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 .
Cannabis use and risk of schizophrenia: a Mendelian randomization study
Cannabis use is observationally associated with an increased risk of schizophrenia  , but whether the relationship is causal is not known . Using a genetic approach , we took 10 independent genetic variants previously identified to associate with cannabis use in 32 330 individuals to determine the nature of the association between cannabis use and risk of schizophrenia . Genetic variants were employed as instruments to recapitulate a r and omized controlled trial involving two groups (  cannabis users vs nonusers ) to estimate the causal effect of cannabis use on risk of schizophrenia  in 34 241 cases and 45 604 controls from predominantly European descent . Genetically-derived estimates were compared with a meta- analysis of observational studies reporting ever use of cannabis and risk of schizophrenia or related disorders . Based on the genetic approach , use of cannabis was associated with increased risk of schizophrenia ( odds ratio ( OR ) of schizophrenia for users vs nonusers of cannabis : 1.37 ; 95 % confidence interval ( CI ) , 1.09–1.67 ; P-value=0.007 ) . The corresponding estimate from observational analysis was 1.43 ( 95 % CI , 1.19–1.67 ; P-value for heterogeneity = 0.76 ) . The genetic markers did not show evidence of pleiotropic effects and accounting for tobacco exposure did not alter the association ( OR of schizophrenia for users vs nonusers of cannabis , adjusted for ever vs never smoker : 1.41 ; 95 % CI , 1.09–1.83 ) . This adds to the substantial evidence base that has previously identified cannabis use to associate with increased risk of schizophrenia , by suggesting that the relationship is causal . Such robust evidence may inform public health messages about cannabis use , especially regarding its potential mental health consequences
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 .