How could MDMA (ecstasy) help anxiety disorders? A neurobiological rationale
Abstract
Abstract Exposure therapy is known to be an effective treatment for anxiety disorders. Nevertheless, exposure is not used as much as it should be, and instead patients are often given supportive medications such as serotonin reuptake inhibitors (SSRIs) and benzodiazepines, which may even interfere with the extinction learning that is the aim of treatment. Given that randomized controlled trials are now investigating a few doses of ±3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) in combination with psychotherapy for treatment-resistant anxiety disorders, we would like to suggest the following three mechanisms for this potentially important new approach: 1) MDMA increases oxytocin levels, which may strengthen the therapeutic alliance; 2) MDMA increases ventromedial prefrontal activity and decreases amygdala activity, which may improve emotional regulation and decrease avoidance and 3) MDMA increases norepinephrine release and circulating cortisol levels, which may facilitate emotional engagement and enhance extinction of learned fear associations. Thus, MDMA has a combination of pharmacological effects that, in a therapeutic setting, could provide a balance of activating emotions while feeling safe and in control, as described in case reports of MDMA-augmented psychotherapy. Further clinical and preclinical studies of the therapeutic value of MDMA are indicated.
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The drug's supposed empathogenic properties are a key reason it has been proposed as an adjunct in psychotherapy.
“MDMA’s apparent empathogenic effects are also central to the rationale for the use of the drug as a psychotherapeutic adjunct [1, 5–6].”
From Is Ecstasy an “Empathogen”? Effects of +/- 3,4-Methylenedioxymethamphetamine on Prosocial Feelings and Identification of Emotional States in Others (2010) · cites this paper as [6]
MDMA enhances activity in the ventromedial prefrontal cortex, which is key for extinction.
“This drug enhances activity in the ventromedialpre frontal cortex, which is key for extinction.”
From Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges (2019) · cites this paper as [147]
MDMA increases cortisol release, which can promote emotional engagement and enhance extinction.
“Furthermore, it increases cortisol release, which can promote emotional engagement and enhance extinction 147 .”
From Post‐traumatic stress disorder: a state‐of‐the‐art review of evidence and challenges (2019) · cites this paper as [147]
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- Authors
- Johansen, P., & Krebs, T.
- Affiliations
- Norwegian University of Science and Technology (NO)
- Department of Neuroscience, Faculty of Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway,
- Venue
- Journal of Psychopharmacology
- Publisher
- SAGE Publications
- Published
- 2009-03-09
- Volume
- 23
- Issue
- 4
- Pages
- 389-391
- ISSN
- 0269-8811 (ISSN-L)
- 1461-7285
- OpenAlex
- W2105541798
- Cited by
- 96
- References
- 25
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 5 · 2023: 5 · 2022: 4 · 2021: 5 · 2020: 6 · 2019: 3 · 2018: 6 · 2017: 6 · 2016: 8 · 2015: 4 · 2014: 10 · 2013: 6 · 2012: 9
- FWCI
- 8.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Psychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Norges Forskningsråd
- Topics
- Social Sciences › Psychology › Clinical Psychology › Psychedelics and Drug Studies
- Social Sciences › Psychology › Clinical Psychology › Psychotherapy Techniques and Applications
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- MDMA, ecstasy, anxiety disorders, MDMA-assisted psychotherapy, exposure therapy, fear extinction, oxytocin, therapeutic relationship, ventromedial prefrontal cortex, amygdala, norepinephrine, cortisol, emotion regulation, avoidance, serotonin reuptake inhibitors, benzodiazepines
- MeSH terms
- Anxiety Disorders, Avoidance Learning, Brain, Empathy, Fear, Humans, Psychotherapy, Stress Disorders, Post-Traumatic, N-Methyl-3,4-methylenedioxyamphetamine
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