MDEA

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Summary sheet: MDEA
MDEA
Molecular structure of 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, Methylenedioxyethylamphetamine, MDEA, MDE, and colloquially as Eve) is an obscure, synthetic entactogen of the substituted amphetamine class that produces modified MDMA-like entactogenic effects when administered. It is a closely related structural analog of MDMA and MDA[1] that acts via the same pharmacological mechanism as a serotonin, norepinephrine, and dopamine releasing agent and reuptake inhibitor.[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]

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]

Very little data exists about the pharmacological properties, metabolism, and toxicity of MDEA, and it has little history of human usage. 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 has been shown to act as a releasing agent and reuptake inhibitor of the key monoamine neurotransmitters serotonin, dopamine and noradrenaline[2] which are the neurotransmitters responsible for modulating focus, motivation, pleasure, and reward. This is done by inhibiting the reuptake and reabsorption of monoamine neurotransmitters after they have performed their function of transmitting a neural impulse, allowing them to accumulate in the synaptic cleft and be reused in a manner which causes physically stimulating, sedating, disinhibiting and euphoric effects.[7] The often-reported "stoning" effects have been theorized to arise from the higher relative activity MDEA has on releasing serotonin over dopamine compared to MDMA.

It has also been noted that MDEA, even at lower doses, 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.[8]

Subjective effects

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The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed 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 and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include 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 health concerns

Short-term physical health risks of MDEA consumption include dehydration, insomnia, hyperthermia,[9][10] and hyponatremia.[11] 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.

Long-term health concerns

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.[12] Other studies have suggested that the brain may recover from serotonergic damage.[13][14][15]

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.[16] 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.[17]

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 on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

Serotonin syndrome risk

Combinations in the list below may increase the amount of neurotransmitters such as serotonin and dopamine to dangerous or even fatal levels.

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.

Legality

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As such, it may contain incomplete or wrong information. You can help by expanding it.

  • Brazil - Possession, production and sale is illegal as it is listed on Portaria SVS/MS nº 344 as "MDE".[20]
  • United Kingdom: MDEA is a Class A drug.
  • United States: MDEA is a Schedule I drug.

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. New Insights into the Mechanism of Action of Amphetamines | http://www.annualreviews.org/doi/abs/10.1146/annurev.pharmtox.47.120505.105140
  8. Passie, Torsten, MD. Healing with Entactogens. Santa Cruz: Multidisciplinary Association for Psychedelic Studies, n.d. Print.
  9. Drug-induced hyperthermia | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2044.1993.tb07423.x/abstract;jsessionid=FC30A9B157A2BAFC81048D8595714565.f02t03
  10. 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
  11. Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population | http://jop.sagepub.com/content/20/3/400
  12. 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
  13. 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
  14. 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.
  15. 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
  16. Drug-induced Valvulopathy: An Update | tpx.sagepub.com/content/38/6/837.full
  17. Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805
  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