Equivalent effects of acute tryptophan depletion on REM sleep in ecstasy users and controls.
Robin Carhart-Harris, David Nutt, Marcus R. Munafò, David M Christmas, Sue Wilson
Psychopharmacology July 8, 2009 DOI: 10.1007/s00213-009-1595-3 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Cross-over observational study Peer reviewed |
|---|---|
| Sample size | 24 |
| Population | 12 ecstasy users and 12 controls |
| Intervention | tryptophan-supplemented control mixture |
| Duration | Three nights of sleep measurement |
| Measures | Ambulatory polysomnography |
| Topics | MDMA |
| Keywords | Humans Substance-related disorders N-methyl-3,4-methylenedioxyamphetamine Tryptophan Hallucinogens Pain measurement Polysomnography Cross-over studies Double-blind method Reaction time Sleep, rem Time factors Young adult |
| Key findings | Acute tryptophan depletion shortened REM sleep onset latency, increased REM sleep, and increased stage 2 sleep in the first three hours, but ecstasy users and controls did not differ in sleep on the screening night or after depletion. The authors conclude that the ecstasy users had not suffered significant serotonergic damage as indexed by sleep. |
Abstract
Introduction: This study sought to test the association between 3,4-methylenedioxymethamphetamine use, serotonergic function and sleep.
Materials and Methods: Ambulatory polysomnography was used to measure three nights sleep in 12 ecstasy users and 12 controls after screening (no intervention), a tryptophan-free amino acid mixture (acute tryptophan depletion (ATD)) and a tryptophan-supplemented control mixture.
Results: ATD significantly decreased rapid eye movement (REM) sleep onset latency, increased the amount of REM sleep and increased the amount of stage 2 sleep in the first 3 h of sleep. There was no difference between ecstasy users' and controls' sleep on the screening night or after ATD.
Discussion: These findings imply that the ecstasy users had not suffered significant serotonergic damage as indexed by sleep.
Comparable studies
Other randomized controlled trials on MDMA, most cited first.
Citations in the library
Cited by 5
- A reconsideration and response to Parrott AC (2013) "Human psychobiology of MDMA or 'Ecstasy': an overview of 25 years of empirical research". Human Psychopharmacology: Clinical and Experimental March 1, 2014
- Strategic control, consolidation and poly-drug use; the relative contributions to verbal memory impairment in recreational ecstasy users UTAS Research Repository August 1, 2014
- Serotonergic psychedelics as potential therapeutics for post-COVID-19 syndrome (or Long COVID): A comprehensive review. Progress in Neuro-Psychopharmacology and Biological Psychiatry March 20, 2025
- MDMA is certainly damaging after 25 years of empirical research: a reply and refutation of Doblin et al. (2014). Human Psychopharmacology: Clinical and Experimental March 2014
- Acute MDMA administration alters the distribution and circadian rhythm of wheel running activity in the rat. Brain Research September 26, 2010
Cites 30
- Positron emission tomographic evidence of toxic effect of MDMA (“Ecstasy”) on brain serotonin neurons in human beings The Lancet October 1, 1998
- The molecular mechanism of "ecstasy" [3,4-methylenedioxy-methamphetamine (MDMA)]: serotonin transporters are targets for MDMA-induced serotonin release. Proceedings of the National Academy of Sciences March 1, 1992
- Hallucinogenic Amphetamine Selectively Destroys Brain Serotonin Nerve Terminals Science September 6, 1985
- Altered Serotonin Innervation Patterns in the Forebrain of Monkeys Treated with (±)3,4-Methylenedioxymethamphetamine Seven Years Previously: Factors Influencing Abnormal Recovery Journal of Neuroscience June 15, 1999
- Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") Journal of Neuroscience August 1, 1995
and 25 more in the library