Electronic Letters to:
|
|
eLetters: Electronic letters published:
-
![[Read eLetter]](/icons/misc/sectionDOWN.gif)
Lack of long-term effect of ‘ecstasy’ use on serotonin binding fits with known risk profile of MDMA
- Teri S. Krebs, Pål-Ørjan Johansen (7 April 2009)
|
|
|||
|
Teri S. Krebs, Research fellow Dept of Neuroscience, Norwegian University of Science and Technology, Pål-Ørjan Johansen
Send letter to journal:
krebs{at}ntnu.no Teri S. Krebs, et al.
|
Selvaraj et al. found no evidence of effects on serotonin transporter binding in the brains of former heavy users of ecstasy (an unregulated street-drug version of (+/-)-3,4-methylenedioxymethamphetamine; MDMA), with lifetime use between 60 and 864 tablets and abstinence between 390 and 1825 days. These findings fit well with a recent prospective study that found no changes in serotonin transporter binding after initial use of ecstasy (1). A recent report by the UK Academic Council on Misuse of Drugs (ACMD) concluded that any effect of MDMA on human serotonin functioning appears small and temporary (2). A few days of exposure to ethanol is known to kill brain cells in laboratory animals. In contrast, low doses of MDMA have few long-term effects in animals, and even high or repeated doses of MDMA do not typically destroy neurons but rather may induce temporary or prolonged changes in various measures of serotonin functioning (3). Serotonin transporters are regulated by many feedback loops, and serotonin functioning is known to fluctuate in response to anti-depressants, time of year, and other factors. Thus, any differences in serotonin functioning in ecstasy users should not be assumed to represent neuronal damage but may be pre-existing or due to adaptive plasticity (3). The ACMD report also notes the low incidence of serious adverse effects among ecstasy users, with approximately one death per two million ecstasy tablets consumed in the UK, and most ecstasy-related deaths also involved alcohol or other dangerous drugs (2). According to the ACMD, overall risks from illicit ecstasy are similar to amphetamine, but with less potential for compulsive use, or for risky and aggressive behavior, or for psychiatric and cognitive problems (2). Retrospective surveys have found small, clinically-insignificant associations between ecstasy use and depression and memory deficits (2). These non-randomized surveys mostly ignored potential confounders that may explain both repeated ecstasy use and mood and cognitive problems, such as childhood anxiety and depression (4). Research priorities are guided by a public health perspective. Exposure to industrial chemicals, some prescription drugs, alcohol, and childhood poverty and neglect are all likely far more significant causes of brain damage than exposure to ecstasy. Taken together, the Selvaraj et al. study and the ACMD report are reassuring to the millions of people who have taken moderate amounts of ecstasy. These findings add to the many clinical and preclinical studies that indicate, in the judgment of health authorities in the UK and elsewhere, a favorable risk-benefit profile of a few doses of pharmaceutical MDMA, administered in scientific research, with appropriate medical screening and supervision, as seen in numerous completed and on-going trials of MDMA in healthy volunteers and anxiety patients. Future neuroimaging studies could explore the biological basis of the noteworthy, and potentially medically useful, effects of MDMA on affiliation and emotional regulation (5). References 1. de Win MM, Jager G, Booij J, Reneman L, Schilt T, Lavini C, Olabarriaga SD, den Heeten GJ, van den Brink W. Sustained effects of ecstasy on the human brain: a prospective neuroimaging study in novel users. Brain 2008; 131:2936-45. [Pubmed 18842607] 2. Advisory Council on the Misuse of Drugs. MDMA (ecstasy): a review of its harms and classification under the Misuse of Drugs Act 1971. Home Office, 2009. http://drugs.homeoffice.gov.uk/publication-search/acmd/mdma-report 3. Baumann MH, Wang X, Rothman RB. 3,4-Methylenedioxymethamphetamine (MDMA) neurotoxicity in rats: a reappraisal of past and present findings. Psychopharmacology (Berl) 2007; 189:407-24. [Pubmed 16541247] 4. Huizink AC, Ferdinand RF, van der Ende J, Verhulst FC. Symptoms of anxiety and depression in childhood and use of MDMA: prospective, population based study. BMJ 2006; 332:825-8. [Pubmed 16500927] 5. Johansen P, Krebs T. How could MDMA (ecstasy) help anxiety disorders? A neurobiological rationale. J Psychopharmacol 2009 (in press). [Pubmed 19273493] Declaration of interest TS Krebs has previously received funding support from the US nonprofit Multidisciplinary Association of Psychedelic Studies (www.maps.org), sponsor of clinical research on MDMA. PØ Johansen is director of Evidence Knowledge Exchange (www.evidence.no), a Norwegian nonprofit offering continuing education courses. Teri S. Krebs, Dept of Neuroscience, and Pål-Ørjan Johansen, Dept of Psychology, Norwegian University of Science and Technology (NTNU) |
|||