect::Pain relief]]'''- Mild to Moderate pain relief is noted on low to high doses of Blue Lotus. This is thought to be down to the disinhibited and drowsy state it causes. |
| }}
| | *'''[[Effect::Sedation]]'''- Sedation is intense on all doses of Blue Lotus and is one of many of the most prominent effects. |
| ===Experience reports===
| | *'''[[Effect::Muscle relaxation]]'''- Along with sedation, many report muscle relaxation, a feeling of melting into surroundings. |
| Anecdotal reports which describe the effects of this compound within our [[experience index]] include:
| | *'''[[Effect::Headache]]'''- Extremely high doses of Blue Lotus commonly cause Headaches but these can also occur at any dosage depending on the person. |
| {{#ask: [[Category:MDMA]][[Category:Experience]]|format=ul|Columns=1}}
| | *'''[[Effect::Nausea]]'''- Nausea is common depending on the method of consumption. It is most noted to occur when drunk in a tea or smoked as a resin. |
| Additional experience reports can be found here:
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| *[https://www.erowid.org/experiences/subs/exp_MDMA.shtml Erowid Experience Vaults: MDMA]
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| ==Names and forms==
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| ===Names===
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| [[File:Ecstasy_monogram.jpg|150px|thumbnail|right|MDMA Pills, commonly called '''Ecstasy''']]
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| [[File:1g_MDMA-HCl.jpg|150px|thumbnail|right|Off-white MDMA crystals, commonly called '''Molly''']]
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| Since the 1980s, MDMA has become widely known as "'''Ecstasy'''" (shortened to "'''E'''", "'''X'''", or "'''XTC'''"), usually referring to its street forms as illicitly pressed pills or tablets.<ref>The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”) - A. Richard Green et al. | http://pharmrev.aspetjournals.org/content/55/3/463.short</ref> The American term "'''Molly'''" and the British equivalent term "'''Mandy'''" originally referred to crystal or powder MDMA that was purported to be of high purity and free of adulteration.<ref>3 cases of primary intracranial hemorrhage associated with “Molly”, a purified form of 3,4-methylenedioxymethamphetamine (MDMA) | http://www.jns-journal.com/article/S0022-510X(12)00483-2/abstract</ref> However, it has since evolved into a generic street term for any number of euphoric [[stimulants]] that are sold in powder or crystal form.{{citation needed}}
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| ===Forms===
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| MDMA can be found in the following forms:
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| *'''Pills''' are the most common form in which MDMA is sold, and are commonly referred to as '''Ecstasy'''. They often contain other substances or adulterants that range from anything from [[MDA]], [[MDEA]], [[amphetamine]], [[methamphetamine]], [[caffeine]], [[2C-B]] or mCPP to synthesis by-products such as MDP2P, MDDM or [[2C-H]]. They can also contain an array random substances such as [[research chemicals]], prescription drugs, over-the-counter drugs, poisons or nothing at all. It is strongly recommended to take [[harm reduction]] measures such as using a reagent testing kit when ingesting unknown pills.<br />The average concentration of MDMA in ecstasy pills, tested in a drug checking program in Zurich, doubled between 2010 and 2018. The percentage of pills containing more than 120 mg MDMA rose from 4% to 73%. In the same period, the rate of pills containing other psychoactive compounds dropped from 53% to 7%.<ref>{{cite web|url=https://www.saferparty.ch/tl_files/images/download/file/aktuelles%202019/XTC_Auswertung_2018.pdf|website=saferparty.ch|publisher=Sozialdepartement Zürich|language=de|year=2018|access-date=January 18, 2020|title=MDMA Auswertung 2018|trans-title=MDMA Evaluation 2018}}</ref>
| | }} |
| *'''Crystals''' or '''powder''' (commonly called '''Molly''') is a white to brownish substance which can be dissolved, crushed, put into gel capsules or edible paper ("parachutes"). It can be administered [[Route of administration#Oral|orally]], [[Route of administration#Sublingual|sublingually]], buccally or via [[Route of administration#Insufflation|insufflation]] ("snorting" or "sniffing").
| | {{effects/visual| |
| | While subtle, if enough is ingested (Most often through smoking), Blue Lotus can cause visual effects and enhancements. |
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| ==Research==
| | You may select visual effects to add below [[Subjective effect index#Visual effects|here]]. |
| ===MDMA-assisted psychotherapy for PTSD===
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| In 2011, a pilot study on 20 patients demonstrated promising results in the treatment of post-traumatic stress disorder (PTSD). After two or three MDMA-assisted psychotherapy sessions, 83% of the patients no longer met the criteria for PTSD, compared to only 25% in the control group where MDMA was replaced with a placebo. The results sustained at two and twelve months after the treatment. The MDMA and placebo group both received non-drug psychotherapy before and after the sessions. In the study, a dose of 125mg MDMA plus a 62.5mg supplemental dose after 2 hours have been administered.<ref name="mithoefer">Mithoefer, Michael C., et al. “Durability of Improvement in Post-Traumatic Stress Disorder Symptoms and Absence of Harmful Effects or Drug Dependency after 3,4-Methylenedioxymethamphetamine-Assisted Psychotherapy: A Prospective Long-Term Follow-up Study.” Journal of Psychopharmacology (Oxford, England) 27.1 (2013): 28–39. https://doi.org/ 10.1177/0269881112456611</ref> After completion of the study, the patients from the placebo group also received MDMA-assisted psychotherapy, and a long-term follow-up study of 19 patients published in 2013 shows that even after three years the positive results maintained.<ref name="mithoefer2">Mithoefer, Michael C., et al. “Durability of Improvement in Post-Traumatic Stress Disorder Symptoms and Absence of Harmful Effects or Drug Dependency after 3,4-Methylenedioxymethamphetamine-Assisted Psychotherapy: A Prospective Long-Term Follow-up Study.” Journal of Psychopharmacology (Oxford, England) 27.1 (2013): 28–39. https://doi.org/10.1177/0269881112456611</ref>
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| In 2017, the FDA granted MDMA a breakthrough therapy designation for PTSD, meaning if studies show promise, a review for potential medical use could occur more quickly.<ref>Wan, William (26 August 2017). "Ecstasy could be 'breakthrough' therapy for soldiers, others suffering from PTSD". Washington Post. Archived from the original on 29 August 2017. Retrieved 29 August 2017.</ref> Phase 3 clinical trials to look at effectiveness and safety have already begun, and are expected to be completed in 2021, meaning the FDA could approve treatment as early as 2022.<ref>Feduccia, AA; Holland, J; Mithoefer, MC (February 2018). "Progress and promise for the MDMA drug development program". Psychopharmacology. 235 (2): 561–571. doi:10.1007/s00213-017-4779-2. PMID 29152674.</ref> <ref> https://maps.org/articles/6094-inverse-mdma-steps-closer-to-fda-approval-as-a-drug,-but-now-it-needs-to-leap </ref>
| | ====Enhancements==== |
| | *'''[[Effect::Color enhancement]] '''- Blue Lotus can have subtle color enhancements, especially when smoked, colors seem to be noticeably more vibrant and enhanced. |
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| ===R-MDMA=== | | ====Distortions==== |
| MDMA is typically produced and consumed in its [[racemic]] form (known as SR-MDMA) which consists of equal parts S-MDMA and R-MDMA. A 2017 study found that high doses of R-MDMA administered in mice increased prosocial behavior and facilitated fear-extinction learning but did not produce hyperthermia or signs of neurotoxicity. This is thought to owe itself to the lower dopamine release R-MDMA displays relative to SR-MDMA. This result suggests that R-MDMA may be a safer and more viable therapeutic than racemic MDMA.<ref>Curry, D. W., Young, M. B., Tran, A. N., Daoud, G. E., & Howell, L. L. (2018). Separating the agony from ecstasy: R (–)-3, 4-methylenedioxymethamphetamine has prosocial and therapeutic-like effects without signs of neurotoxicity in mice. Neuropharmacology, 128, 196-206. https://doi.org/10.1016/j.neuropharm.2017.10.003</ref> However, more research is needed to validate this finding.
| | *'''[[Effect::Tracers]]'''- Minor tracers can appear at any dose and have been reported from low doses as well as high doses. This is most noticed when the head is moved. |
| | *'''[[Effect::Brightness alteration]]'''- In combination with [[Effect::Color enhancement]], the scenery is often described as brighter or more vibrant. |
| | *'''[[Effect::Perspective distortion]]'''- In massive doses, many report their environment seeming to grow and shrink behind objects they are focusing on. Changes in body size while lying down are common at all doses. |
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| == Reagent results ==
| | }} |
| Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.
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| {| class="wikitable"
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| !Marquis
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| !Mecke
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| !Mandelin
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| !Liebermann
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| !Froehde
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| ! colspan="2" |Gallic
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| |-
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| |Purple - Black
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| |Green - Blue / Black
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| |Purple / Blue - Black
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| |Intense brown - Black
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| |Yellow/green - Dark blue
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| | colspan="2" |Green to brown
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| |-
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| !Robadope
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| !Ehrlich
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| !Hofmann
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| !Simon’s
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| !Zimmermann
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| !Scott
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| !Folin
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| |-
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| |No reaction
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| |No reaction
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| |No reaction
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| |Dark blue
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| |No reaction
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| |No reaction
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| |Orange
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| |}
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| ==Toxicity and harm potential==
| | |{{effects/cognitive| |
| [[File:harmchart.png|thumb|right|315px|Radar plot showing relative physical harm, social harm, and dependence of MDMA<ref>Nutt, D., King, L. A., Saulsbury, W., & Blakemore, C. (2007). Development of a Rational Scale to Assess the Harm of Drugs of Potential Misuse, 1047–1053. http://dx.doi.org/10.1016/S0140-6736(07)60464-4</ref>]]
| | Blue Lotus has most of its cognitive effects manifest themself in sleep. This leads many to use it as a sleep aid or lucid dreaming aid. |
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| The short-term physical health risks of MDMA consumption include [[dehydration]], bruxism, [[insomnia]], [[hyperthermia]],<ref>Nimmo, S. M., Kennedy, B. W., Tullett, W. M., Blyth, A. S., & Dougall, J. R. (1993). Drug‐induced hyperthermia. ''Anaesthesia'', 48(10), 892-895. https://doi.org/10.1111/j.1365-2044.1993.tb07423.x</ref><ref>Malberg, J. E., & Seiden, L. S. (1998). Small changes in ambient temperature cause large changes in 3, 4-methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat. ''Journal of Neuroscience'', 18(13), 5086-5094. PMID: 9634574. https://www.ncbi.nlm.nih.gov/pubmed/9634574</ref> and hyponatremia.<ref>Wolff, K., Tsapakis, E. M., Winstock, A. R., Hartley, D., Holt, D., Forsling, M. L., & Aitchison, K. J. (2006). Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population. ''Journal of Psychopharmacology'', 20(3), 400-410. https://doi.org/10.1177/0269881106061514</ref> MDMA generally does not cause any serious or life threatening effects by itself unless it is associated with other extraneous factors such as exposure to prolonged high ambient temperature and humidity, prolonged physical activities, poor intake of water and lack of acclimatization.<ref>https://www.sciencedirect.com/science/article/pii/S1752928X17300537</ref>
| | You may select from a list of cognitive effects to add below [[Subjective effect index#Cognitive effects|here]]. |
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| Continuous activity without sufficient rest or rehydration may cause the user's body temperature to rise to dangerous levels, and loss of fluid via excessive sweating puts the body at further risk as the stimulating and euphoric qualities of MDMA may cause the user to become oblivious to their physical condition. Diuretics such as [[alcohol]] may exacerbate these risks further due to causing excessive amounts of dehydration. Users are advised to pay close attention to their water intake, drinking neither too much nor too little, and to take care not to overexert themselves to avoid heat-stroke, which can be fatal.
| | *'''[[Effect::Increased music appreciation]]'''- Music can sound crisp or higher quality, leading to a greater appreciation of music. This effect seems to be potent and pronounced at all dosages, but mostly noticeable when smoked. |
| | *'''[[Effect::Empathy, affection, and sociability enhancement]]'''- Many report the urge to interact or be around others, similar to a drunk feeling. However many also report the sleepiness and drowsiness makes socialising unbearable. |
| | *'''[[Effect::Dream potentiation]]'''- Perhaps the most potent effect of Blue Lotus is the dreams it can bring on. It is most commonly used as a lucid dreaming aid, placing Blue Lotus also into the [[Oneirogen]] category. |
| | *'''[[Effect::Derealization]]'''- Many users report a feeling of dissociation to their surroundings or themselves. This is most common when trying to fall asleep. |
| | *'''[[Effect::Sleepiness]]'''- Blue Lotus causes a drowsy sleepy effect at all dosages. This has lead it to become a common sleep aid. |
| | *'''[[Effect::Disinhibition]]'''- Blue Lotus causes an drunk like disinhibition in some, but in others has the opposite effect. |
| | *'''[[Effect::Focus suppression]]'''- It is noticeably hard to concentrate on high doses of Blue Lotus due to the disinhibition and drowsiness it causes. |
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| ===Toxic dose===
| | }} |
| The [[Toxicity::exact toxic dosage is unknown]], but considered to be far greater than its effective dose.{{citation needed}}
| | {{effects/auditory| |
| | Blue Lotus most prominent auditory effect is the enhancement of music. This can be described as the music sounding sharper or more clear. |
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| ===Neurotoxicity===
| | You may select from a list of auditory effects to add below [[Subjective effect index#Auditory effects|here]]. |
| The neurotoxicity of MDMA use is the subject of considerable debate. Scientific study has resulted in the general agreement that, although it is physically safe to try in a responsible context, the administration of repeated or high dosages of MDMA is most certainly neurotoxic in some form.
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| Administration of MDMA causes subsequent down-regulation of [[serotonin]] reuptake transporters in the brain. The rate at which the brain recovers from serotonergic changes is unclear. One study demonstrated lasting serotonergic changes in some animals exposed to MDMA.<ref>Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/7643196</ref> Other studies have suggested that the brain may recover from serotonergic damage.<ref>Scheffel, U., Szabo, Z., Mathews, W. B., Finley, P. A., Dannals, R. F., Ravert, H. T., ... & Ricaurte, G. A. (1998). In vivo detection of short‐ and long‐term MDMA neurotoxicity—a positron emission tomography study in the living baboon brain. ''Synapse'', 29(2), 183-192. https://doi.org/10.1002/(SICI)1098-2396(199806)29:2<183::AID-SYN9>3.0.CO;2-3</ref><ref>Reneman, L., Lavalaye, J., Schmand, B., de Wolff, F. A., van den Brink, W., den Heeten, G. J., & Booij, J. (2001). Cortical serotonin transporter density and verbal memory in individuals who stopped using 3, 4-methylenedioxymethamphetamine (MDMA or ecstasy): preliminary findings. ''Archives of General Psychiatry'', 58(10), 901-906.
| | *'''[[Effect::Auditory acuity enhancement]]'''- Music can sound crisp or higher quality, leading to a greater appreciation of music. This effect seems to be potent and pronounced at all dosages, but mostly noticeable when smoked. |
| Chicago. https://doi.org/10.1001/archpsyc.58.10.901</ref><ref>Selvaraj, S., Hoshi, R., Bhagwagar, Z., Murthy, N. V., Hinz, R., Cowen, P., ... & Grasby, P. (2009). Brain serotonin transporter binding in former users of MDMA (‘ecstasy’). The ''British Journal of Psychiatry'', 194(4), 355-359. https://doi.org/10.1192/bjp.bp.108.050344</ref>
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| It is thought that MDMA's metabolites play a large role in the in the uncertain levels of neurotoxicity. For example, a metabolite of MDMA called [https://en.wikipedia.org/wiki/Alpha-Methyldopamine alpha-Methyldopamine] (α-Me-DA, which is known to be toxic to [[dopamine]] [[neurons]]<ref>Neurotoxic thioether adducts of 3,4-methylenedioxymethamphetamine identified in human urine after ecstasy ingestion (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19349378 | http://dmd.aspetjournals.org/content/37/7/1448.full.pdf</ref><ref name="miller">2,5-Bis-(glutathion-S-yl)-alpha-methyldopamine, a putative metabolite of (+/-)-3,4-methylenedioxyamphetamine, decreases brain serotonin concentrations (PubMed.gov / NCBI) - Miller RT et al. | http://www.ncbi.nlm.nih.gov/pubmed/9128836</ref>) was thought believed to be involved in the toxicity of MDMA to [[serotonin]] [[receptors]]. However, one study found this to not be the case as direct administration of α-Me-DA did not cause neurotoxicity.<ref name="miller">2,5-Bis-(glutathion-S-yl)-alpha-methyldopamine, a putative metabolite of (+/-)-3,4-methylenedioxyamphetamine, decreases brain serotonin concentrations (PubMed.gov / NCBI) - Miller RT et al. | http://www.ncbi.nlm.nih.gov/pubmed/9128836</ref> Additionally, MDMA injected directly into the brain was found to not be toxic, implying a metabolite is responsible for the toxicity when MDMA is administered via insufflation or oral consumption.<ref name="miller">2,5-Bis-(glutathion-S-yl)-alpha-methyldopamine, a putative metabolite of (+/-)-3,4-methylenedioxyamphetamine, decreases brain serotonin concentrations (PubMed.gov / NCBI) - Miller RT et al. | http://www.ncbi.nlm.nih.gov/pubmed/9128836</ref>
| | }} |
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| This study found that although α-Me-DA is involved, it is a further metabolite of α-Me-DA involving glutathione that is primarily responsible for the selective damage to [[5-HT receptors]] triggered by MDMA/[[MDA]].<ref name="miller">2,5-Bis-(glutathion-S-yl)-alpha-methyldopamine, a putative metabolite of (+/-)-3,4-methylenedioxyamphetamine, decreases brain serotonin concentrations (PubMed.gov / NCBI) - Miller RT et al. | http://www.ncbi.nlm.nih.gov/pubmed/9128836</ref>This metabolite forms in higher concentrations when core temperature is elevated. It is taken up into [[serotonin]] [[receptors]] by its transporters and metabolized by [[MAO-B]] into a reactive oxygen species which can cause neurological damage.<ref name="miller" /><ref>Drug-induced Valvulopathy: An Update - Chandikumar S. Elangbam | http://tpx.sagepub.com/content/38/6/837.full</ref>
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| ===Cardiotoxicity=== | | }} |
| | ===Experience reports=== |
| | {{Experience reports|Blue Lotus|https://www.erowid.org/experiences/subs/exp_Lotus_I_Lily_Group.shtml}} <!-- Check the link to see if it exists --> |
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| Long-term heavy use of MDMA has been shown to be cardiotoxic and may lead to valvulopathy (heart valve damage) through its actions on the 5-HT<sub>2B</sub> receptor.<ref name="5ht2btox">Huang, X. P., Setola, V., Yadav, P. N., Allen, J. A., Rogan, S. C., Hanson, B. J., ... & Roth, B. L. (2009). Parallel functional activity profiling reveals valvulopathogens are potent 5-hydroxytryptamine2B receptor agonists: implications for drug safety assessment. ''Molecular Pharmacology'', 76(4), 710-722. https://doi.org/10.1161/01.CIR.102.23.2836</ref><ref>Drug-induced Valvulopathy: An Update - Chandikumar S. Elangbam | http://tpx.sagepub.com/content/38/6/837.full</ref> In one study, 28% of long-term users (2-3 doses per week for a mean of 6 years, mean of age 24.3 years) had developed clinically evident valvular heart disease.<ref>Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805</ref>
| | ==Toxicity and harm potential== |
| | The toxicity of Blue Lotus is misunderstood and poorly researched. Only the pure alkaloids have been tested with little toxicity, however, mixing Blue Lotus with other substances could present a risk. |
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| It is strongly recommended that one use [[responsible drug use|harm reduction practices]] when using this substance. | | It is strongly recommended that one use [[responsible use|harm reduction practices]] when using this substance. |
| | ===Lethal dosage=== |
| | There are no studies on aporphine in animals. However, studies on subcutaneous apomorphine injection, the bioactive form of aporphine, have been carried out. In a 5-day study, mice were administered up to 10 mg/kg apomorphine subcutaneously daily. No adverse effects were observed other than a slight increase in dopamine levels. |
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| ===Dependence and abuse potential=== | | ===Tolerance and addiction potential=== |
| As with other [[stimulant]]s, the chronic use of MDMA can be considered [[Addiction potential::moderately addictive with a high potential for abuse]] and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and [[withdrawal effects]] may occur if one suddenly stops their usage.
| | Blue Lotus is not thought to be addictive. Its compounds have been used in the treatment of alcohol and morphine addiction. |
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| Tolerance to many of the effects of MDMA develops [[Time to full tolerance::with prolonged and repeated use]]. This results in users having to administer increasingly larger doses to achieve the same effects. Upon a single administration, it takes about [[Time to half tolerance::1 month]] for the tolerance to be reduced to half and [[Time to zero tolerance::2.5 months]] to be back at baseline (in the absence of further consumption). MDMA presents cross-tolerance with [[Cross-tolerance::all [[dopaminergic]] and [[serotonergic]] [[stimulant]]s]], meaning that after the consumption of MDMA all [[stimulant]]s will have a reduced effect.
| | ===Dangerous interactions=== |
| | The main and absolute contraindication to using Blue Lotus, is the concurrent use of adrenergic receptor antagonists; combined, they cause a severe drop in blood pressure and fainting. |
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| ===Dangerous interactions===
| | <small>L</small>-DOPA and Blue Lotus could pose risks and cause symptoms such as [[sleepiness]], [[dizziness]], [[Runny nose|runny nose]], [[sweating]] and [[Muscle twitching|tremors]]. |
| {{DangerousInteractions/Intro}} | | {{DangerousInteractions/Intro}} |
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| *'''[[UnsafeInteraction::25x-NBOMe|25x-NBOMe]]''' - Due to the highly unpredictable and physically straining effects of 25x-NBOMe, combinations with MDMA are strongly discouraged.
| | ==Legal status== |
| *'''[[UncertainInteraction::5-MeO-xxT|5-MeO-xxT]]''' - 5-MeO tryptamines are considered to be unpredictable and should be mixed with MDMA with care.
| | ''Nymphaea caerulea'' has been illegal in Latvia since November 2009. It is a schedule 1 drug. Possession of large quantities can be punished by up to 15 years in prison. |
| *'''[[UncertainInteraction::Alcohol|Alcohol]]''' - Both MDMA and alcohol cause dehydration and bodily strain. Approach this combination with caution, moderation and sufficient hydration. More than a small amount of alcohol will dull the euphoria of MDMA.
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| *'''[[UncertainInteraction::Cocaine|Cocaine]]''' - Cocaine blocks some of the desirable effects of MDMA while increasing the risk of heart attack.{{citation needed}}
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| *'''[[UncertainInteraction::DOx|DOx]]''' - The combined stimulating effects of DOx and MDMA can become overbearing, particularly during the come-up phase. Additionally, coming down on the MDMA while the DOx is still active can produce significant anxiety and bodily discomfort.
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| *'''[[UncertainInteraction::GHB|GHB]]'''/'''[[UncertainInteraction::GBL|GBL]]''' - Large amounts of GHB/GBL may overwhelm the effects of MDMA on the comedown and place the user at risk of sudden loss of consciousness.
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| *'''[[UncertainInteraction::MXE|MXE]]''' - There have been reports of concerning serotonergic interactions when the two are taken at the same time, but MXE taken to the end of an MDMA experience does not appear to cause the same issues.
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| *'''[[UnsafeInteraction::PCP|PCP]]''' - PCP with MDMA may increase the risk of excessive stimulation, [[mania]], and [[psychosis]].
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| *'''[[DangerousInteraction::Tramadol|Tramadol]]''' - Tramadol is well-documented to lower the seizure threshold<ref>{{cite journal|last1=Talaie|first1=H.|last2=Panahandeh|first2=R.|last3=Fayaznouri|first3=M. R.|last4=Asadi|first4=Z.|last5=Abdollahi|first5=M.|title=Dose-independent occurrence of seizure with tramadol|year=2009|journal=Journal of Medical Toxicology|volume=5|issue=2|pages=63-67|doi=10.1007/BF03161089|issn=1556-9039|eissn=1937-6995|oclc=163567183|pmid=19415589|pmc=3550327}}</ref> and this risk is especially elevated when tramadol is taken with MDMA.
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| ===[[Serotonin syndrome]] risk===
| | ''Nymphaea caerulea'' was also banned in Poland in March 2009. |
| Combinations with the following substances can lead to dangerously high [[serotonin]] levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.
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| *'''[[DangerousInteraction::MAOIs|MAOIs]]''' such as '''[[syrian rue]]''', '''[[banisteriopsis caapi]]''', '''phenelzine''', '''selegiline''', and '''moclobemide'''<ref>Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210</ref> - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with MDMA will lead to hypertensive crises.
| | ''Nymphaea caerulea'' has been illegal in [[Russia]] since April 2009. |
| *'''[[UnsafeInteraction::Serotonin releasers]]''' such as '''[[MDMA]]''', '''[[4-FA]]''', '''[[methamphetamine]]''', '''[[methylone]]''' and '''[[αMT]]'''
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| *'''[[UncertainInteraction::ΑMT|AMT]]'''
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| *'''[[UnsafeInteraction::2C-T-x|2C-T-x]]'''
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| *'''[[DangerousInteraction::DXM|DXM]]'''
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| *'''[[UnsafeInteraction::5-HTP|5-HTP]]''' - 5-HTP is a supplement that acts as a precursor for serotonin. It is sometimes recommended to be used after MDMA experiences to try to restore depleted serotonin reserves. However, taking 5-HTP shortly before or with MDMA may cause excessive serotonin levels in the brain, which can lead to serotonin syndrome.<ref>{{cite journal|title=Qualitative Review of Serotonin Syndrome, Ecstasy (MDMA) and the use of Other Serotonergic Substances: Hierarchy of Risk|last1=Silins|first1=E.|last2=Copeland|first2=J.|last3=Dillon|first3=P.|pages=649-655|year=2007|volume=41|issue=8|journal=Australian and New Zealand Journal of Psychiatr|doi=10.1080/00048670701449237|pmid=17620161|issn=0004-8674|eissn=1440-1614}}</ref> As a result, it is advised to wait until the day after the MDMA has been used before consuming 5-HTP.
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| *'''[[DangerousInteraction::SSRIs|SSRIs]]''' - SSRI antidepressants such as sertraline (Zoloft), fluoxetine (Prozac), citalopram (Celexa), escitalopram (Lexapro), fluvoxamine (Luvox), and paroxetine (Paxil) can lead to serotonin syndrome when combined with MDMA.<ref>Dobry, Y., Rice, T., & Sher, L. (2013). Ecstasy use and serotonin syndrome: a neglected danger to adolescents and young adults prescribed selective serotonin reuptake inhibitors. International Journal of Adolescent Medicine and Health, 25(3). doi:10.1515/ijamh-2013-0052</ref>
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| ==Legal status==
| | ''Nymphaea caerulea'' is completely prohibited in the state of Louisiana, making it the only state to ban the flower. |
| Internationally, MDMA was added to the UN Convention on Psychotropic Substances as a Schedule I controlled substance in February 1986.<ref>{{cite web|url=http://www.unodc.org/documents/commissions/CND/Drug_Resolutions/1980-1989/1986/CND_Decision-1986-07_S-IX.pdf|title=Decision to place MDMA into Schedule I|publisher=Commission on Narcotic Drugs |date=11 February 1986|website=UNODC|access-date=November 11, 2019}}</ref>
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| *'''Austria''': MDMA is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).<ref>Suchtgiftverordnung, aktuelle Fassung | https://ris.bka.gv.at/GeltendeFassung.wxe?Abfrage=Bundesnormen&Gesetzesnummer=10011053</ref>
| | ''Nymphaea caerulea,'' if sold for human consumption, could fall under the UK's ''Psychoactive Substances Act 2016,'' however, this law is rarely imposed on plants and small scale possession. |
| *'''Belgium''': MDMA is illegal to possess, produce and sell in Belgium.<ref>EMCDDA Country legal profiles - Belgium | http://www.emcdda.europa.eu/html.cfm/index5174EN.html?pluginMethod=eldd.countryprofiles&country=BE</ref>
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| *'''Brazil''': MDMA is illegal to possess, produce and sell under Portaria SVS/MS nº 344.<ref>List of controlled substances: Portaria SVS/MS nº 344 (Portuguese) | http://portal.anvisa.gov.br/lista-de-substancias-sujeitas-a-controle-especial</ref>
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| *'''Canada''': MDMA is a Schedule I drug in Canada.<ref>Canada controlled drugs and substances | http://laws-lois.justice.gc.ca/eng/acts/C-38.8/</ref>
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| *'''Denmark''': MDMA is illegal to possess, produce and sell in Denmark.<ref>EMCDDA Country legal profiles - Denmark | http://www.emcdda.europa.eu/html.cfm/index5174EN.html?pluginMethod=eldd.countryprofiles&country=DK</ref>
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| *'''Egypt''': MDMA is a Schedule III drug in Egypt.{{citation needed}}
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| *'''Finland''': MDMA is illegal to possess, produce and sell in Finland.{{citation needed}}
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| *'''Germany''': MDMA is controlled under Anlage I BtMG (''Narcotics Act, Schedule I'')<ref>{{cite web|url=https://www.gesetze-im-internet.de/btmg_1981/anlage_i.html|title=Anlage I BtMG|publisher=Bundesministerium der Justiz und für Verbraucherschutz|access-date=December 18, 2019|language=de}}</ref> as of August 1, 1986.<ref>{{cite web|url=https://dejure.org/ext/90385d7b0f00e371c060c0f7a577c245|title=Zweite Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften|publisher=Bundesanzeiger Verlag|access-date=December 18, 2019|language=de}}</ref> It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.<ref>{{cite web|url=https://www.gesetze-im-internet.de/btmg_1981/__29.html|title=§ 29 BtMG|publisher=Bundesministerium der Justiz und für Verbraucherschutz|access-date=December 18, 2019|language=de}}</ref>
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| *'''Latvia''': MDMA is a Schedule I drug in Latvia.<ref>Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (3,4-Metilēndioksifeniletānamīni) | http://likumi.lv/doc.php?id=121086</ref>
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| *'''Luxembourg''': MDMA is a prohibited substance.<ref>Règlement grand-ducal du 13 juin 1986 complétant l'annexe du règlement grand-ducal du 20 mars 1974 concernant certaines substances psychotropes. | http://legilux.public.lu/eli/etat/leg/rgd/1986/06/13/n2/jo</ref>
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| *'''The Netherlands''': MDMA is illegal to possess, produce and sell in the Netherlands.<ref>Opiumwet | https://wetten.overheid.nl/BWBR0001941/2019-07-19&xid=17259,15700022,15700186,15700191,15700256,15700259,15700262,15700265,15700271,15700283&usg=ALkJrhg0a81esxOUix1UMvvAvbVALDP2-Q#BijlageI</ref>
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| *'''New Zealand''': MDMA is a Class B1 drug in New Zealand.<ref>Misuse of Drugs Act 1975 No 116 | http://www.legislation.govt.nz/act/public/1975/0116/latest/whole.html#DLM436190</ref>
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| *'''Norway''': MDMA is illegal to possess, produce and sell in Norway.{{citation needed}}
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| *'''Portugal''': MDMA is illegal to produce, sell or trade in Portugal. However, since 2001, individuals found in possession of small quantities (up to 1 gram) are considered sick individuals instead of criminals. The drugs are confiscated and the suspects may be forced to attend a dissuasion session at the nearest CDT (Commission for the Dissuasion of Drug Addiction) or pay a fine, in most cases.<ref name="greenwald2009">GREENWALD, Glenn. Drug decriminalization in Portugal: lessons for creating fair and successful drug policies. Cato Institute Whitepaper Series, 2009.</ref>
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| *'''Russia''': MDMA is classified as a Schedule I prohibited substance.<ref>Resolution of the Government of the Russian Federation | https://www.consultant.ru/cons/cgi/online.cgi?req=doc&base=LAW&n=314201&fld=134&dst=100034,0&rnd=0.41568319511755825#047741519652799347</ref>
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| *'''Sweden''': MDMA is illegal to possess, produce and sell in Sweden.{{citation needed}}
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| *'''Switzerland''': MDMA is a controlled substance specifically named under Verzeichnis D.<ref>{{cite web|url=https://www.admin.ch/opc/de/classified-compilation/20101220/index.html|title=Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien|publisher=Bundeskanzlei [Federal Chancellery of Switzerland]|access-date=January 1, 2020|language=de}}</ref>
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| *'''United Kingdom''': MDMA is a Class A drug in the UK.<ref>Misuse of Drugs Act 1971 | https://www.legislation.gov.uk/ukpga/1971/38/schedule/2</ref>
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| *'''United States''': MDMA is classified as a Schedule I drug under the Controlled Substance Act. This means it is illegal to manufacture, buy, possess, process, or distribute without a license from the Drug Enforcement Administration (DEA).<ref>DEA / Drug Scheduling | https://www.dea.gov/druginfo/ds.shtml</ref>
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| *'''Czech Republic''': MDMA is a Schedule I controlled substance.<ref>https://www.zakonyprolidi.cz/cs/2013-463#f5150333</ref>
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| ==See also== | | ==See also== |
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| *[[Responsible use]] | | *[[Responsible use]] |
| *[[Entactogen]]
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| *[[Stimulant]]
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| *[[MDA]]
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| *[[Methylone]]
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| *[[4-FA]]
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| ==External links== | | ==External links== |
| | (List along order below) |
| | |
| | *[https://en.wikipedia.org/wiki/Nymphaea_nouchali_var._caerulea Blue Lotus (Wikipedia)] |
| | *[https://www.erowid.org/plants/lotus/ Blue Lotus (Erowid Vault)] |
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| *[http://en.wikipedia.org/wiki/MDMA MDMA (Wikipedia)]
| | ==Literature== |
| *[http://www.erowid.org/chemicals/mdma/mdma.shtml MDMA (Erowid Vault)]
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| *[https://isomerdesign.com/PiHKAL/read.php?domain=pk&id=109 MDMA (PiHKAL / Isomer Design)]
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| ===Harm reduction===
| | *APA formatted reference |
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| *[http://www.ecstasydata.org EcstasyData]
| | Please see the [[citation formatting guide]] if you need assistance properly formatting citations. |
| *[https://www.pillreports.net/ Pill Reports]
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| *[http://www.rollsafe.org/ RollSafe]
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| **[https://rollsafe.org/mdma-wiki/ MDMA Wiki] (archived)
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| ==References== | | ==References== |
| {{reflist|2}}
| | <references /> |
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| [[Category:Psychoactive substance]] | | [[Category:Psychoactive substance]] |
| [[Category:Depressant]]
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| [[Category:Stimulant]]
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| {{#set:Featured=true}}
| | <br /> |