MDEA

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Summary sheet: MDEA
MDEA
MDEA.svg
Chemical Nomenclature
Common names MDEA, MDE, Eve
Substitutive name 3,4-methylenedioxy-N-ethylamphetamine
Systematic name (RS)-1-(benzo[d][1,3]dioxol-5-yl)-N-ethylpropan-2-amine
Class Membership
Psychoactive class Entactogen
Chemical class Amphetamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.



Oral
Dosage
Threshold 50 - 70 mg
Light 70 - 120 mg
Common 120 - 180 mg
Strong 180 - 225 mg
Heavy 225 mg +
Duration
Total 3 - 5 hours
Onset 20 - 60 minutes
Come up 15 - 30 minutes
Peak 1.5 - 2 hours
Offset 1 - 2 hours
After effects 12 - 48 hours









DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

3,4-Methylenedioxy-N-ethylamphetamine (also known as MDEA, MDE, and colloquially as Eve) is a lesser-known entactogen substance of the amphetamine class. MDEA is chemically similar to MDMA and MDA.[1] It produces its effects by increasing levels of serotonin, norepinephrine, and dopamine in the brain.[2]

The first recorded human use of MDEA was in 1976 by Alexander Shulgin, who noted its similarity to MDMA in both effects and potency, though faster to act and shorter in duration.[3] The synthesis and pharmacological evaluation of MDEA and a series of related compounds were published in 1980.[4] MDEA is included in Shulgin's 1991 book "PiHKAL" ("Phenethylamines I Have Known and Loved").[1]

In the United States, MDEA was introduced recreationally in 1985 as a legal substitute to the newly banned MDMA before it was made a Schedule I substance two years later.[5] Since then, MDEA has rarely been sold on its own and has largely been used as an occasional additive or substitute ingredient in pills of "Ecstasy".[2]

Very little data exists about the pharmacological properties, metabolism, and toxicity of MDEA,. As a result it is highly advised to approach this potentially habit-forming entactogenic substance with the proper amount of precaution and harm reduction practices if choosing to use it.

History and culture

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In the United States, MDEA was introduced recreationally in 1985 as a legal substitute to the newly banned MDMA before it was made a Schedule I substance two years later on August 13, 1987 under the Federal Analogue Act.[6] Since then, MDEA has rarely been sold on its own and has largely been used as an occasional additive or substitute ingredient in pills of "Ecstasy" (for instance, studies conducted in the 1990s found MDEA present in approximately four percent of ecstasy tablets).[2]

While MDEA shares many of the core entactogenic properties of MDMA, it is slightly less potent and considered to be more "stoning", lacking the pro-socializing and energizing "magic" most party-goers seek in their MDMA experiences. As a result, it is largely considered by most people to be a less desirable variant of MDMA and is thus rarely produced and sold in the illicit drug market, typically showing up only in small batches synthesized and distributed by hobbyist clandestine chemists.[citation needed]

Chemistry

Generic structure of a phenethylamine molecule

MDEA, also known as 3,4-Methylenedioxy-N-ethylamphetamine, is a synthetic molecule of the substituted amphetamine chemical class. Molecules of the amphetamine class contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα. Additionally, MDEA contains an ethyl substitution on RN, which is a single carbon extension of the methyl group present in MDMA. MDEA also contains substitutions at R3 and R4 of the phenyl ring with oxygen groups that are incorporated into a methylenedioxy ring through a methylene bridge. MDEA shares this methylenedioxy ring with other entactogens like MDMA, MDA and MDAI.

Pharmacology

MDEA acts as a releasing agent and reuptake inhibitor of the monoamine neurotransmitters serotonin, dopamine and noradrenaline[2]. These neurotransmitters are responsible for modulating focus, motivation, pleasure, and reward.

The "stoning" effects of MDEA are thought to arise from the higher relative activity MDEA has on releasing serotonin over dopamine compared to MDMA.

MDEA stimulates the release of oxytocin and prolactin, two hormones that are currently being studied for their potential roles in modulating the feeling of trust and love.[7]

Subjective effects

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This subjective effects section is a stub.

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The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects
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Visual effects
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Cognitive effects
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Transpersonal effects
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After effects
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Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Short-term physical health risks of MDEA consumption include dehydration, insomnia, hyperthermia,[8][9] and hyponatremia.[10] Continuous activity without sufficient rest or rehydration may cause body temperature to rise to dangerous levels, and loss of fluid via excessive perspiration puts the body at further risk as the stimulatory and euphoric qualities of the drug may render the user oblivious to their energy expenditure for quite some time. Diuretics such as alcohol may exacerbate these risks further.

The exact toxic dosage is unknown, but considered to be far greater than its active dose.

Neurotoxicity

As with MDMA, the neurotoxicity of MDEA use has long been the subject of 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 MDEA is likely to be neurotoxic and cardiotoxic in some form.

Like other powerful serotonin releasing agents, MDEA is thought to cause 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, which likely applies to MDEA as well.[11] Other studies have suggested that the brain may recover from serotonergic damage.[12][13][14]

Cardiotoxicity

Like with MDMA, the long-term heavy use of MDEA is likely similarly cardiotoxic, leading to valvulopathy through its actions on the 5-HT2B receptor.[15] In one study, 28% of long-term MDMA 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.[16]

It is strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

As with other stimulants, the chronic use of MDEA can be considered 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 a person suddenly stops their usage.

Tolerance to many of the effects of MDEA develops with prolonged and repeated use. This results in users having to administer increasingly larger doses to achieve the same effects. After that, it takes about 1-1.5 months for the tolerance to be reduced to half and 2-3 months to be back at baseline (in the absence of further consumption). MDEA presents cross-tolerance with all dopaminergic and serotonergic stimulants and entactogens, meaning that after the consumption of MDEA all of these will have a reduced effect.

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The following lists some known dangerous combinations, but may not include all of them. A combination that appears to be safe in low doses can still increase the risk of injury or death. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume.

  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other amphetamines.
  • Cocaine - This combination may increase strain on the heart.
  • Stimulants - MDEA can be potentially dangerous in combination with other stimulants as it can increase one's heart rate and blood pressure to dangerous levels.
  • 25x-NBOMe & 25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be strictly avoided due to DXM's effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Tramadol lowers the seizure threshold.[17] Combinations with stimulants may further increase this risk.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, 2C-T-2, 2C-T-7, αMT, and some antidepressants.[18]
  • Stimulants - The neurotoxic effects of MDEA may be increased when combined with other stimulants.
  • Cocaine - This combination may increase strain on the heart.

Serotonin syndrome risk

Combinations with the following substances can cause dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

There is an increased risk of serotonin syndrome when MDEA is taken with many antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). Additionally, if MDEA is taken with SSRIs and SNRIs, the MDEA will be significantly less powerful or may have no distinguishable effects at all.

Legal status

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  • Austria: MDEA is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Brazil: MDEA is illegal to possess, produce or sell as it is listed on Portaria SVS/MS nº 344 as "MDE".[20]
  • United Kingdom: MDEA is a Class A drug.[citation needed]
  • United States: MDEA is a Schedule I drug.[citation needed]

See also

External links

Literature

References

  1. 1.0 1.1 "Read #22 2C-C | PiHKAL · info". isomerdesign.com (in English). 
  2. 2.0 2.1 2.2 2.3 Freudenmann RW, Spitzer M (2004). "The Neuropsychopharmacology and Toxicology of 3,4-methylenedioxy-N-ethyl-amphetamine (MDEA)". CNS Drug Reviews. 10 (2): 89–116. https://doi.org10.1111/j.1527-3458.2004.tb00007.x. PMID 15179441.
  3. Shulgin, Alexander. "Pharmacology Lab Notes #2". Lafayette, CA. (1976-1980). p206 (Erowid.org) | https://erowid.org/library/books_online/shulgin_labbooks/shulgin_labbook2_searchable.pdf
  4. Braun U, Shulgin AT, Braun G. "Centrally active N-substituted analogs of 3,4-methylenedioxyphenylisopropylamine (3,4-methylenedioxyamphetamine)." J Pharm Sci. 1980 Feb;69(2):192-5. | https://www.ncbi.nlm.nih.gov/pubmed/6102141
  5. PiHKAL|http://isomerdesign.com/PiHKAL/read.php?domain=pk&id=106
  6. PiHKAL|http://isomerdesign.com/PiHKAL/read.php?domain=pk&id=106
  7. Passie, Torsten, MD. Healing with Entactogens. Santa Cruz: Multidisciplinary Association for Psychedelic Studies, n.d. Print.
  8. Drug-induced hyperthermia | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2044.1993.tb07423.x/abstract;jsessionid=FC30A9B157A2BAFC81048D8595714565.f02t03
  9. Small changes in ambient temperature cause large changes in 3,4-methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/9634574
  10. Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population | http://jop.sagepub.com/content/20/3/400
  11. Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDEA, "ecstasy") (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/7643196
  12. In vivo detection of short- and long-term MDEA neurotoxicity--a positron emission tomography study in the living baboon brain (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/9593108
  13. Reneman L, Lavalaye J, Schmand B, de Wolff FA, van den Brink W, den Heeten GJ, Booij J (2001). "Cortical serotonin transporter density and verbal memory in individuals who stopped using 3,4-methylenedioxymethamphetamine (MDEA or "ecstasy"): preliminary findings". Arch. Gen. Psychiatry 58 (10): 901–6.
  14. Selvaraj, S. et al (2009) "Brain Serotonin transporter binding in former users of MDEA ("ecstasy")." British Journal of Psychiatry. 194: 355-359. | https://www.ncbi.nlm.nih.gov/pubmed/19336788
  15. Drug-induced Valvulopathy: An Update | tpx.sagepub.com/content/38/6/837.full
  16. Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805
  17. Talaie, H., Panahandeh, R., Fayaznouri, M. R., Asadi, Z., & Abdollahi, M. (2009). Dose-independent occurrence of seizure with tramadol. Journal of Medical Toxicology, 5(2), 63-67. https://doi.org/10.1007/BF03161089
  18. 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
  19. 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
  20. http://portal.anvisa.gov.br/documents/10181/3115436/%281%29RDC_130_2016_.pdf/fc7ea407-3ff5-4fc1-bcfe-2f37504d28b7