Causal association between cannabis and psychosis: examination of the evidence

Arseneault, Louise; Cannon, Mary; Witton, John; Murray, Robin M.

doi:10.1192/bjp.184.2.110

Cited by 768 publications

(236 citation statements)

References 40 publications

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“…This is consistent with earlier examinations of the cannabis–psychosis relationship (Andreasson, Allebeck, Engstrom, & Rydberg, 1987; Arseneault, Cannon, Witton, & Murray, 2004; Arseneault et al., 2002; Compton et al., 2009; Di Forti et al., 2009, 2014; Kelley et al., 2016; McLaren, Silins, Hutchinson, Mattick, & Hall, 2010; Moore et al., 2007) (for a meta‐analysis, see Large, Sharma, Compton, Slade, & Nielssen, 2011). The effect of gender on AoP was significant in our study, with males being at risk of developing psychosis earlier than females.…”

Section: Discussionsupporting

confidence: 91%

Investigation of the COMT Val158Met variant association with age of onset of psychosis, adjusting for cannabis use

et al. 2017

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Objective COMT rs4680 (Val158Met) genotype moderates the effect of cannabis on the age of onset of psychosis (AoP). We investigated the association between rs4680 and AoP, after adjusting for relevant covariates, in a Canadian Caucasian sample.MethodsOne hundred and sixty‐nine subjects with psychosis were recruited. AoP, defined as age of DSM‐IV diagnosis was established using the Structured Clinical Interview for DSM‐IV. Cannabis use data were collected using a self‐report computerized questionnaire. DNA was extracted from saliva and genotyping of the COMT Val158Met polymorphism was done by SNaPshot and TaqMan assays. Logistic regression and Kaplan–Meier analysis results are reported.ResultsIn those who had used cannabis before 20 years of age, rs4680 had a trend level effect on AoP (median AoP: Val/Val < Val/Met < Met/Met 19.37, 20.95, 21.24 years, respectively; log‐rank test p = .051).ConclusionOur data are indicative of the need to further investigate the association between the COMT rs4680 variant and AoP in the context of adolescent cannabis use.

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Section: Discussionsupporting

confidence: 91%

Investigation of the COMT Val158Met variant association with age of onset of psychosis, adjusting for cannabis use

et al. 2017

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“…Nonetheless, such a result would be consistent with our results, because one might predict that complete blockade of emotional learning with a CB1 antagonist, as with abnormal potentiation of typically nonsalient stimuli with a CB1 agonist, would be profoundly disruptive to emotional learning processes. Indeed, cannabis use has been identified as a major risk factor in the development of schizophrenia (Arsenault et al, 2004;Semple et al, 2005). This evidence, combined with the reported abnormalities in CB1 receptor expression and in the levels of endogenous cannabinoids in schizophrenia subjects (Dean et al, 2001;Giuffrida et al, 2004;Zavitsanou et al, 2004), further implicates this system as a potential mediator of the aberrant emotional processing observed in this disorder.…”

Section: Discussionmentioning

confidence: 77%

Cannabinoids Potentiate Emotional Learning Plasticity in Neurons of the Medial Prefrontal Cortex through Basolateral Amygdala Inputs

Laviolette

Grace

2006

Journal of Neuroscience

165

144

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Cannabinoids represent one of the most commonly used hallucinogenic drug classes. In addition, cannabis use is a primary risk factor for schizophrenia in susceptible individuals and can potently modulate the emotional salience of sensory stimuli. We report that systemic activation or blockade of cannabinoid CB1 receptors modulates emotional associative learning and memory formation in a subpopulation of neurons in the mammalian medial prefrontal cortex (mPFC) that receives functional input from the basolateral amygdala (BLA). Using in vivo single-unit recordings in rats, we found that a CB1 receptor agonist potentiated the response of medial prefrontal cortical neurons to olfactory cues paired previously with a footshock, whereas this associative responding was prevented by a CB1 receptor antagonist. In an olfactory fear-conditioning procedure, CB1 agonist microinfusions into the mPFC enabled behavioral responses to olfactory cues paired with normally subthreshold footshock, whereas the antagonist completely blocked emotional learning. These results are the first demonstration that cannabinoid signaling in the mPFC can modulate the magnitude of neuronal emotional learning plasticity and memory formation through functional inputs from the BLA.

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“…Indeed, prenatal cannabinoid exposure is associated with lower IQs and delinquent behaviors in children [2,3]. Moreover, adolescent cannabis use is associated with an increased risk of developing schizophrenia and/or accelerated onset of symptoms [5,46,47,48,49]. Emerging evidence suggests that cannabinoid exposure may have complex interactions with genetic factors associated with schizophrenia and other neuropsychiatric disorders (reviewed in [50,51]), such as the link between CNR1 gene polymorphisms and cannabinoid exposure on both brain structure and clinical outcome in schizophrenia patients [30].…”

Section: Discussionmentioning

confidence: 99%

THC Treatment Alters Glutamate Receptor Gene Expression in Human Stem Cell-Derived Neurons

et al. 2017

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Given the cognitive and behavioral effects following in utero Δ9-tetrahydrocannabinol (THC) exposure that have been reported in humans and rodents, it is critical to understand the precise consequences of THC on developing human neurons. Here, we utilize excitatory neurons derived from human-induced pluripotent stem cells (hiPSCs), and report that in vitro THC exposure reduced expression of glutamate receptor subunit genes (GRIA1, GRIA2, GRIN2A, and GRIN2B). By expanding these studies across hiPSC-derived neurons from individuals with a variety of genotypes, we believe that a hiPSC-based model will facilitate studies of the interaction of THC exposure and the genetic risk factors underlying neuropsychiatric disease vulnerability.

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Causal association between cannabis and psychosis: examination of the evidence

Abstract: Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Research is needed to understand the mechanisms by which cannabis causes psychosis.

Cited by 768 publications

References 40 publications

Investigation of the COMT Val158Met variant association with age of onset of psychosis, adjusting for cannabis use

Investigation of the COMT Val158Met variant association with age of onset of psychosis, adjusting for cannabis use

Cannabinoids Potentiate Emotional Learning Plasticity in Neurons of the Medial Prefrontal Cortex through Basolateral Amygdala Inputs

THC Treatment Alters Glutamate Receptor Gene Expression in Human Stem Cell-Derived Neurons

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