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Dissemination of Erroneous Research Findings and Subsequent Retraction in High-Circulation Newspapers: A Case Study of Alleged MDMA-Induced Dopaminergic Neurotoxicity in Primates

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Abstract

Ensuring the public is informed of retractions has proven difficult for the scientific community. While it is possible that newspapers focus differential attention on publication of scientific articles and their subsequent retractions, this topic has received minimal attention from researchers. To learn more, we analyzed newspaper coverage of the high-profile 2002 article Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA (“ecstasy”) and its retraction in a case study. We searched the 50 largest American newspapers with available online archives for stories about the article’s publication and retraction. Of the 50 newspapers, 26 (52%) covered the article’s publication and 20 (40%) its retraction. Six of the 50 newspapers (12%) published stories on the article’s retraction without covering its initial publication. Of the 26 newspapers covering the article’s publication, only 14 (54%) covered its retraction. Stories about the retraction were balanced, but shorter than those on the article’s publication and often lacking in context and detail. While the decrease in coverage of the article’s retraction was moderate among the entire sample, the much lower retraction coverage in newspapers that had already covered the article’s publication is concerning and emphasizes the need for increased media coverage of retractions.

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Background Posttraumatic stress disorder is a prevalent mental health condition with substantial impact on daily functioning that lacks sufficient treatment options. Here we evaluate six phase 2 trials in a pooled analysis to determine the study design for phase 3 trials of MDMA-assisted psychotherapy for PTSD. Methods Six randomized, double-blind, controlled clinical trials at five study sites were conducted from April 2004 to February 2017. Active doses of MDMA (75–125 mg, n = 72) or placebo/control doses (0–40 mg, n = 31) were administered to individuals with PTSD during manualized psychotherapy sessions in two or three 8-h sessions spaced a month apart. Three non-drug 90-min therapy sessions preceded the first MDMA exposure, and three to four followed each experimental session. Results After two blinded experimental sessions, the active group had significantly greater reductions in CAPS-IV total scores from baseline than the control group [MMRM estimated mean difference (SE) between groups − 22.0 (5.17), P < 0.001]. The between-group Cohen’s d effect size was 0.8, indicating a large treatment effect. After two experimental sessions, more participants in the active group (54.2%) did not meet CAPS-IV PTSD diagnostic criteria than the control group (22.6%). Depression symptom improvement on the BDI-II was greatest for the active group compared to the control group, although only trended towards significant group differences [MMRM, estimated mean difference (SE) between groups − 6.0 (3.03), P = 0.053]. All doses of MDMA were well tolerated, with some expected reactions occurring at greater frequency for the active MDMA group during experimental sessions and the 7 days following. Conclusions MDMA-assisted psychotherapy was efficacious and well tolerated in a large sample of adults with PTSD. These studies supported expansion into phase 3 trials and led to FDA granting Breakthrough Therapy designation for this promising treatment. Trial registration ClinicalTrials.gov Identifier: NCT00090064, NCT00353938, NCT01958593, NCT01211405, NCT01689740, NCT01793610.
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Background: Post-traumatic stress disorder (PTSD) is prevalent in military personnel and first responders, many of whom do not respond to currently available treatments. This study aimed to assess the efficacy and safety of 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for treating chronic PTSD in this population. Methods: We did a randomised, double-blind, dose-response, phase 2 trial at an outpatient psychiatric clinic in the USA. We included service personnel who were 18 years or older, with chronic PTSD duration of 6 months or more, and who had a Clinician-Administered PTSD Scale (CAPS-IV) total score of 50 or greater. Using a web-based randomisation system, we randomly assigned participants (1:1:2) to three different dose groups of MDMA plus psychotherapy: 30 mg (active control), 75 mg, or 125 mg. We masked investigators, independent outcome raters, and participants until after the primary endpoint. MDMA was administered orally in two 8-h sessions with concomitant manualised psychotherapy. The primary outcome was mean change in CAPS-IV total score from baseline to 1 month after the second experimental session. Participants in the 30 mg and 75 mg groups subsequently underwent three 100-125 mg MDMA-assisted psychotherapy sessions in an open-label crossover, and all participants were assessed 12 months after the last MDMA session. Safety was monitored through adverse events, spontaneously reported expected reactions, vital signs, and suicidal ideation and behaviour. This study is registered with ClinicalTrials.gov, number NCT01211405. Findings: Between Nov 10, 2010, and Jan 29, 2015, 26 veterans and first responders met eligibility criteria and were randomly assigned to receive 30 mg (n=7), 75 mg (n=7), or 125 mg (n=12) of MDMA plus psychotherapy. At the primary endpoint, the 75 mg and 125 mg groups had significantly greater decreases in PTSD symptom severity (mean change CAPS-IV total scores of -58·3 [SD 9·8] and -44·3 [28·7]; p=0·001) than the 30 mg group (-11·4 [12·7]). Compared with the 30 mg group, Cohen's d effect sizes were large: 2·8 (95% CI 1·19-4·39) for the 75 mg group and 1·1 (0·04-2·08) for the 125 mg group. In the open-label crossover with full-dose MDMA (100-125 mg), PTSD symptom severity significantly decreased in the group that had previously received 30 mg (p=0·01), whereas no further significant decreases were observed in the group that previously achieved a large response after 75 mg doses in the blinded segment (p=0·81). PTSD symptoms were significantly reduced at the 12-month follow-up compared with baseline after all groups had full-dose MDMA (mean CAPS-IV total score of 38·8 [SD 28·1] vs 87·1 [16·1]; p<0·0001). 85 adverse events were reported by 20 participants. Of these adverse events, four (5%) were serious: three were deemed unrelated and one possibly related to study drug treatment. Interpretation: Active doses (75 mg and 125 mg) of MDMA with adjunctive psychotherapy in a controlled setting were effective and well tolerated in reducing PTSD symptoms in veterans and first responders. Funding: Multidisciplinary Association for Psychedelic Studies.
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In the wake of large-scale retraction scandals, we urge scientific publishers to be more proactive in stamping out fake peer-reviewing practices. They should work with editors, authors and research institutes to implement an effective system of precautions and penalties. Fraudulent peer review can arise when editors rely on authors' recommended reviewers. These names are often genuine but have a false e-mail address that enables the authors to write a favourable review of their own paper. Springer Nature, also the publisher of Nature, this year retracted 107 papers from one of its journals on the basis of fake peer review (see T. Stigbrand Tumor Biol. doi.org/b7gg; 2017). Two years ago, it retracted 64 articles in 10 of its journals on similar grounds (see Nature doi.org/b7gh; 2015). In our view, retracting such papers is not enough. Editors need to double-check the authenticity of potential reviewers and insist that authors provide academic identities for their suggested reviewers, including institutional e-mail addresses, ORCID identifiers and Scopus Author IDs. Journals should confidentially share each other's databases of falsified reviewers' details and of offending authors. Publishers could then reject new submissions from those authors for a set period. National academic committees and research institutes might consider revoking research funding for such authors and demoting them.
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Responds to comments by M. Mithoefer, et al (see record 2003-06079-001) on the article by G. A. Ricaurte, et al (see record 2002-18729-002) which reported dopamine neurotoxicity in primates injected repeatedly with MDMA. The original authors remain of the opinion that there are not sufficient data to conclude that clinical MDMA research can be conducted without running the risk of monoaminergic brain neural injury. (PsycINFO Database Record (c) 2007 APA, all rights reserved) DOI: doi:10.1126/science.300.5625.1504
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Turning to the question of serotonergic neurotoxicity, Halpern et al. [1] suggested that that their relatively ‘modest’ performance deficits may have been be due to other confounds, and that ‘our findings indicate that the neurotoxicity of ecstasy use remains incompletely resolved’[note: median last ecstasy usage was 121 days, hence their findings are pertinent for the question of enduring toxicity]. There are, however, many neuroimaging studies which have found significant serotonergic deficits. In a review of this neuroimaging literature, Cowan [23] concluded that the most robust finding was a reduction in serotonin transporter (SERT) density. That review included several large studies, including those by McCann's group in the United States, Reneman's group in the Netherlands, Buchert's group in Germany and others. In a recent Canadian study, Kish et al. [13] has again confirmed extensive serotonergic neurotoxicity. In a comparison of 49 abstinent ecstasy users with 50 non-user controls, SERT binding was reduced significantly in every region of the cerebral cortex (reductions ranging from −19% to −46%) and hippocampus (−21%). These SERT reductions were associated statistically with cumulative life-time MDMA usage and maximum single-occasion use. These serotonergic deficits also remained after controlling for a wide range of potential confounds, including other psychoactive drug use. They also correlated significantly with various aspects of cognitive performance. This agrees with McCann et al. [10], who had earlier reported significant correlations between reduced SERT binding and neurocognitive deficits. In a functional magnetic resonance imaging (fMRI) study of adolescent ecstasy users, Jacobsen et al. [24] reported abnormal function of the left hippocampus during performance of a high-load working memory task. In an event-related potential study, Burgess et al. [25] showed that ecstasy users had a significantly reduced late-positive response in the left parietal cortex during performance of a word recognition task. These are just a selection of the empirical reports showing modified neural activity and/or neurocognitive changes.
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In field studies assessing cognitive function in illicit ecstasy users, there are several frequent confounding factors that might plausibly bias the findings toward an overestimate of ecstasy-induced neurocognitive toxicity. We designed an investigation seeking to minimize these possible sources of bias. We compared illicit ecstasy users and non-users while (1) excluding individuals with significant life-time exposure to other illicit drugs or alcohol; (2) requiring that all participants be members of the 'rave' subculture; and (3) testing all participants with breath, urine and hair samples at the time of evaluation to exclude possible surreptitious substance use. We compared groups with adjustment for age, gender, race/ethnicity, family-of-origin variables and childhood history of conduct disorder and attention deficit hyperactivity disorder. We provide significance levels without correction for multiple comparisons. Field study. Fifty-two illicit ecstasy users and 59 non-users, aged 18-45 years. Battery of 15 neuropsychological tests tapping a range of cognitive functions. We found little evidence of decreased cognitive performance in ecstasy users, save for poorer strategic self-regulation, possibly reflecting increased impulsivity. However, this finding might have reflected a pre-morbid attribute of ecstasy users, rather than a residual neurotoxic effect of the drug. In a study designed to minimize limitations found in many prior investigations, we failed to demonstrate marked residual cognitive effects in ecstasy users. This finding contrasts with many previous findings-including our own-and emphasizes the need for continued caution in interpreting field studies of cognitive function in illicit ecstasy users.
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3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") was first synthesised 80 years ago, but has recently received prominence as an illegally synthesised recreational drug of abuse. There is a widely held belief among misusers that it is safe. In the last 2-3 years there have been a number of reports of the drug producing severe acute toxicity and death and there are concerns that it may cause long term toxic damage to 5-hydroxytryptamine (5-HT) nerve terminals. There is a considerable literature on the acute pharmacological effects of MDMA in experimental animals, and this is reviewed. The drug produces both hyperthermia and the "serotonin syndrome", a series of behavioural changes which result from increased 5-HT function. Acute clinical toxicity problems following MDMA ingestion also include hyperthermia and the appearance of the serotonin syndrome. The hyperthermia appears to precipitate other severe clinical problems and the outcome can be fatal. In agreement with others, we suggest that the recent increase in the number of reports of MDMA toxicity probably results from the widespread use of the drug at all night dance parties or "raves". The phenomenon of amphetamine aggregation toxicity in mice was reported 40 years ago. If applicable to MDMA-induced toxicity in humans, all the conditions necessary to induce or enhance toxicity are present at raves: crowded conditions (aggregation), high ambient temperature, loud noise and dehydrated subjects. Administration of MDMA to rodents and non-human primates results in a long term neurotoxic decrease in 5-HT content in several brain regions and there is clear biochemical and histological evidence that this reflects neurodegeneration of 5-HT terminals. Unequivocal data demonstrating that similar changes occur in human brain do not exist, but limited and indirect clinical evidence gives grounds for concern. There are also data suggesting that long term psychiatric changes can occur, although there are problems of interpretation and these are reviewed. Suggestions for the rational treatment of the acute toxicity are made on the basis of both pharmacological studies in animals and current clinical practice. Cases presenting clinically are usually emergencies and unlikely to allow carefully controlled studies. Proposals include decreasing body temperature (possibly with ice), the use of dantrolene and anticonvulsant and sedative medication, particularly benzodiazepines. The use of neuroleptics requires care because of the theoretical risk of producing the neuroleptic malignant syndrome and the possibility of precipitating seizures. In rats, chlormethiazole antagonises the hyperthermia produced by MDMA and has been shown clinically to block MDMA-induced convulsive activity.
Article
The prevailing view is that the popular recreational drug (±)3,4-methylenedioxymethamphetamine (MDMA, or “ecstasy”) is a selective serotonin neurotoxin in animals and possibly in humans. Nonhuman primates exposed to several sequential doses of MDMA, a regimen modeled after one used by humans, developed severe brain dopaminergic neurotoxicity, in addition to less pronounced serotonergic neurotoxicity. MDMA neurotoxicity was associated with increased vulnerability to motor dysfunction secondary to dopamine depletion. These results have implications for mechanisms of MDMA neurotoxicity and suggest that recreational MDMA users may unwittingly be putting themselves at risk, either as young adults or later in life, for developing neuropsychiatric disorders related to brain dopamine and/or serotonin deficiency.
Article
A substantial literature suggests that users of illicit 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") display residual cognitive deficits. Most MDMA users, however, use other illicit drugs as well, so it is difficult to be certain that these deficits are due to MDMA, as opposed to other drug use or additional confounding factors. We administered a battery of neuropsychological tests to 23 young MDMA users who reported minimal exposure to any other drugs, including alcohol, and to 16 comparison individuals equally involved with the rave subculture, but reporting no MDMA use. We compared the groups by regression analyses adjusting for numerous potentially confounding variables. To test for a possible dose-response effect, we also performed a median split of 12 moderate MDMA users (22-50 lifetime uses) and 11 heavy users (60-450 uses), and compared these subgroups with non-users. MDMA users as a whole performed worse than non-users on most test measures, but these comparisons rarely reached statistical significance. This picture changed markedly in the subgroup analysis: although moderate users displayed virtually no differences from non-users on any measures, the heavy users displayed significant deficits on many measures, particularly those associated with mental processing speed and impulsivity. These differences did not appear explainable by differences in family-of-origin variables, verbal IQ, levels of depression, or time since last MDMA use. The presence of residual cognitive deficits, even among unusually "pure" frequent users of illicit MDMA, analyzed with adjustment for confounding variables, augments the evidence that MDMA itself, rather than some associated factor, is responsible for the deficits observed.
Article
In October 2004, a flawed systematic review entitled "Interactive Health Communication Applications for People with Chronic Disease" was published in the Cochrane Library, accompanied by several press releases in which authors warned the public of the negative health consequences of interactive health communication applications, including the Internet. Within days of the review's publication, scientists identified major coding errors and other methodological problems that invalidated the principal conclusions of the study and led to a retraction. While the original study results and their negative conclusions were widely publicized in the media, the retraction seemed to go unnoticed. This paper aims to document an unprecedented case of misinformation from a Cochrane review and its impact on media, scientists, and patients. As well, it aims to identify the generic factors leading to the incident and suggest remedies. This was a qualitative study of the events leading to the retraction of the publication and of the reactions from media, scientists, and patients. This includes a review and content analysis of academic and mass media articles responding to the publication and retraction. Mass media articles were retrieved in May 2005 from LexisNexis Academic and Google and were classified and tallied. The extended case method is employed, and the analysis is also applied to comparable publishing events. A search on LexisNexis Academic database with the query "Elizabeth Murray AND health" for the period of June 2004 to May 2005 revealed a total of 15 press reports, of which only 1 addressed the retraction. Google was searched for references to the review, and the first 200 retrieved hits were analyzed. Of these, 170 pages were not related to the review. Of the remaining 30 pages, 23 (77%) were reports about the original publication that did not mention the retraction, 1 (3%) was a bibliography not mentioning the retraction, and 6 (20%) addressed the retraction, of which only 1 was a non-Cochrane-related source. Analyzed retrievals showed that the mass media gave more coverage to the Cochrane review than to the retraction or to a related systematic review with a similar scope but a different conclusion. Questionable results were prematurely disseminated, oversimplified, and sensationalized, while the retraction was hardly noticed by the public. Open commentary by scientists and patients helped to rapidly identify the errors but did not prevent or correct the dissemination of misinformation.
Article
To explore how often newspapers cover the retraction of a medical journal article and whether newspaper coverage corresponds with the appearance of a press release about the retraction. Fifty citations were identified in PubMed that had been indexed with the Medical Subject Heading 'Retracted Publication'. Next, the archives of LexisNexis's 'Major Newspapers' and EurekAlert's press releases were searched to find references to those retracted publications. Newspaper articles addressed exactly three of the 50 retracted publications, and press releases, exactly four of the 50 retracted publications. All three retracted publications that received newspaper coverage also had a press release. In other words, newspapers only covered a retraction that had been introduced by a press release. One would expect that newspaper coverage would increase after a press release, but the suggested relationships among a medical journal article retraction, a press release and newspaper coverage should be further investigated. If the linkage suggested by the data of this study holds, and if newspaper coverage stimulates library patron interest, then a medical library might prepare itself for information requests following a press release.
Drug panics in the twenty-first century: Ecstasy, prescription drugs, and the reframing of the war on drugs
  • D Ahrens
Ahrens, D. 2013. Drug panics in the twenty-first century: Ecstasy, prescription drugs, and the reframing of the war on drugs. Albany Government Law Review 6:397-437.
Top 100 newspapers in the United States
  • Infoplease
Infoplease. 2007. Top 100 newspapers in the United States. https://www.infoplease.com/arts-entertainment/newspa pers-and-magazines/top-100-newspapers-united-states.
Study in primates shows brain damage from doses of ecstasy
  • D G Mcneil
McNeil, D. G. 2002. Study in primates shows brain damage from doses of ecstasy. New York Times, September 27.
Ecstasy's after-effects
Nature Editorial Board. 2003. Ecstasy's after-effects. Nature. doi:10.1038/425223a.
Ecstasy as a remedy for PTSD? You probably have some questions
  • D Philipps
Philipps, D. 2018. Ecstasy as a remedy for PTSD? You probably have some questions. New York Times, https://www.nytimes. com/2018/05/01/us/ecstasy-molly-ptsd-mdma.html.
MDMA-and p-chlorophenylalanineinduced reduction in 5-HT concentrations: Effects on serotonin transporter densities
  • G A Ricaurte
  • P Brendon
  • Annis O Boot
  • Una D Mechan
  • George A Mccann
  • Ricaurte
Ricaurte, G. A. 2004. MDMA-and p-chlorophenylalanineinduced reduction in 5-HT concentrations: Effects on serotonin transporter densities. Brendon P. Boot, Annis O. Mechan, Una D. McCann, George A. Ricaurte [Eur.
Oops ! “ Killer “ ecstasy article retracted, NIDA credibility on the line, RAVE act still law
  • P S Smith
Smith, P. S. 2003. Oops ! " Killer " ecstasy article retracted, NIDA credibility on the line, RAVE act still law. DRC-Net. http://www.maps.org/research-archive/mdma/retraction/ drc-net091203.html.
Recreational use of ecstasy causes new brain damage
  • T Stockton
Stockton, T. 2002. Recreational use of ecstasy causes new brain damage. The Johns Hopkins Gazette, September 30.
Retracted ecstasy paper “ an outrageous scandal“
  • R Walgate
Walgate, R. 2003. Retracted ecstasy paper " an outrageous scandal". The Scientist. https://www.the-scientist.com/ news-analysis/retracted-ecstasy-paper-an-outrageousscandal-51068.
Ecstasy Thought to Cause Brain Damage According to Study Published in Science
  • K Wren
Wren, K. 2002. Ecstasy Thought to Cause Brain Damage According to Study Published in Science. American Association for the Advancement of Science.