Summary sheet: MDA
MDA
MDA.svg
Chemical Nomenclature
Common names MDA, Sass, Sally, Tenamfetamine
Substitutive name 3,4-Methylenedioxyamphetamine
Systematic name (R) 1-(benzo[1,3]dioxol-5-yl)propan-2-amine
Class Membership
Psychoactive class Entactogen / Stimulant / Psychedelic
Chemical class Amphetamine / MDxx
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 20 mg
Light 40 - 60 mg
Common 60 - 100 mg
Strong 100 - 145 mg
Heavy 145 mg +
Duration
Total 5 - 8 hours
Onset 30 - 90 minutes
Come up 15 - 45 minutes
Peak 2.5 - 4 hours
Offset 2 - 3 hours
After effects 4 - 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.

Interactions
Alcohol
MXE
Dissociatives
DXM
MDMA
Stimulants
25x-NBOMe
25x-NBOH
Tramadol
SNRIs
MAOIs
Serotonin releasers
SSRIs
5-HTP


3,4-Methylenedioxyamphetamine (also known as MDA, and Tenamfetamine, or colloquially as "Sally", "Sass", or "Sass-a-frass") is a synthetic entactogen of the amphetamine chemical class. It produces long-lived entactogenic, stimulant and mild psychedelic effects that include stimulation, anxiety suppression, enhanced feelings of empathy, affection, and sociability, and euphoria when administered.

MDA was first synthesized in 1910 but its psychoactive effects were not discovered until in 1930. It was used in animal and human trials between 1939 and 1941 and from 1949 to 1957. More than 500 human subjects were given MDA in an investigation of its potential use as either an antidepressant or anorectic.[1] By 1958, it was successfully patented as a cough suppressant and ataractic. By 1961 it was patented as an anorectic under the trade name "Amphedoxamine".[citation needed]

Contemporary reports suggest that MDA emerged as a recreational drug towards the end of 1967, meaning its use predates its more widely used relative MDMA (Ecstasy).[2]

As with MDMA, MDA is thought to act primarily as a serotonin-norepinephrine-dopamine reuptake inhibitor and releasing agent.[citation needed] However, MDA is significantly more potent by weight and subjective intensity relative to MDMA. It also has a notably longer duration (six to eight hours instead of three to five) and produces more traditional serotonergic psychedelic effects (such as visual distortions) along with appreciably higher activity on dopamine, which is also believed to be responsible for the greater degree of neurotoxicity it produces.[3]

Today, possession of MDA is illegal in most countries, although some limited exceptions exist for scientific and medical research.

History and culture

MDA was originally synthesized by G. Mannish and W. Jacobson in 1910.[1] However, its psychoactive effects were not discovered until the self-experiments of Gordon Alles in July 1930. Alles would later license the drug to Smith, Kline & French. The first animal tests occurred in 1939, followed by human trials in 1941 that explored it as a possible therapy for Parkinson's disease. From 1949 to 1957, more than 500 human subjects were given MDA in an investigation of its potential use as an antidepressant and anorectic by Smith, Kline & French.[citation needed]

The United States Army also experimented with the drug, code-named EA-1298, while working to develop a truth drug or incapacitating agent. A man named Harold Blauer died in January 1953 after being intravenously injected with 450 mg of the drug.[4]

MDA was eventually patented as a cough suppressant by H. D. Brown in 1958, as an ataractic by Smith, Kline & French in 1960, and as an anorectic under the trade name "Amphedoxamine" in 1961. MDA began to appear on the recreational drug scene around 1967. In early 1968, the Bureau of Drug Abuse Control reported the seizure of over 1.4 kilograms of MDA and 11 kilograms of precursors from a clandestine laboratory in New York[5].

In 1992, a huge batch of pills known as "Snowballs" came into mass circulation in Europe, that unexpectedly contained MDA instead of MDMA. The batch unleashed a wave of extraordinary hallucinations across the UK and Europe that year, since the chemists had inaccurately dosed the pills with almost 200 mg of the active substance, which is generally enjoyed at lower amounts.[6]

Several researchers, including Claudio Naranjo and Richard Yensen, have explored utilizing MDA in the field of psychotherapy.[7][8] In 2010, Matthew Baggott and colleagues studied the ability of MDA to invoke mystical experiences and alter vision in healthy volunteers.[9]

Chemistry

MDA, also known as 3,4-methylenedioxyamphetamine, is a synthetic molecule of the amphetamine family. 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. MDA also contains substitutions at R3 and R4 of the phenyl ring with oxygen groups. These oxygen groups are incorporated into a methylenedioxy ring through a methylene chain. MDA shares this methylenedioxy ring with MDMA, MDAI and more obscure variants like MDEA or MMDA.

Pharmacology

Further information: Serotonergic psychedelic

MDA acts as a releasing agent and reuptake inhibitor of the neurotransmitters known as serotonin, dopamine and norepinephrine.[10][11] It also functions as a 5-HT2A,[12] 5-HT2B,[13] and 5-HT2C[14] receptor agonist and shows affinity for the TAAR1, α2A-, α2B-, α2C-adrenergic receptors and 5-HT1A and 5-HT7 receptors.[15]

The effect on serotonin may explain the similar euphoric and empathogenic effects of the two compounds MDMA and MDA. However, MDA has a higher efficacy in stimulating the 5-HT2A receptor than MDMA; thus MDA tends to cause more psychedelic-like effects, such as visual geometry and hallucinations. While MDMA can also produce psychedelic-like visual effects, these are less pronounced than those of MDA or require a heavier dose to become apparent. It is worth noting that the role of these interactions and how they result in the psychedelic experience continues to remain elusive.

Subjective effects

While MDA is similar to MDMA, users report that MDA has more stimulant and psychedelic qualities and less intense entactogenic effects than MDMA. MDA is also considered to be less predictable than MDMA, with effects varying greatly from person to person.

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects
 

Visual effects
 

Cognitive effects
 

Transpersonal effects
 

After effects
 

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Toxicity and harm potential

Anecdotal evidence from people within the Psychonaut community who have tried MDA suggests that there are no negative health effects attributed to simply trying the drug by itself at low to moderate doses and using it very sparingly (but nothing can be completely guaranteed). Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

Harold Blauer[17] died in January 1953 after being intravenously injected with 450 mg of MDA.

MDA is also known to be more neurotoxic when compared to substances such as MDMA or MDE.[18]

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 MDA 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 the psychedelic effects of MDA is built almost immediately after ingestion. However, tolerance to the stimulant and entactogenic effects are built up after repeated and heavy usage in a manner that varies between individuals. After that, it takes about 3 days for the tolerance to be reduced to half and 7 days to be back at baseline (in the absence of further consumption). MDA presents cross-tolerance with all psychedelics and most stimulants, meaning that after the consumption of MDA all psychedelics and some stimulants will have a reduced effect.

Dangerous interactions

  • 25x-NBOMe & 25x-NBOH - 25x compounds are highly stimulating and physically straining. Combinations with MDA should be strictly avoided due to the risk of excessive stimulation and heart strain. This can result in increased blood pressure, vasoconstriction, panic attacks, thought loops, seizures, and heart failure in extreme cases.
  • Alcohol - Combining alcohol with stimulants can be dangerous due to the risk of accidental over-intoxication. Stimulants mask alcohol's depressant effects, which is what most people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects will be left unopposed, which can result in blackouts and severe respiratory depression. If mixing, the user should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be avoided due to its inhibiting effects on serotonin and norepinephrine reuptake. There is an increased risk of panic attacks and hypertensive crisis, or serotonin syndrome with serotonin releasers (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
  • MDMA - Any neurotoxic effects of MDMA are likely to be increased when other stimulants are present. There is also a risk of excessive blood pressure and heart strain (cardiotoxicity).
  • MXE - Some reports suggest combinations with MXE may dangerously increase blood pressure and increase the risk of mania and psychosis.
  • Dissociatives - Both classes carry a risk of delusions, mania and psychosis, and these risk may be multiplied when combined.
  • Stimulants - MDA may be dangerous to combine with other stimulants like cocaine as they can increase one's heart rate and blood pressure to dangerous levels.
  • Tramadol - Tramadol is known to lower the seizure threshold[19] and combinations with stimulants may further increase this risk.
  • Cocaine - This combination may increase strain on the heart.
  • Amphetamine - This combination may cause suicidal mania, paranoia, and hallucinations five days after cessation of long term amphetamine usage. This is caused by neural network disequilibrium likely related to the lack of calcium channel action by MDA.

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.

Legal status

Internationally, MDA is part of the the Convention on Psychotropic Substances of 1971 as a Schedule I substance.[21]

  • Australia: MDA is a controlled substance.[22]
  • Austria: MDA is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Canada: MDA is listed on the CSDA in Schedule I.[23]
  • Germany: MDA is controlled under Anlage I BtMG (Narcotics Act, Schedule I) as of September 1, 1984.[24][25] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[26]
  • Russia: MDA is classed as a Schedule I prohibited substance.[27]
  • Switzerland: MDA is a controlled substance specifically named under Verzeichnis D.[28]
  • The Netherlands: MDA is illegal to possess, produce and sell in the Netherlands[29]
  • United Kingdom: MDA is a class A drug.[citation needed]
  • United States: MDA is a Schedule I drug.[30]

See also

External links

Literature

  • Green, A.J., Mechan, A.O., Elliott, J.M., O'shea, E., & Colado, M.I. (2003). The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacological Reviews, 55 3, 463-508. https://doi.org/10.1124/pr.55.3.3

References

  1. 1.0 1.1 Mannich, C., Jacobsohn, W., Mannich, C. (January 1910). "Über Oxyphenyl‐alkylamine und Dioxyphenyl‐alkylamine". Berichte der deutschen chemischen Gesellschaft. 43 (1): 189–197. doi:10.1002/cber.19100430126. ISSN 0365-9496. 
  2. Schoenfeld, Eugene. "Hippocrates". Berkeley Barb November 24-30, 1967: 7 (Independent Voices) | http://voices.revealdigital.com/cgi-bin/independentvoices?a=d&d=BFBJFGD19671124.1.7
  3. [1]
  4. $700,000 Awarded to Estate of Army Drug Test Victim, 1987 
  5. "Methylenedioxy Amphetamine (MDA)." Microgram. Bureau of Drug Abuse Control. Feb 1968. 1(5):4-5 (Erowid.org) | https://erowid.org/library/periodicals/microgram/microgram_1968_02_v01n05.pdf
  6. Power, Mike (2 May 2013). Drugs 2.0: The Web Revolution That's Changing How the World Gets High. Portobello Books Ltd. ISBN 9781846274596. 
  7. Naranjo, C., Shulgin, A. T., Sargent, T. (1967). "Evaluation of 3,4-Methylenedioxyamphetamine (MDA) as an Adjunct to Psychotherapy". Pharmacology. 17 (4): 359–364. doi:10.1159/000137100. ISSN 0031-7012. 
  8. Yensen, R., Di Leo, F. B., Rhead, J. C., Richards, W. A., Soskin, R. A., Turek, B., Kurland, A. A. (October 1976). "MDA-assisted psychotherapy with neurotic outpatients: a pilot study". The Journal of Nervous and Mental Disease. 163 (4): 233–245. doi:10.1097/00005053-197610000-00002. ISSN 0022-3018. }}
  9. Baggott, M. J., Siegrist, J. D., Galloway, G. P., Robertson, L. C., Coyle, J. R., Mendelson, J. E. (2 December 2010). "Investigating the Mechanisms of Hallucinogen-Induced Visions Using 3,4-Methylenedioxyamphetamine (MDA): A Randomized Controlled Trial in Humans". PLOS ONE. 5 (12): e14074. doi:10.1371/journal.pone.0014074. ISSN 1932-6203. 
  10. Lewin, A. H., Miller, G. M., Gilmour, B. (1 December 2011). "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Bioorganic & Medicinal Chemistry. 19 (23): 7044–7048. doi:10.1016/j.bmc.2011.10.007. ISSN 1464-3391. 
  11. Wallach, J. V. (January 2009). "Endogenous hallucinogens as ligands of the trace amine receptors: a possible role in sensory perception". Medical Hypotheses. 72 (1): 91–94. doi:10.1016/j.mehy.2008.07.052. ISSN 0306-9877. 
  12. Giovanni, G. D., Matteo, V. D., Esposito, E. (11 November 2008). Serotonin-Dopamine Interaction: Experimental Evidence and Therapeutic Relevance. Elsevier. ISBN 9780444532350. 
  13. Rothman, R. B., Baumann, M. H. (May 2009). "Serotonergic drugs and valvular heart disease". Expert Opinion on Drug Safety. 8 (3): 317–329. doi:10.1517/14740330902931524. ISSN 1744-764X. 
  14. Nash, J. F., Roth, B. L., Brodkin, J. D., Nichols, D. E., Gudelsky, G. A. (15 August 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): 111–115. doi:10.1016/0304-3940(94)90057-4. ISSN 0304-3940. 
  15. Ray, T. S. (2 February 2010). "Psychedelics and the human receptorome". PloS One. 5 (2): e9019. doi:10.1371/journal.pone.0009019. ISSN 1932-6203. 
  16. Johnson, M. P., Hoffman, A. J., Nichols, D. E. (December 1986). "Effects of enantiomers of MDA, MDMA and related analogues on [3H]serotonin and [3H]dopamine release from superfused rat brain slices". European Journal of Pharmacology. 132 (2–3): 269–276. doi:10.1016/0014-2999(86)90615-1. ISSN 0014-2999. 
  17. The History Channel documented details of his death here http://www.youtube.com/watch?v=ySw-0uY4CUA See minute 2:38 onward.
  18. http://www.drogen-info-berlin.de/htm/mda.html
  19. 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. doi:10.1007/BF03161089. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. 
  20. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210 . eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  21. "CONVENTION ON PSYCHOTROPIC SUBSTANCES 1971" (PDF). United Nations. Retrieved December 15, 2019. 
  22. "Criminal Code Regulations 2019". Office of Parliamentary Counsel. Retrieved December 15, 2019. 
  23. "Controlled Drugs and Substances Act - SCHEDULE I". Government of Canada. Retrieved December 15, 2019. 
  24. "Erste Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften" (in German). Bundesanzeiger Verlag. Retrieved December 15, 2019. 
  25. "Anlage I BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 15, 2019. 
  26. "§ 29 BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 15, 2019. 
  27. Resolution of the Government of the Russian Federation 
  28. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  29. Koninkrijksrelaties, M. van B. Z. en, Opiumwet 
  30. Passie, T., Benzenhöfer, U. (June 2016). "The History of MDMA as an Underground Drug in the United States, 1960-1979". Journal of Psychoactive Drugs. 48 (2): 67–75. doi:10.1080/02791072.2015.1128580. ISSN 0279-1072.