World Library  
Flag as Inappropriate
Email this Article


MDMA structure
3,4-methylenedioxy-methamphetamine 3d model
Systematic (IUPAC) name
Clinical data
Legal status
Routes Oral, sublingual, insufflation, inhalation (vaporization), injection,[3] rectal
Pharmacokinetic data
Metabolism Hepatic, CYP450 extensively involved, including CYP2D6
Onset of action Immediate
Half-life (R)-MDMA: 5.8 ± 2.2 hours[4]
(S)-MDMA: 3.6 ± 0.9 hours[4]
Excretion Renal
CAS number  YesY[]
ATC code None
IUPHAR ligand
ChemSpider  YesY
Synonyms 3,4-MDMA, Ecstasy, Molly
PDB ligand ID B41 (, )
Chemical data
Formula C11H15NO2 
Mol. mass 193.24 g/mol
Physical data
Boiling point 105 °C (221 °F) at 0.4 mmHg (experimental)

MDMA (contracted from 3,4-methylenedioxy-methamphetamine) is a psychoactive drug of the phenethylamine and amphetamine classes of drugs. It is consumed primarily for its euphoric and empathogenic effects. Pharmacologically, MDMA acts as a serotonin-dopamine-norepinephrine releasing agent and reuptake inhibitor. MDMA is neurotoxic and can cause symptoms of dependency due to its effects on the mesocorticolimbic projection.

MDMA has become widely known as "ecstasy" (shortened to "E", "X", or "XTC"), usually referring to its tablet street form, although this term may also include the presence of possible adulterants. The UK term "Mandy" and the US term "Molly" colloquially refer to MDMA in a crystalline powder form that is relatively free of adulterants.[5][6] "Molly" can sometimes also refer to the related drugs methylone, MDPV, mephedrone or any other of the pharmacological group of compounds commonly known as bath salts.[12]

Possession of MDMA is illegal in most countries. Some limited exceptions exist for scientific and medical research. For 2012, the UNODC estimated between 9.4 and 28.24 million people globally used MDMA at least once in the past year. This was broadly similar to the number of cocaine, amphetamine, and opioid users, but far fewer than the global number of cannabis users.[13] It is taken in a variety of contexts far removed from its roots in psychotherapeutic settings, and is commonly associated with dance parties (or "raves") and electronic dance music.[14]

Medical reviews have noted that MDMA has some limited therapeutic benefits in certain mental health disorders, but has potential adverse effects associated with its use.[15][16] More research is needed in order to determine if its usefulness in posttraumatic stress disorder (PTSD) treatment outweighs the risk of persistent neuropsychological harm to a patient.[15][16]


  • Uses 1
    • Medical 1.1
      • Research 1.1.1
    • Recreational 1.2
      • Recreational effects 1.2.1
      • Purity and adulterants 1.2.2
  • Adverse effects 2
    • Immediate effects 2.1
    • After-effects 2.2
  • Overdose 3
    • Chronic use and addiction 3.1
  • Interactions 4
  • Pharmacology 5
    • Pharmacodynamics 5.1
    • Pharmacokinetics 5.2
  • Physical and chemical properties 6
    • Detection of use 6.1
  • History, society, and culture 7
    • Harm assessment 7.1
    • Legal status 7.2
    • Cost and distribution 7.3
      • Europe 7.3.1
      • North America 7.3.2
      • Australia 7.3.3
  • References 8
  • External links 9


Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and legal services engaged in delphic analysis regarding 20 popular recreational drugs; ecstasy was ranked 16th in addictiveness, harmfulness, and social harm.[17]


MDMA currently has no accepted medical uses.[18][19]


A review of the safety and efficacy of MDMA as a treatment for various disorders, particularly PTSD, indicated that MDMA has therapeutic efficacy in some patients;[16] however, it emphasized that MDMA is not a safe medical treatment due to lasting neurotoxic and cognition impairing effects in humans.[16] The author noted that oxytocin and D-cycloserine are potentially safer co-drugs in PTSD treatment, albeit with limited evidence of efficacy.[16] This review and a second corroborating review by a different author both concluded that, because of MDMA's demonstrated potential to cause lasting harm in humans (e.g., serotonergic neurotoxicity and persistent memory impairment), "considerably more research must be performed" on its efficacy in PTSD treatment to determine if the potential treatment benefits outweigh its potential to cause long-term harm to a patient.[15][16]


MDMA is often considered the drug of choice within the rave culture and is also used at clubs, festivals and house parties.[20] In the rave environment, the sensory effects from the music and lighting setup including as lasers are often highly synergistic with the drug. The psychedelic amphetamine quality of MDMA offers multiple reasons for its appeals to users in the "rave" setting. Some users enjoy the feeling of mass communion from the inhibition-depressing effects of the drug, while others use it as party fuel because of the drug's stimulatory effects.[21]

MDMA is occasionally known for being taken in conjunction with psychedelic drugs, such as LSD or psilocybin mushrooms, or even common drugs such as cannabis. As this practice has become more prevalent,[22] most of the more common combinations have been given nicknames, such as “candy flipping” for MDMA combined with LSD, “hippie flipping” for MDMA with psilocybin mushrooms, or “kitty flipping” for MDMA with ketamine.[23] The term “flipping” may come from the subjective effects of using MDMA with a psychedelic in which the user may shift rapidly between a more lucid state and a more psychedelic state several times during their experiences. Many users use mentholated products while taking MDMA for its cooling sensation while experiencing the drug’s effects. Examples include menthol cigarettes, Vicks VapoRub, NyQuil,[24] and lozenges.

Recreational effects

In general, users begin reporting subjective effects within 30 to 60 minutes of consumption, hitting a peak at about 75 to 120 minutes which plateaus for about 3.5 hours.[25]

The desired short-term psychoactive effects of MDMA include:

  • Euphoria – a sense of general well-being and happiness[15][26]
  • Increased sociability and feelings of communication being easy or simple[15][26]
  • Entactogenic effects – increased empathy or feelings of closeness with others[15][26]
  • A sense of inner peace[26]
  • Mild hallucination (e.g., colors and sounds are enhanced and mild closed-eye visuals)[26]
  • Enhanced sensation, perception, or sexuality[15][26]

Purity and adulterants

The average tablet contains 60–70 mg (base equivalent) of MDMA, usually as the hydrochloride salt.[19] Powdered MDMA is typically 30–40% pure, due to bulking agents (e.g., lactose) and binding agents.[19] Tablets sold as ecstasy sometimes only contain 3,4-methylenedioxyamphetamine (MDA) instead of MDMA;[4][19] the proportion of seized ecstasy tablets with MDMA-like impurities has varied annually and by country.[19]

Ecstasy tablets
Ecstasy tablets which allegedly contain MDMA, but may contain adulterants
Impure MDMA

Adverse effects

MDMA use has been shown to produce brain lesions, a form of brain damage, in the serotonergic neural pathways of humans and other animals.[1][4] In addition, long-term exposure to MDMA in humans has been shown to produce marked neurotoxicity in serotonergic axon terminals.[20][26][27] Neurotoxic damage to axon terminals has been shown to persist for more than two years.[27] Brain temperature during MDMA use is positively correlated with MDMA-induced neurotoxicity in animals.[20] Adverse neuroplastic changes to brain microvasculature and white matter also seem to occur in humans using low doses of MDMA.[20] Reduced gray matter density in certain brain structures has also been noted in human MDMA users.[20] In addition, MDMA has immunosuppressive effects in the periphery, but pro-inflammatory effects in the central nervous system.[28] Babies of mothers who used MDMA during pregnancy exhibit impaired motor function at 4 months of age, which may reflect either a delay in development or a persistent neurological deficit.[16][29]

MDMA also produces persistent cognitive impairments in human users.[2][15][16] Impairments in multiple aspects of cognition, including memory, visual processing, and sleep have been noted in humans;[15][16] the magnitude of these impairments is correlated with lifetime ecstasy or MDMA usage.[2][15][16] Memory is significantly impacted by ecstasy use, which is associated with marked impairments in all forms of memory (e.g., long-term, short-term, working).[15][16]

The most serious short-term physical health risks of MDMA are hyperthermia and dehydration;[26][30] this is due to a life-threatening complication – hyponatremia (excessively low sodium concentration in the blood) – associated with drinking large quantities of water without replenishing electrolytes.[26][30][31]

Immediate effects

The immediate adverse effects of MDMA use can include:


The effects that last up to a week[15][33] following cessation of moderate MDMA use include:

  • Trismus[15]
  • Loss of appetite[33]
  • Insomnia[33]
  • Anxiety or paranoia[33]
  • Depression[15][33]
  • Irritability[33]
  • Impulsiveness[33]
  • Restlessness[33]
  • Memory impairment, some of which becomes permanent[15]
  • Anhedonia[33]


Overdose symptoms vary widely with MDMA; they include:


Chronic use and addiction

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction

This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methylphenidate, phenethylamine, and cocaine. Following presynaptic dopamine and glutamate co-release by such psychostimulants, postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP pathway and calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[37][38] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-fos gene with the help of corepressors.[38] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for one or two months, slowly accumulates following repeated exposure to stimulants through this process.[39][40] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[39][40]

Some studies indicate repeated recreational users of MDMA have increased rates of depression and anxiety, even after quitting the drug.[41][42][43] Other meta analyses have reported possibility of impairment of executive functioning.[44] MDMA has been shown to induce ΔFosB in the nucleus accumbens.[45] Since MDMA releases dopamine in the mesocorticolimbic projection, the mechanisms by which it induces ΔFosB in the nucleus accumbens are analogous to other psychostimulants.[45][46] Therefore, chronic use of MDMA at high doses can result in altered brain structure and drug addiction, which occur as a consequence of ΔFosB overexpression in the nucleus accumbens.[46]

Approximately 60% of MDMA users experience withdrawal symptoms, including, but not limited to: fatigue, loss of appetite, depression, and trouble concentrating.[4] Tolerance is expected to occur with consistent MDMA use.[4]


A number of drug interactions can occur between MDMA and other drugs, including serotonergic drugs.[4][47] MDMA also interacts with drugs which inhibit CYP450 enzymes, like ritonavir (Norvir), particularly CYP2D6 inhibitors.[4] Concurrent use of MDMA with another serotonergic drug can result in a life-threatening condition called serotonin syndrome.[4] Severe overdose resulting in death has also been reported in people who took MDMA in combination with certain monoamine oxidase inhibitors,[4] such as phenelzine (Nardil), tranylcypromine (Parnate), or moclobemide (Aurorix, Manerix).[48]



MDMA acts primarily as a presynaptic releasing agent of serotonin, norepinephrine, and dopamine, which arises from its activity at trace amine-associated receptor 1 (TAAR1) and vesicular monoamine transporter 2 (VMAT2).[4][49][50] MDMA is a monoamine transporter substrate (i.e., a substrate for DAT, NET, and SERT), so it enters monoamine neurons via these neuronal membrane transport proteins;[49] by acting as a monoamine transporter substrate, MDMA produces competitive reuptake inhibition at the neuronal membrane transporters (i.e., it competes with endogenous monoamines for reuptake).[49][51] MDMA inhibits both vesicular monoamine transporters (VMATs), the second of which (VMAT2) is highly expressed within monoamine neurons at vesicular membranes.[50] Once inside a monoamine neuron, MDMA acts as a VMAT2 inhibitor and a TAAR1 agonist.[49][50] Inhibition of VMAT2 by MDMA results in increased concentrations of the associated neurotransmitter (serotonin, norepinephrine, or dopamine) in the cytosol of a monoamine neuron.[50][52] Activation of TAAR1 by MDMA triggers protein kinase A and protein kinase C signaling events which then phosphorylates the associated monoamine transporters – DAT, NET, or SERT – of the neuron.[49] In turn, these phosphorylated monoamine transporters either reverse transport direction – i.e., move neurotransmitters from the cytosol to the synaptic cleft – or withdrawal into the neuron, respectively producing neurotransmitter efflux and noncompetitive reuptake inhibition at the neuronal membrane transporters.[49]

In summary, MDMA enters monoamine neurons by acting as a monoamine transporter substrate.[49] MDMA activity at VMAT2 moves neurotransmitters out from synaptic vesicles and into the cytosol;[50] MDMA activity at TAAR1 moves neurotransmitters out of the cytosol and into the synaptic cleft.[49]

MDMA also has weak agonist activity at postsynaptic serotonin receptors 5-HT1 and 5-HT2 receptors, and its more efficacious metabolite MDA likely augments this action.[53][54][55][56] A placebo-controlled study in 15 human volunteers found 100 mg MDMA increased blood levels of oxytocin, and the amount of oxytocin increase was correlated with the subjective prosocial effects of MDMA.[57](S)-MDMA is more effective in eliciting 5-HT, NE, and DA release, while (D)-MDMA is overall less effective, and more selective for 5-HT and NE release (having only a very faint efficacy on DA release).[58]

MDMA is a ligand at both sigma receptor subtypes, though its interactions at the receptors have not yet been elucidated.[59]


(R)/(–)-enantiomer of MDMA (top)
(S)/(+)-enantiomer of MDMA (bottom)

MDMA reaches maximal concentrations in the blood stream between 1.5 and 3 hr after ingestion.[60] It is then slowly metabolized and excreted, with levels of MDMA and its metabolites decreasing to half their peak concentration over the next several hours.[61]

Metabolites of MDMA that have been identified in humans include 3,4-methylenedioxyamphetamine (MDA), 4-hydroxy-3-methoxy-methamphetamine (HMMA), 4-hydroxy-3-methoxyamphetamine (HMA), 3,4-dihydroxyamphetamine (DHA) (also called alpha-methyldopamine (α-Me-DA)), 3,4-methylenedioxyphenylacetone (MDP2P), and 3,4-Methylenedioxy-N-hydroxyamphetamine (MDOH). The contributions of these metabolites to the psychoactive and toxic effects of MDMA are an area of active research. Sixty-five percent of MDMA is excreted unchanged in the urine (in addition, 7% is metabolized into MDA) during the 24 hours after ingestion.[62]

MDMA is known to be metabolized by two main metabolic pathways: (1) O-demethylenation followed by catechol-O-methyltransferase (COMT)-catalyzed methylation and/or glucuronide/sulfate conjugation; and (2) N-dealkylation, deamination, and oxidation to the corresponding benzoic acid derivatives conjugated with glycine. The metabolism may be primarily by cytochrome P450 (CYP450) enzymes (CYP2D6 (in humans, but CYP2D1 in mice), and CYP3A4) and COMT. Complex, nonlinear pharmacokinetics arise via autoinhibition of CYP2D6 and CYP2D8, resulting in zeroth order kinetics at higher doses. It is thought that this can result in sustained and higher concentrations of MDMA if the user takes consecutive doses of the drug.

MDMA and metabolites are primarily excreted as conjugates, such as sulfates and glucuronides.[63] MDMA is a chiral compound and has been almost exclusively administered as a racemate. However, the two enantiomers have been shown to exhibit different kinetics. The disposition of MDMA may also be stereoselective, with the S-enantiomer having a shorter elimination half-life and greater excretion than the R-enantiomer. Evidence suggests[64] that the area under the blood plasma concentration versus time curve (AUC) was two to four times higher for the (R)-enantiomer than the (S)-enantiomer after a 40 mg oral dose in human volunteers. Likewise, the plasma half-life of (R)-MDMA was significantly longer than that of the (S)-enantiomer (5.8 ± 2.2 hours vs 3.6 ± 0.9 hours).[4] However, because MDMA excretion and metabolism have nonlinear kinetics,[65] the half-lives would be higher at more typical doses (100 mg is sometimes considered a typical dose[60]).

Physical and chemical properties

A powdered salt of MDMA
Reactors used in synthesis
Reactors used to synthesize MDMA on an industrial scale in a chemical factory in Cikande, Indonesia

The free base of MDMA is a colorless oil that is insoluble in water.[19] The most common salt of MDMA is the hydrochloride salt;[19] pure MDMA hydrochloride is water soluble and appears as a white or off-white powder or crystal.[19] Safrole, a colorless or slightly yellow oily liquid that is extracted from the root-bark or the fruit of the sassafras tree, is the primary precursor for all manufacture of MDMA. There are numerous synthetic methods available in the literature to convert safrole into MDMA via different intermediates.[66][67][68][69] One common route is via the MDP2P (3,4-methylenedioxyphenyl-2-propanone, also known as piperonyl acetone) intermediate, which can be produced in at least two different ways. One method is to isomerize safrole to isosafrole in the presence of a strong base, and then oxidize isosafrole to MDP2P. Another method is to make use of the Wacker process to oxidize safrole directly to the MDP2P (3,4-methylenedioxy phenyl-2-propanone) intermediate. This can be done with a palladium catalyst. Once the MDP2P intermediate has been prepared, a reductive amination leads to racemic MDMA (an equal parts mixture of (R)-MDMA and (S)-MDMA). Another method for the synthesis of racemic MDMA is addition of hydrogen bromide to safrole and reaction of the adduct with methylamine. Safrole is not required for MDMA production, and other precursor chemicals are often used instead, for example piperonal.

Relatively small quantities of essential oil are required to make large amounts of MDMA. The essential oil of Ocotea cymbarum typically contains between 80 and 94% safrole. This would allow 500 ml of the oil, which retails at between $20 and $100, to be used to produce between 150 and 340 grams of MDMA.[70]

Detection of use

MDMA and MDA may be quantitated in blood, plasma or urine to monitor for use, confirm a diagnosis of poisoning or assist in the forensic investigation of a traffic or other criminal violation or a sudden death. Some drug abuse screening programs rely on hair, saliva, or sweat as specimens. Most commercial amphetamine immunoassay screening tests cross-react significantly with MDMA or its major metabolites, but chromatographic techniques can easily distinguish and separately measure each of these substances. The concentrations of MDA in the blood or urine of a person who has taken only MDMA are, in general, less than 10% those of the parent drug.[71][72][73]

History, society, and culture

MDMA was first synthesized in 1912 by Merck chemist Anton Köllisch. At the time, Merck was interested in developing substances that stopped abnormal bleeding. Merck wanted to avoid an existing patent held by Bayer for one such compound: hydrastinine. Köllisch developed a preparation of a hydrastinine analogue, methylhydrastinine, despite the wishes of his superiors, Walther Beckh and Otto Wolfes. MDMA was an intermediate compound in the synthesis of methylhydrastinine, and Merck was not interested in its properties at the time.[74] On 24 December 1912, Merck filed two patent applications that described the synthesis of MDMA[75] and its subsequent conversion to methylhydrastinine.[76]

Merck records indicate that its researchers returned to the compound sporadically. In 1927, Max Oberlin studied the pharmacology of MDMA and observed that its effects on blood sugar and smooth muscles were similar to ephedrine's. Researchers at Merck conducted experiments with MDMA in 1952 and 1959.[74] In 1953 and 1954, the United States Army commissioned a study of toxicity and behavioral effects in animals injected with mescaline and several analogues, including MDMA. These originally classified investigations were declassified and published in 1973.[77]

MDMA was being used recreationally in the United States by 1970.[78] In the mid-1970s, Alexander Shulgin, then at University of California, Berkeley, heard from students about unusual effects of MDMA. One such effect was that the drug had helped a student overcome their stutter. Intrigued, Shulgin synthesized MDMA and tried it himself in 1976.[79] Two years later, he and David E. Nichols published the first report on the drug's psychotropic effect in humans. They described it as an "altered state of consciousness with emotional and sensual overtones" that can be compared "to marijuana, and to psilocybin devoid of the hallucinatory component".[80]

Shulgin took to occasionally using MDMA for relaxation, referring to it as "my low-calorie martini", and giving the drug to his friends, researchers, and other people whom he thought could benefit from it. One such person was psychotherapist Leo Zeff, who had been known to use psychedelics in his practice. Zeff was so impressed with the effects of MDMA that he came out of his semi-retirement to proselytize for it. Over the following years, Zeff traveled around the U.S. and occasionally to Europe, training other psychotherapists in the use of MDMA.[79][81]

In the early 1980s, people started using MDMA in Ibiza’s discos.[82] Subsequently, the drug emerged in the other parts of Europe and the United States. In the U.S., MDMA rose to prominence as "Adam" in trendy nightclubs and gay dance clubs in the Dallas area.[83] From there, use spread to raves in major cities around the country, and then to mainstream society. "Ecstasy" was recognized as slang for MDMA as early as June 1982.[84] The drug was first proposed for scheduling by the Drug Enforcement Administration (DEA) in July 1984[85] and was classified as a Schedule I controlled substance in the U.S. on 31 May 1985 on an emergency basis.[86] No double blind studies had yet been conducted as to the efficacy of MDMA for psychotherapy.

In the late 1980s, MDMA began to be widely used in the UK and other parts of Europe, becoming an integral element of rave culture and other psychedelic-influenced music scenes. Spreading along with rave culture, illicit MDMA use became increasingly widespread among young adults in universities and later, in high schools. MDMA became one of the four most widely used illicit drugs in the U.S., along with cocaine, heroin, and cannabis.[87] According to some estimates as of 2004, only marijuana attracts more first time users in the U.S.[87]

After MDMA was criminalized, most medical use stopped, although some therapists continued to prescribe the drug illegally. Later, Charles Grob initiated an ascending-dose safety study in healthy volunteers. Subsequent legally-approved MDMA studies in humans have taken place in the U.S. in Detroit (Wayne State University), Chicago (University of Chicago), San Francisco (UCSF and California Pacific Medical Center), Baltimore (NIDANIH Intramural Program), and South Carolina, as well as in Switzerland (University Hospital of Psychiatry, Zürich), the Netherlands (Maastricht University), and Spain (Universitat Autònoma de Barcelona).[88]

In 2010, the BBC reported that use of MDMA had decreased in the UK in previous years. This may be due to increased seizures during use and decreased production of the precursor chemicals used to manufacture MDMA. Unwitting substitution with other drugs, such as mephedrone and methamphetamine,[89] as well as legal alternatives to MDMA, such as BZP, MDPV, and methylone, are also thought to have contributed to its decrease in popularity.[90]

Harm assessment

A UK study placed great weight on the risk for acute physical harm, the propensity for physical and psychological dependency on the drug, and the negative familial and societal impacts of the drug. They did not evaluate or rate the negative impact of 'ecstasy' on the cognitive health of ecstasy users, e.g., impaired memory and concentration. Based on these factors, the study placed MDMA at number 18 in the list of 20 harmful drugs.[91]

David Nutt, a former chairman of the UK Advisory Council on the Misuse of Drugs, stated in the Journal of Psychopharmacology in January 2009, that 'ecstasy' use compared favorably with horse riding in terms of risk, with the drug leading to around 30 deaths a year in the UK compared to about 10 from horse riding, and "acute harm to person" occurring in about one in 10,000 episodes of 'ecstasy' use compared to about one in 350 episodes of horse riding.[92] Dr. Nutt noted the lack of a balanced risk assessment in public discussions of MDMA.[92] A spokesperson for the ACMD said, "The recent article by Professor David Nutt published in the Journal of Psychopharmacology was done in respect of his academic work and not as chair of the ACMD."[93]

Legal status

MDMA is legally controlled in most of the world under the UN Convention on Psychotropic Substances and other international agreements, although exceptions exist for research and limited medical use. In general, the unlicensed use, sale or manufacture of MDMA are all criminal offences.

In Australia, MDMA was declared illegal in 1986 because of its harmful effects and potential for abuse. It is classed as a Schedule 9 Prohibited Substance in the country, meaning it is available for scientific research purposes only. Any other type of sale, use or manufacture is strictly prohibited by law. Permits for research uses on humans must be approved by a recognized ethics committee on human research.

In the United Kingdom, MDMA was made illegal in 1977 by a modification order to the existing Misuse of Drugs Act 1971. Although MDMA was not named explicitly in this legislation, the order extended the definition of Class A drugs to include various ring-substituted phenethylamines,[94] thereby making it illegal to sell, buy, or possess the drug without a licence. Penalties include a maximum of seven years and/or unlimited fine for possession; life and/or unlimited fine for production or trafficking.

In the United States, MDMA is currently placed in Schedule I of the Controlled Substances Act.[95] In a 2011 federal court hearing the American Civil Liberties Union successfully argued that the sentencing guideline for MDMA/ecstasy is based on outdated science, leading to excessive prison sentences.[96]

In the Netherlands, the Expert Committee on the List (Expertcommissie Lijstensystematiek Opiumwet) issued a report in June 2011 which discussed the evidence for harm and the legal status of MDMA, arguing in favor of maintaining it on List I.[97][98]

In Canada, MDMA is listed as a Schedule 1[99] as it is an analogue of amphetamine.[100] The CDSA was updated as a result of the Safe Streets Act changing amphetamines from Schedule 3 to Schedule 1 on March 2012.[101]

In 1985 the 1971 Convention on Psychotropic Substances, which is its current status.[102]

Cost and distribution


In 2008 the European Monitoring Centre for Drugs and Drug Addiction noted that although there were some reports of tablets being sold for as little as 1, most countries in Europe then reported typical retail prices in the range of €3 to €9 per tablet, typically containing 25–65 mg of MDMA.[103] By 2014 the EMCDDA reported that the range was more usually between €5 and €10 per tablet, typically containing 57–102 mg of MDMA, although MDMA in powder form was becoming more common.[104]

North America

The United Nations Office on Drugs and Crime claimed in its 2008 World Drug Report that typical U.S. retail prices are US$20 to $25 per tablet, or from $3 to $10 per tablet if bought in batches.[105] A new research area named Drug Intelligence aims to automatically monitor distribution networks based on image processing and machine learning techniques, in which an Ecstasy pill picture is analyzed to detect correlations among different production batches.[106] These novel techniques allow police scientists to facilitate the monitoring of illicit distribution networks.


MDMA is particularly expensive in Australia, costing A$15–A$30 per tablet. In terms of purity data for Australian MDMA, the average is around 34%, ranging from less than 1% to about 85%. The majority of tablets contain 70–85 mg of MDMA. Most MDMA enters Australia from the Netherlands, the UK, Asia, and the U.S.[107]


  1. ^ a b 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.  
  2. ^ a b c "3,4-METHYLENEDIOXYMETHAMPHETAMINE". Hazardous Substances Data Bank. National Library of Medicine. 28 August 2008. Retrieved 22 August 2014. /EPIDEMIOLOGY STUDIES/ /Investigators/ compared the prevalence of Diagnostic and Statistical Manual version IV (DSM-IV) mental disorders in 30 current and 29 former ecstasy users, 29 polydrug and 30 drug-naive controls. Groups were approximately matched by age, gender and level of education. The current ecstasy users reported a life-time dose of an average of 821 and the former ecstasy users of 768 ecstasy tablets. Ecstasy users did not significantly differ from controls in the prevalence of mental disorders, except those related to substance use. Substance-induced affective, anxiety and cognitive disorders occurred more frequently among ecstasy users than polydrug controls. The life-time prevalence of ecstasy dependence amounted to 73% in the ecstasy user groups. More than half of the former ecstasy users and nearly half of the current ecstasy users met the criteria of substance-induced cognitive disorders at the time of testing. Logistic regression analyses showed the estimated life-time doses of ecstasy to be predictive of cognitive disorders, both current and life-time. ... Cognitive disorders still present after over 5 months of ecstasy abstinence may well be functional consequences of serotonergic neurotoxicity of 3,4-methylenedioxymethamphetamine (MDMA) [Thomasius R et al; Addiction 100(9):1310-9 (2005)] **PEER REVIEWED** PubMed Abstract 
  3. ^ "Methylenedioxymethamphetamine (MDMA, ecstasy)". Drugs and Human Performance Fact Sheets.  
  4. ^ a b c d e f g h i j k l m "3,4-METHYLENEDIOXYMETHAMPHETAMINE". Hazardous Substances Data Bank. National Library of Medicine. 28 August 2008. Retrieved 22 August 2014. 
  5. ^ Luciano, Randy L.; Perazella, Mark A. (25 March 2014). "Nephrotoxic effects of designer drugs: synthetic is not better!". Nature Reviews Nephrology 10 (6): 314–324.  
  6. ^ "DrugFacts: MDMA (Ecstasy or Molly)". National Institute on Drug Abuse. Retrieved 2 December 2014. 
  7. ^
  8. ^
  9. ^
  10. ^
  11. ^
  12. ^ [7][8][9][10][11]
  13. ^ World Drug Report 2014. Vienna, Austria: United Nations Office on Drugs and Crime. June 2014. p. 2.  
  14. ^ World Health Organization (2004). Neuroscience of Psychoactive Substance Use and Dependence. World Health Organization. pp. 97–.  
  15. ^ a b c d e f g h i j k l m n o p q Meyer JS (2013). "3,4-methylenedioxymethamphetamine (MDMA): current perspectives". Subst Abuse Rehabil 4: 83–99.  
  16. ^ a b c d e f g h i j k Parrott AC (2014). "The potential dangers of using MDMA for psychotherapy". J Psychoactive Drugs 46 (1): 37–43.  
  17. ^  
  18. ^ Mohan J, ed. (June 2014). "World Drug Report 2014". United Nations Office on Drugs and Crime. pp. 3, 123–152. Retrieved 18 August 2014. 
  19. ^ a b c d e f g h "Methylenedioxymethamphetamine (MDMA or 'Ecstasy')". EMCDDA. European Monitoring Centre for Drugs and Drug Addiction. Retrieved 17 October 2014. 
  20. ^ a b c d e f g h i j k l m n Carvalho M, Carmo H, Costa VM, Capela JP, Pontes H, Remião F, Carvalho F, Bastos Mde L (August 2012). "Toxicity of amphetamines: an update". Arch. Toxicol. 86 (8): 1167–1231.  
  21. ^ Reynolds, Simon (1999). Generation Ecstasy: Into the World of Techno and Rave Culture. Routledge. p. 81.  
  22. ^ "Mixing". The Good Drugs Guide. Retrieved 17 October 2014. 
  23. ^ University of Maryland, College Park Center for Substance Abuse Research. "Ecstasy:CESAR". 
  24. ^ "Director's Report to the National Advisory Council on Drug Abuse". National Institute on Drug Abuse. May 2000. 
  25. ^ Liechti ME, Gamma A, Vollenweider FX (2001). "Gender Differences in the Subjective Effects of MDMA". Psychopharmacology 154 (2): 161–168.  
  26. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah Greene SL, Kerr F, Braitberg G (October 2008). "Review article: amphetamines and related drugs of abuse". Emerg. Med. Australas 20 (5): 391–402. PMID 18973636. doi:10.1111/j.1742-6723.2008.01114.x. Clinical manifestation ...
    hypertension, aortic dissection, arrhythmias, vasospasm, acute coronary syndrome, hypotension ... Agitation, paranoia, euphoria, hallucinations, bruxism, hyperreflexia, intracerebral haemorrhage ... pulmonary oedema/ARDS ... Hepatitis, nausea, vomiting, diarrhoea, gastrointestinal ischaemia ... Hyponatraemia (dilutional/SIADH), acidosis ... Muscle rigidity, rhabdomyolysis
    Desired effects
    [entactogen] – euphoria, inner peace, social facilitation, ‘heightens sexuality and expands consciousness’, mild hallucinogenic effects ...
    Clinical associations
    Bruxism, hyperthermia, ataxia, confusion, hyponatraemia (SIADH), hepatitis, muscular rigidity, rhabdomyolysis, DIC, renal failure, hypotension, serotonin syndrome, chronic mood/memory disturbances ... human data have shown that long-term exposure to MDMA is toxic to serotonergic neurones.75,76
  27. ^ a b Halpin LE, Collins SA, Yamamoto BK (February 2014). "Neurotoxicity of methamphetamine and 3,4-methylenedioxymethamphetamine". Life Sci. 97 (1): 37–44.  
  28. ^ Boyle NT, Connor TJ (September 2010). "Methylenedioxymethamphetamine ('Ecstasy')-induced immunosuppression: a cause for concern?" (PDF). British Journal of Pharmacology 161 (1): 17–32.  
  29. ^ Singer LT, Moore DG, Fulton S, Goodwin J, Turner JJ, Min MO, Parrott AC (2012). "Neurobehavioral outcomes of infants exposed to MDMA (Ecstasy) and other recreational drugs during pregnancy". Neurotoxicol Teratol 34 (3): 303–10.  
  30. ^ a b c d e f g Keane M (February 2014). "Recognising and managing acute hyponatraemia". Emerg Nurse 21 (9): 32–6; quiz 37.  
  31. ^ a b c d e f Michael White C (March 2014). "How MDMA's pharmacology and pharmacokinetics drive desired effects and harms". J Clin Pharmacol 54 (3): 245–52.  
  32. ^ Zemishlany, Z; Aizenberg, D; Weizman, A (March 2001). "Subjective effects of MDMA (‘Ecstasy’) on human sexual function". European Psychiatry 16 (2): 127–130.  
  33. ^ a b c d e f g h i "3,4-METHYLENEDIOXYMETHAMPHETAMINE". Hazardous Substances Data Bank. National Library of Medicine. 28 August 2008. Retrieved 22 August 2014. Over the course of a week following moderate use of the drug, many MDMA users report feeling a range of emotions, including anxiety, restlessness, irritability, and sadness that in some individuals can be as severe as true clinical depression. Similarly, elevated anxiety, impulsiveness, and aggression, as well as sleep disturbances, lack of appetite, and reduced interest in and pleasure from sex have been observed in regular MDMA users. 
  34. ^ a b c d e f John; Gunn, Scott; Singer, Mervyn; Webb, Andrew Kellum. Oxford American Handbook of Critical Care. Oxford University Press (2007). ASIN: B002BJ4V1C. Page 464.
  35. ^ de la Torre R, Farré M, Roset PN, Pizarro N, Abanades S, Segura M, Segura J, Camí J (2004). "Human pharmacology of MDMA: pharmacokinetics, metabolism, and disposition". Ther Drug Monit 26 (2): 137–144.  
  36. ^ Chummun H, Tilley V, Ibe J (2010). "3,4-methylenedioxyamfetamine (ecstasy) use reduces cognition". Br J Nurs 19 (2): 94–100.  
  37. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. 
  38. ^ a b Renthal W, Nestler EJ (2009). "Chromatin regulation in drug addiction and depression". Dialogues Clin. Neurosci. 11 (3): 257–268.  
  39. ^ a b
  40. ^ a b Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clin. Psychopharmacol. Neurosci. 10 (3): 136–143.  
  41. ^ Verheyden SL, Henry JA, Curran HV (2003). "Acute, sub-acute and long-term subjective consequences of 'ecstasy' (MDMA) consumption in 430 regular users". Hum Psychopharmacol 18 (7): 507–17.  
  42. ^ Verheyden SL, Maidment R, Curran HV (2003). "Quitting ecstasy: an investigation of why people stop taking the drug and their subsequent mental health". J. Psychopharmacol. (Oxford) 17 (4): 371–8.  
  43. ^ Laws KR, Kokkalis J (2007). "Ecstasy (MDMA) and memory function: a meta-analytic update". Human Psychopharmacology: Clinical and Experimental 22 (6): 381–88.  
  44. ^ Rodgers J, Buchanan T, Scholey AB, Heffernan TM, Ling J, Parrott AC (2003). "Patterns of drug use and the influence of gender on self-reports of memory ability in ecstasy users: a web-based study". J. Psychopharmacol. (Oxford) 17 (4): 389–96.  
  45. ^ a b Olausson P, Jentsch JD, Tronson N, Neve RL, Nestler EJ, Taylor JR (September 2006). "DeltaFosB in the nucleus accumbens regulates food-reinforced instrumental behavior and motivation". J. Neurosci. 26 (36): 9196–204.  
  46. ^ a b Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637.  
  47. ^ Silins E, Copeland J, Dillon P (2007). "Qualitative review of serotonin syndrome, ecstasy (MDMA) and the use of other serotonergic substances: Hierarchy of risk". Australian and New Zealand Journal of Psychiatry 41 (8): 649–655.  
  48. ^ Vuori E, Henry JA, Ojanperä I, Nieminen R, Savolainen T, Wahlsten P, Jäntti M (2003). "Death following ingestion of MDMA (ecstasy) and moclobemide". Addiction 98 (3): 365–8.  
  49. ^ a b c d e f g h Miller GM (January 2011). "The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity". J. Neurochem. 116 (2): 164–176.  
  50. ^ a b c d e 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: 86–98.  
  51. ^ Fitzgerald JL, Reid JJ (1990). "Effects of methylenedioxymethamphetamine on the release of monoamines from rat brain slices". European Journal of Pharmacology 191 (2): 217–20.  
  52. ^ Bogen IL, Haug KH, Myhre O, Fonnum F (2003). "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.  
  53. ^ Battaglia G, Brooks BP, Kulsakdinun C, De Souza EB (1988). "Pharmacologic profile of MDMA (3,4-methylenedioxymethamphetamine) at various brain recognition sites". European Journal of Pharmacology 149 (1–2): 159–63.  
  54. ^ 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.  
  55. ^ Nash JF, Roth BL, Brodkin JD, Nichols DE, Gudelsky GA (1994). "Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors". Neuroscience Letters 177 (1–2): 111–5.  
  56. ^ Setola V, Hufeisen SJ, Grande-Allen KJ, Vesely I, Glennon RA, Blough B, Rothman RB, Roth BL (2003). "3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro". Molecular Pharmacology 63 (6): 1223–9.  
  57. ^ Dumont GJ, Sweep FC, van der Steen R, Hermsen R, Donders AR, Touw DJ, van Gerven JM, Buitelaar JK, Verkes RJ (2009). "Increased oxytocin concentrations and prosocial feelings in humans after ecstasy (3,4-methylenedioxymethamphetamine) administration". Soc Neurosci 4 (4): 359–366.  
  58. ^ Baumann MH, Rothman RB (6 November 2009). "NEURAL AND CARDIAC TOXICITIES ASSOCIATED WITH 3,4-METHYLENEDIOXYMETHAMPHETAMINE (MDMA)". International Review of Neurobiology. International Review of Neurobiology 88 (1): 257–296.  
  59. ^ Matsumoto RR (July 2009). "Targeting sigma receptors: novel medication development for drug abuse and addiction". Expert Rev Clin Pharmacol 2 (4): 351–8.  
  60. ^ a b R. De La Torre, M. Farré, J. Ortuño, M. Mas, R. Brenneisen, P. N. Roset, et al. (February 2000). "Non-linear pharmacokinetics of MDMA ('ecstasy') in humans". Annals of the New York Academy of Sciences 49 (2): 104–109.  
  61. ^ R. DE LA TORRE, M. FARRÉ, P. N. ROSET, C. HERNÁNDEZ LÓPEZ, M. MAS, J. ORTUÑO, et al. (September 2000). "Pharmacology of MDMA in humans". Annals of the New York Academy of Sciences 914 (1): 225–237.  
  62. ^ Verebey K, Alrazi J, Jaffe JH (1988). "The complications of 'ecstasy' (MDMA)". JAMA 259 (11): 1649–1650.  
  63. ^ Shima N, Kamata H, Katagi M, Tsuchihashi H, Sakuma T, Nemoto N (2007). "Direct Determination of Glucuronide and Sulfate of 4-Hydroxy-3-methoxymethamphetamine, the Main Metabolite of MDMA, in Human Urine". J. Chromatogr. B Analyt. Technol. Biomed. Life Sci. 857 (1): 123–129.  
  64. ^ Fallon JK, Kicman AT, Henry JA, Milligan PJ, Cowan DA, Hutt AJ (1 July 1999). "Stereospecific Analysis and Enantiomeric Disposition of 3,4-Methylenedioxymethamphetamine (Ecstasy) in Humans". Clinical Chemistry 45 (7): 1058–1069.  
  65. ^ Mueller M, Peters FT, Maurer HH, McCann UD, Ricaurte GA (October 2008). "Nonlinear Pharmacokinetics of (±)3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy") and Its Major Metabolites in Squirrel Monkeys at Plasma Concentrations of MDMA That Develop After Typical Psychoactive Doses". JPET 327 (1): 38–44.  
  66. ^ Milhazes N, Martins P, Uriarte E, Garrido J, Calheiros R, Marques MP, Borges F (2007). "Electrochemical and spectroscopic characterisation of amphetamine-like drugs: application to the screening of 3,4-methylenedioxymethamphetamine (MDMA) and its synthetic precursors". Anal. Chim. Acta 596 (2): 231–41.  
  67. ^ Milhazes N, Cunha-Oliveira T, Martins P, Garrido J, Oliveira C, Rego AC, Borges F (2006). "Synthesis and cytotoxic profile of 3,4-methylenedioxymethamphetamine ("ecstasy") and its metabolites on undifferentiated PC12 cells: A putative structure-toxicity relationship". Chem. Res. Toxicol. 19 (10): 1294–304.  
  68. ^ Reductive aminations of carbonyl compounds with borohydride and borane reducing agents. Baxter, Ellen W.; Reitz, Allen B. Organic Reactions (Hoboken, New Jersey, United States) (2002), 59.
  69. ^ Gimeno P, Besacier F, Bottex M, Dujourdy L, Chaudron-Thozet H (2005). "A study of impurities in intermediates and 3,4-methylenedioxymethamphetamine (MDMA) samples produced via reductive amination routes". Forensic Sci. Int. 155 (2–3): 141–57.  
  70. ^ Nov 2005 DEA Microgram newsletter, p. 166. (11 November 2005). Retrieved on 12 August 2013.
  71. ^ Kolbrich EA, Goodwin RS, Gorelick DA, Hayes RJ, Stein EA, Huestis MA. Plasma pharmacokinetics of 3,4-methylenedioxymethamphetamine after controlled oral administration to young adults. Ther. Drug Monit. 30: 320–332, 2008.
  72. ^ Barnes AJ, De Martinis BS, Gorelick DA, Goodwin RS, Kolbrich EA, Huestis MA (2009). "Disposition of MDMA and metabolites in human sweat following controlled MDMA administration". Clinical chemistry 55 (3): 454–62.  
  73. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 9th edition, Biomedical Publications, Seal Beach, California, 2011, pp. 1078–1080.
  74. ^ a b Bernschneider-Reif S, Oxler F, Freudenmann RW (2006). "The origin of MDMA ('Ecstasy') – separating the facts from the myth". Pharmazie 61 (11): 966–972.  
  75. ^ Firma E. Merck in Darmstadt (16 May 1914). "German Patent 274350: Verfahren zur Darstellung von Alkyloxyaryl-, Dialkyloxyaryl- und Alkylendioxyarylaminopropanen bzw. deren am Stickstoff monoalkylierten Derivaten.". Kaiserliches Patentamt. Retrieved 12 April 2009. 
  76. ^ Firma E. Merck in Darmstadt (15 October 1914). "German Patent 279194: Verfahren zur Darstellung von Hydrastinin Derivaten.". Kaiserliches Patentamt. 
  77. ^ Hardman HF, Haavik CO, Seevers MH (1973). "Relationship of the Structure of Mescaline and Seven Analogs to Toxicity and Behavior in Five Species of Laboratory Animals". Toxicology Applied Pharmacology 25 (2): 299–309.  
  78. ^ The first confirmed sample was seized and identified by Chicago Police in 1970, seeSreenivasan VR (1972). "Problems in Identification of Methylenedioxy and Methoxy Amphetamines". Journal of Criminal Law, Criminology & Police Science (The Journal of Criminal Law, Criminology, and Police Science, Vol. 63, No. 2) 63 (2): 304–312.  
  79. ^ a b Ann Shulgin; Alexander Shulgin (1991). PiHKAL: A Chemical Love Story. Part I. Chapter 12. Transform Press.  
  80. ^ Shulgin AT; Nichols DE (1978). "Characterization of Three New Psychotomimetics". In Willette, Robert E.; Stillman, Richard Joseph. The Psychopharmacology of Hallucinogens.. New York: Pergamon Press. pp. 74–83.  
  81. ^ Bennett, Drake (30 January 2005). "Dr. Ecstasy.". New York Times Magazine. 
  82. ^ McKinley, Jr., James C. (12 September 2013). "Overdoses of ‘Molly’ Led to Electric Zoo Deaths". The New York Times. Retrieved 9 December 2013. 
  83. ^ ''The Austin Chronicle'' – "Countdown to Ecstasy." by Marc Savlov. Retrieved on 11 June 2011.
  84. ^ Idol, Billy. Billy Idol. Track 9, "It's So Cruel"
  85. ^ "Pharmaceutical Company Unravels Drug's Chequered Past". 2005. 
  86. ^ Erowid MDMA Vault: Info No. 3 on Scheduling. Retrieved on 11 June 2011.
  87. ^ a b ''Primetime'' with Peter Jennings. Retrieved on 11 June 2011.
  88. ^ Bibliography of Psychedelic Research Studies. collected by the Multidisciplinary Association for Psychedelic Studies
  89. ^ "Mephedrone (4-Methylmethcathinone) appearing in "Ecstasy" in the Netherlands". 19 September 2010. Retrieved 31 December 2012. 
  90. ^ "Why ecstasy is 'vanishing' from UK nightclubs". BBC News. 19 January 2010. Retrieved 14 February 2010. 
  91. ^ Scientists want new drug rankings, BBC News (23 March 2007).
  92. ^ a b Nutt DJ (2009). "Equasy-- an overlooked addiction with implications for the current debate on drug harms". J Psychopharmacol 23 (1): 3–5.  
  93. ^ Ecstasy 'not worse than riding', BBC News, 7 February 2009
  94. ^ Misuse of Drugs Act 1971. (5 January 1998). Retrieved on 11 June 2011.
  95. ^ Schedules of Controlled Substances; Scheduling of 3,4-Methylenedioxymethamphetamine (MDMA) Into Schedule I of the Controlled Substances Act; Remand, 53 Fed. Reg. 5,156 (DEA 22 February 1988).
  96. ^ Court Rejects Harsh Federal Drug Sentencing Guideline as Scientifically Unjustified | American Civil Liberties Union. (15 July 2011). Retrieved on 29 August 2012.
  97. ^ Rapport Drugs in Lijsten | Rapport. (27 June 2011). Retrieved on 29 August 2012.
  98. ^ "Committee: the current system of the Opium Act does not have to be changed". 24 June 2011. Retrieved 29 August 2012. As regards MDMA, better known as XTC, the committee concludes that investigations show that damage to the health of the individual in the long term is less serious than was initially assumed. But the extent of the illegal production and involvement of organised crime leads to damage to society, including damage to the image of the Netherlands abroad. This argues in favour of maintaining MDMA on List I. 
  99. ^ "Schedule I". Controlled Drugs and Substances Act. Isomer Design. Retrieved 9 December 2013. 
  100. ^ "Definitions and interpretations". Controlled Drugs and Substances Act. Isomer Design. Retrieved 9 December 2013. 
  101. ^ "Backgrounder: The Safe Streets and Communities Act Four Components Coming Into Force". Canadian Department of Justice. Retrieved 9 December 2013. 
  102. ^ 22nd report of the Expert Committee on Drug Dependence World Health Organization, 1985. (PDF) . Retrieved on 29 August 2012.
  103. ^ European Monitoring Centre for Drugs and Drug Addiction (2008). Annual report: the state of the drugs problem in Europe (PDF). Luxembourg: Office for Official Publications of the European Communities. p. 49.  
  104. ^ European Drug Report 2014, page 26
  105. ^ United Nations Office on Drugs and Crime (2008). World drug report (PDF). United Nations Publications. p. 271.  
  106. ^ Camargo J, Esseiva P, González F, Wist J, Patiny L (30 November 2012). "Monitoring of illicit pill distribution networks using an image collection exploration framework". Forensic Science International 223 (1): 298–305.  
  107. ^ Drugtext – 10 years of ecstasy and other party drug use in Australia: What have we done and what is there left to do?. Retrieved on 11 June 2011.

External links

  • MDMA Facts and Statistics
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.