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 .
GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal effect of schizophrenia liability
Cannabis use is a heritable trait that has been associated with adverse mental health outcomes . In the largest genome-wide association study ( GWAS ) for lifetime cannabis use to date ( N = 184,765 ) , we identified eight genome-wide significant independent single nucleotide polymorphisms in six regions . All measured genetic variants combined explained 11 % of the variance . Gene-based tests revealed 35 significant genes in 16 regions , and S-PrediXcan analyses showed that 21 genes had different expression levels for cannabis users versus nonusers . The strongest finding across the different analyses was CADM2 , which has been associated with substance use and risk-taking . Significant genetic correlations were found with 14 of 25 tested substance use and mental health – related traits , including smoking , alcohol use , schizophrenia and risk-taking . Mendelian r and omization analysis showed evidence for a causal positive influence of schizophrenia risk on cannabis use . Overall , our study provides new insights into the etiology of cannabis use and its relation with mental health . A GWAS of lifetime cannabis use reveals new risk loci , shows that cannabis use has genetic overlap with smoking and alcohol use , and indicates that the likelihood of initiating cannabis use is causally influenced by schizophrenia
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 .