Evidence map›Paper›PMID 25477825›Full record

ArticleFrontiers in psychiatry2014

The Cannabis Pathway to Non-Affective Psychosis may Reflect Less Neurobiological Vulnerability.

Else-Marie Løberg, Siri Helle, Merethe Nygård, Jan Øystein Berle, Rune A Kroken, Erik Johnsen

Open access · goldAbstract read
In one paragraph

Article 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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  16. Cannabis and development of dual diagnoses: A literature review.The American journal of drug and alcohol abuse · 2017
    Review
  17. Article
  18. Traditional marijuana, high-potency cannabis and synthetic cannabinoids: increasing risk for psychosis.World psychiatry : official journal of the World Psychiatric Association (WPA) · 2016
    Article
  19. Cannabinoids and Schizophrenia: Risks and Therapeutic Potential.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
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

6 authors at 2 institutions in 1 country.

Else-Marie LøbergDivision of Psychiatry, Haukeland University Hospital , Bergen , Norway ; Department of Clinical Psychology, University of Bergen , Bergen , Norway.
Siri HelleDivision of Psychiatry, Haukeland University Hospital , Bergen , Norway.
Merethe NygårdLaboratory of Clinical Biochemistry, Haukeland University Hospital , Bergen , Norway.
Jan Øystein BerleDivision of Psychiatry, Haukeland University Hospital , Bergen , Norway.
Rune A KrokenDivision of Psychiatry, Haukeland University Hospital , Bergen , Norway.
Erik JohnsenDivision of Psychiatry, Haukeland University Hospital , Bergen , Norway ; Department of Clinical Medicine, University of Bergen , Bergen , Norway.
Haukeland University Hospital · NOUniversity of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a high prevalence of cannabis use reported in non-affective psychosis. Early prospective longitudinal studies conclude that cannabis use is a risk factor for psychosis, and neurochemical studies on cannabis have suggested potential mechanisms for this effect. Recent advances in the field of neuroscience and genetics may have important implications for our understanding of this relationship. Importantly, we need to better understand the vulnerability × cannabis interaction to shed light on the mediators of cannabis as a risk factor for psychosis. Thus, the present study reviews recent literature on several variables relevant for understanding the relationship between cannabis and psychosis, including age of onset, cognition, brain functioning, family history, genetics, and neurological soft signs (NSS) in non-affective psychosis. Compared with non-using non-affective psychosis, the present review shows that there seem to be fewer stable cognitive deficits in patients with cannabis use and psychosis, in addition to fewer NSS and possibly more normalized brain functioning, indicating less neurobiological vulnerability for psychosis. There are, however, some familiar and genetic vulnerabilities present in the cannabis psychosis group, which may influence the cannabis pathway to psychosis by increasing sensitivity to cannabis. Furthermore, an earlier age of onset suggests a different pathway to psychosis in the cannabis-using patients. Two alternative vulnerability models are presented to integrate these seemingly paradoxical findings.

Indexed as

age of onsetcannabiscognitionpsychosisschizophrenia

Identifiers

PMID25477825
PMCPMC4235385
OpenAlexW1986116097

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.