Second Thoughts on 3,4-Methylenedioxymethamphetamine (MDMA) Neurotoxicity

A letter to the editor critiques a study that attempted to assess serotonergic neurotransmitter damage in MDMA users by measuring serum prolactin response to an intravenous L-tryptophan challenge. The study found a blunted rise in prolactin levels among MDMA users, but this result was not statistically significant. The letter argues that even a significant result would not imply causation and highlights a methodological limitation: subjects were not adequately screened for use of other psychotropic drugs, and toxicology screens were not performed. Three subjects (33%) admitted to marijuana use, raising concerns about confounding factors.

Study at a glance

Abstract

To the Editor.— Recent attention has been drawn to the purported neurotoxic dangers associated with 3, 4-methylenedioxymethamphetamine (MDMA). Price et al1have attempted to assess possible serotonergic neurotransmitter damage by contrasting serum prolactin response to the challenge with intravenous L-tryptophan in subjects with a history of MDMA use vs control subjects. Their primary finding was a blunted rise in the expected serum prolactin level in MDMA users, but not to a statistically significant degree. The importance of this finding appears to be questionable and perhaps misleading. Even if the data had yielded a statistically significant result, would such a correlation necessarily imply causation? A methodological limitation to the study would appear to be that subjects were not adequately screened on selection to exclude those who were using other psychotropic drugs. There is no mention that toxicology screens were ever performed. In fact, three subjects (33%) admitted to marijuana use