Erowid References Database
Ricaurte GA, Finnegan KT, Irwin I, Langston JW.
“Aminergic metabolites in cerebrospinal fluid of humans previously exposed to MDMA: preliminary observations”.
Ann N Y Acad Sci. 1990;600:699-708; discussion.
Recreational use of the neurotoxic drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy') poses a public health problem of uncertain proportions. The reason for this is twofold. First, there is little information regarding the number of individuals that have been exposed to the drug, and even less about how many people are continuing to use it. According to one informal survey, 39% of students on an undergraduate campus reported having experimented with MDMA on at least one occasion. Other informal surveys on different college campuses have yielded lower figures (6-25%). In 1985, Siegel reported that approximately 30,000 dosage units of MDMA were being sold in the United States each month. More recently (1989), Doblin provided an estimate of 100,000 dosage units per month. Whether this represents a true increase in MDMA use, or whether these estimates vary as a function of how they were ascertained is not clear. Howerver, given MDMA's neurotoxic potential (see below), formal epidemiologic efforts to determine the incidence of recreational MDMA use are in order.
The second reason why it is difficut to guage the seriousness of the threat that MDMA poses to public health is that, although the long-term serotonin-depleting effects of MDMA have been convincingly demonstrated in animals, such documentation is lacking in humans. Moreover, the doses, routes, and schedules of MDMA administration used in most (but not all, see reference 11) animal studies have differed significantly from those typically employed by humans. Hence, it is difficult to know to what extent the findings in animals can be generalized to humans.
To the best of our knowledge, thus far only two studies have investigated the neurotoxic potential of MDMA in humans. The first measured the concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) of five individuals with a history of recreational MDMA use. No difference from the controls was found. The second study assessed central serotonergic function in nine recreational MDMA users employing the L-tryptophan challenge test. In this study, L-tryptophan induced a rise in serum prolactin in controls, but not in MDMA subjects, suggesting that serotonergic function in MDMA users might be impaired.
The purpose of the present study was to further evaluate the neurotoxic potential of MDMA in humans by measuring CSF 5-HIAA levels in a group of MDMA users who agreed to undergo lumbar puncture two (or more) weeks after their last use of the drug.
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