MDEA: Difference between revisions

>Unity
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==Toxicity and harm potential==
==Toxicity and harm potential==
===Short-term health concerns===
Short-term physical health risks of MDEA consumption include [[dehydration]], [[insomnia]], [[hyperthermia]],<ref>Drug-induced hyperthermia | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2044.1993.tb07423.x/abstract;jsessionid=FC30A9B157A2BAFC81048D8595714565.f02t03</ref><ref>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</ref> and hyponatremia.<ref>Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population | http://jop.sagepub.com/content/20/3/400</ref> 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.
Short-term physical health risks of MDEA consumption include [[dehydration]], [[insomnia]], [[hyperthermia]],<ref>Drug-induced hyperthermia | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2044.1993.tb07423.x/abstract;jsessionid=FC30A9B157A2BAFC81048D8595714565.f02t03</ref><ref>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</ref> and hyponatremia.<ref>Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population | http://jop.sagepub.com/content/20/3/400</ref> 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 [[Toxicity::exact toxic dosage is unknown]], but considered to be far greater than its active dose.
The [[Toxicity::exact toxic dosage is unknown]], but considered to be far greater than its active dose.


===Long-term health concerns===
===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.
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.<ref>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</ref> Other studies have suggested that the brain may recover from serotonergic damage.<ref>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</ref><ref>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. </ref><ref>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</ref>
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.<ref>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</ref> Other studies have suggested that the brain may recover from serotonergic damage.<ref>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</ref><ref>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. </ref><ref>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</ref>
===Cardiotoxicity===


Like with MDMA, the long-term heavy use of MDEA is likely similarly cardiotoxic, leading to valvulopathy through its actions on the 5-HT<sub>2B</sub> receptor.<ref> Drug-induced Valvulopathy: An Update | tpx.sagepub.com/content/38/6/837.full</ref> 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.<ref>Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805</ref>
Like with MDMA, the long-term heavy use of MDEA is likely similarly cardiotoxic, leading to valvulopathy through its actions on the 5-HT<sub>2B</sub> receptor.<ref> Drug-induced Valvulopathy: An Update | tpx.sagepub.com/content/38/6/837.full</ref> 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.<ref>Possible association between 3,4-methylenedioxymethamphetamine abuse and valvular heart disease. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/17950805</ref>
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