Evidence map›Paper›PMID 30770892›Full record

Trial reportMolecular psychiatry2020

Delta-9-tetrahydrocannabinol increases striatal glutamate levels in healthy individuals: implications for psychosis.

Marco Colizzi, Nathalie Weltens, Philip McGuire, David Lythgoe, Steve Williams, Lukas Van Oudenhove, Sagnik Bhattacharyya

Open access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 4 pooled it
9.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 4 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. The Autism-Psychosis Continuum Conundrum: Exploring the Role of the Endocannabinoid System.International journal of environmental research and public health · 2022
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Acute effects of ΔPsychopharmacology · 2022
    Trial
  7. Trial
  8. Trial
  9. Trial
  10. Article
  11. Adolescent ΔPharmaceuticals (Basel, Switzerland) · 2026
    Article
  12. The Paradoxical Effect of Cannabis Use on Cognition in Chronic Psychotic Disorders.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Substance use and use disorders during pregnancy and the postpartum period.American journal of obstetrics and gynecology · 2025
    Review
  17. Exploring causal mechanisms of psychosis risk.Neuroscience and biobehavioral reviews · 2024
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Marco ColizziNational Institute for Health Research (NIHR) Biomedical Research Centre (BRC), South London and Maudsley NHS Foundation Trust, and Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK.ORCID http://orcid.org/0000-0001-6139-1920
Nathalie WeltensLaboratory for Brain-Gut Axis Studies (LaBGAS), Translational Research Center for Gastrointestinal Disorders (TARGID), Department of Chronic Diseases, Metabolism and Ageing, University of Leuven, Leuven, 3000, Belgium.
Philip McGuireNational Institute for Health Research (NIHR) Biomedical Research Centre (BRC), South London and Maudsley NHS Foundation Trust, and Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK.
David LythgoeDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK.
Steve WilliamsDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK.ORCID http://orcid.org/0000-0003-4299-1941
Lukas Van OudenhoveLaboratory for Brain-Gut Axis Studies (LaBGAS), Translational Research Center for Gastrointestinal Disorders (TARGID), Department of Chronic Diseases, Metabolism and Ageing, University of Leuven, Leuven, 3000, Belgium.
Sagnik BhattacharyyaNational Institute for Health Research (NIHR) Biomedical Research Centre (BRC), South London and Maudsley NHS Foundation Trust, and Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK. sagnik.2.bhattacharyya@kcl.ac.uk.ORCID http://orcid.org/0000-0002-8688-8025
King's College London · GBKU Leuven · BE

Funding

Department of Health NIHR-CS-011-001Medical Research Council MR/J012149/1
6 · The paper itself

Abstract

The neurobiological mechanisms underlying the association between cannabis use and acute or long-lasting psychosis are not completely understood. While some evidence suggests altered striatal dopamine may underlie the association, direct evidence that cannabis use affects either acute or chronic striatal dopamine is inconclusive. In contrast, pre-clinical research suggests that cannabis may affect dopamine via modulation of glutamate signaling. A double-blind, randomized, placebo-controlled, crossover design was used to investigate whether altered striatal glutamate, as measured using proton magnetic resonance spectroscopy, underlies the acute psychotomimetic effects of intravenously administered delta-9-tetrahydrocannabinol (Δ9-THC; 1.19 mg/2 ml), the key psychoactive ingredient in cannabis, in a set of 16 healthy participants (7 males) with modest previous cannabis exposure. Compared to placebo, acute administration of Δ9-THC significantly increased Glutamate (Glu) + Glutamine (Gln) metabolites (Glx) in the left caudate head (P = 0.027). Furthermore, compared to individuals who were not sensitive to the psychotomimetic effects of Δ9-THC, individuals who developed transient psychotic-like symptoms (~70% of the sample) had significantly lower baseline Glx (placebo; P 7= 0.023) and a 2.27-times higher increase following Δ9-THC administration. Lower baseline Glx values (r = -0.55; P = 0.026) and higher previous cannabis exposure (r = 0.52; P = 0.040) were associated with a higher Δ9-THC-induced Glx increase. These results suggest that an increase in striatal glutamate levels may underlie acute cannabis-induced psychosis while lower baseline levels may be a marker of greater sensitivity to its acute psychotomimetic effects and may have important public health implications.

Indexed as

HallucinogensPsychotic DisordersCorpus StriatumDouble-Blind MethodDronabinolGlutamic AcidHumansMaleDronabinolGlutamic AcidHallucinogens

Identifiers

PMID30770892
PMCPMC7714685
OpenAlexW2911748025

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.