Addiction
July 8, 2006
Roland W. Freudenmann, Florian Öxler, Sabine Bernschneider‐reif
201 citations
MDMA was first synthesized by Merck in 1912, but not as an appetite suppressant as commonly claimed. Original documents from Merck's archive show it was an unimportant precursor in a new synthesis for hemostatic substances, patented to evade a competitor's patent. Pharmacological testing occurred in 1927 and 1959, but not in humans. The myth that MDMA was developed as an appetite suppressor likely arose from uncritical copy-paste errors in later literature.
CNS Drug Reviews
June 1, 2004
Roland W. Freudenmann, Manfred Spitzer
41 citations
MDEA, also known as "eve," is a ring-substituted amphetamine chemically and pharmacologically similar to MDMA. It produces psychomotor stimulation, mild perceptual changes, feelings of closeness, positive emotional states, and sympathomimetic physical effects. The term "ecstasy" now refers to a group of nearly identical compounds including MDA, MDMA, MDEA, and MBDB, and many pills contain mixtures. This review describes MDEA-specific pharmacodynamics and kinetics from animal and human challenge studies, and presents case reports of fatalities with toxicologically confirmed MDEA. Evidence for serotonergic neurotoxicity comes only from animal studies; human risk is unclear because users consume impure substances. Future animal studies using human-like dosing patterns and directly comparing individual ring-substituted amphetamines are needed to resolve controversies about neurotoxicity and its functional consequences.
Journal of Psychopharmacology
November 1, 2006
Roland W. Freudenmann, Carlos Schönfeldt-lecuona, Manfred Spitzer et al.
4 citations
Depression in people who formerly used ecstasy heavily may not improve with standard antidepressants like SSRIs, possibly because long-term ecstasy use damages serotonin pathways. A patient with MDMA-induced depression who did not respond to several antidepressants, including an SNRI and an SSRI, achieved stable remission of mood and cognitive symptoms after receiving repeated bilateral electroconvulsive therapy (ECT), with improvement lasting over 1.5 years. Add-on ECT could be a treatment option for former ecstasy users with severe depression that does not respond to antidepressants, though clinical trials are needed to confirm its usefulness.