Evidence map›Paper›PMID 24904437›Full record

ReviewFrontiers in psychiatry2014

Gone to Pot - A Review of the Association between Cannabis and Psychosis.

Rajiv Radhakrishnan, Samuel T Wilkinson, Deepak Cyril D'Souza

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 8 pooled it
32.8field-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

125 citing papers in PubMed, 8 syntheses or guidelines pooled it, 301 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Cannabis use and psychosis: a review of reviews.European archives of psychiatry and clinical neuroscience · 2020
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Risks associated with the non-medicinal use of cannabis.Deutsches Arzteblatt international · 2015
    Pooled it
  9. Trial
  10. Trial
  11. Δ9-THC Disrupts Gamma (γ)-Band Neural Oscillations in Humans.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Trial
  12. GABA Deficits Enhance the Psychotomimetic Effects of Δ9-THC.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Trial
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Observational
  19. Review
  20. Article

65 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Rajiv RadhakrishnanDepartment of Psychiatry, Yale University School of Medicine , New Haven, CT , USA.
Samuel T WilkinsonDepartment of Psychiatry, Yale University School of Medicine , New Haven, CT , USA.
Deepak Cyril D'SouzaDepartment of Psychiatry, Yale University School of Medicine , New Haven, CT , USA ; Abraham Ribicoff Research Facilities, Connecticut Mental Health Center , New Haven, CT , USA ; Schizophrenia and Neuropharmacology Research Group, VA Connecticut Healthcare System , West Haven, CT , USA.
Yale University · USConnecticut Mental Health Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cannabis is the most commonly used illicit drug worldwide, with ~5 million daily users worldwide. Emerging evidence supports a number of associations between cannabis and psychosis/psychotic disorders, including schizophrenia. These associations-based on case-studies, surveys, epidemiological studies, and experimental studies indicate that cannabinoids can produce acute, transient effects; acute, persistent effects; and delayed, persistent effects that recapitulate the psychopathology and psychophysiology seen in schizophrenia. Acute exposure to both cannabis and synthetic cannabinoids (Spice/K2) can produce a full range of transient psychotomimetic symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to symptoms of schizophrenia. In individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Several factors appear to moderate these associations, including family history, genetic factors, history of childhood abuse, and the age at onset of cannabis use. Exposure to cannabinoids in adolescence confers a higher risk for psychosis outcomes in later life and the risk is dose-related. Individuals with polymorphisms of COMT and AKT1 genes may be at increased risk for psychotic disorders in association with cannabinoids, as are individuals with a family history of psychotic disorders or a history of childhood trauma. The relationship between cannabis and schizophrenia fulfills many but not all of the standard criteria for causality, including temporality, biological gradient, biological plausibility, experimental evidence, consistency, and coherence. At the present time, the evidence indicates that cannabis may be a component cause in the emergence of psychosis, and this warrants serious consideration from the point of view of public health policy.

Indexed as

cannabispsychophysiologypsychosisschizophreniaschizotypyspicesynthetic cannabinoids

Identifiers

PMID24904437
PMCPMC4033190
OpenAlexW2040750242

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.