The results show that , in particular , frequent cannabis use , especially daily use , and the consumption of high-potency cannabis are associated with a higher risk of developing psychosis .
Moreover , several genotypes moderate the impact of cannabis use on psychosis risk , particularly those involved in the dopamine function , such as AKT1 .
Finally , cannabis use is associated with an earlier psychosis onset and increased risk of transition in individuals at a clinical high risk of psychosis .
These findings indicate that changing cannabis use behavior could be a harm reduction strategy employed to lower the risk of developing psychosis .
Increasing evidence indicates a relationship between  cannabis use and psychosis risk .
Specific factors , such as determinants of cannabis use or the genetic profile of cannabis users , appear to moderate this association .
The present systematic review presents a detailed and up-to- date literature overview on factors that influence the relationship between cannabis use and psychosis risk .
Assessing causality in associations between cannabis use and schizophrenia risk: a two-sample Mendelian randomization study
Background Observational associations between cannabis and schizophrenia are well documented , but ascertaining causation is more challenging . We used Mendelian r and omization ( MR ) , utilizing publicly available data as a method for ascertaining causation from observational data . Method We performed bi-directional two- sample MR using summary -level genome-wide data from the International Cannabis Consortium ( ICC ) and the Psychiatric Genomics Consortium ( PGC2 ) . Single nucleotide polymorphisms ( SNPs ) associated with cannabis initiation ( p < 10−5 ) and schizophrenia ( p < 5 × 10−8 ) were combined using an inverse-variance-weighted fixed-effects approach . We also used height and education genome-wide association study data  , representing negative and positive control analyses . Results There was some evidence consistent with a causal effect of cannabis initiation on risk of schizophrenia [ odds ratio ( OR ) 1.04 per doubling odds of cannabis initiation , 95 % confidence interval ( CI ) 1.01–1.07 , p = 0.019 ] . There was strong evidence consistent with a causal effect of schizophrenia risk on likelihood of cannabis initiation ( OR 1.10 per doubling of the odds of schizophrenia , 95 % CI 1.05–1.14 , p = 2.64 × 10−5 ) . Findings were as predicted for the negative control ( height : OR 1.00 , 95 % CI 0.99–1.01 , p = 0.90 ) but weaker than predicted for the positive control ( years in education : OR 0.99 , 95 % CI 0.97–1.00 , p = 0.066 ) analyses . Conclusions Our results provide some that cannabis initiation increases the risk of schizophrenia , although the size of the causal estimate is small . We find stronger evidence that schizophrenia risk predicts cannabis initiation , possibly as genetic instruments for schizophrenia are stronger than for cannabis initiation
The results show that , in particular , frequent cannabis use , especially daily use , and the consumption of high-potency cannabis are associated with a higher risk of developing psychosis .
Moreover , several genotypes moderate the impact of cannabis use on psychosis risk , particularly those involved in the dopamine function , such as AKT1 .
Finally , cannabis use is associated with an earlier psychosis onset and increased risk of transition in individuals at a clinical high risk of psychosis .
These findings indicate that changing cannabis use behavior could be a harm reduction strategy employed to lower the risk of developing psychosis .
Increasing evidence indicates a relationship between  cannabis use and psychosis risk .
Specific factors , such as determinants of cannabis use or the genetic profile of cannabis users , appear to moderate this association .
The present systematic review presents a detailed and up-to- date literature overview on factors that influence the relationship between cannabis use and psychosis risk .