1. confounders
    1. socioeconomic (Philip and Johnson)
    2. demographic
    3. common genetic factors (Tsung)
    4. dysregulation of neural circuitory mediating drug reward and reinforcement (Chambers, 01)
  2. hypotheses
    1. vulnerability hypothesis
      1. Use of cannabis actually increases the risk of S
      2. predicts the risk of S should be higher in users
    2. self medication hypothesis
      1. Pt with S take drugs to reduce S/S or ADR
  3. support
    1. cannabis intox leads to brief psycho episode (mahters and godse)
    2. or recurrence of psychosis in people with history of psychosis
    3. IV THC exacerbates +ve s/s in pt and induces them in controls (D'Douza 2000)
    4. NEUROIMAGING
      1. lllar in Fn network impaired by cannabis and those implicated in pathogenesis of S (leuber, todd, 99)
    5. cannabinoid agonists impair cog that are hallmark s/s of S (Emrich, 97)
    6. ENDOGENOUS CANNABINOIDS
      1. ? aetiological role in S
      2. Increase in CSF of S, independent of age, gender or Rx (Leweke, 99)
    7. POST MORTEM STUDIES
      1. Increase binding of CRA in DLPFC of S independent of recent use (Dean 01)
      2. Increases binding of CRA in cingulate cortex of S compared with controls (Zavitsanou)
  4. Sweedish Conscript Cohort (Andreasson, 87)
  5. Other studies
    1. subjects with high vulnerability would report more perceived hostility, strange or unusual impressions (Amorin)
    2. experience sampling (Verdoux, 03)
      1. acute effects of cannabis were modified by vulnerability of psychosis
    3. Neuroimaging
      1. use before age 17 -- low % of cortical grey matter (Wilson, 2000)
    4. Mathematecal modelling study
      1. - cannabis ppt psychosis in vulnerables - use is more likely in S - DID NOT SUPPORT CAUSAL LINK (dEGENHARDT 03)
  6. SR & MA (Semple, Lawrie, McIntosh, 05)
    1. case- contol studies (11)
      1. consistent unadj OR acoss all pop group studied NO BIAS, NO HETEROGENITY
      2. MA of OR (7)
        1. SIMILAR fixed and random effects OR
    2. 6 case control Studies that rated psychotic S/s in users compared to non-useres
      1. High risk pop
        1. did not find increased risk ; possible dose-response relationship
      2. general pop (LARGEST CROSS-SEC STUDY, dEGENHARDT 01)
        1. POSSIBLE dose related effect
    3. Prosp long study (Furguson, 03)
      1. Greater vuln to cannabis in early adolescence
  7. Floating Topic
  8. initial evidence of asso of cannabis and psychosis (Bowers 01)
    1. case reports of cannabis preceeding schizohrenia
    2. psychosis in community survey of cannabis users
    3. obs studies of psychosis in cannabis users
ā€ˇCannabis and ā€ˇpsychosisā€ˇinitial evidence of asso of ā€ˇcannabis and psychosis (Bowers ā€ˇ01)ā€ˇcase reports of cannabis preceeding ā€ˇschizohreniaā€ˇpsychosis in community survey of ā€ˇcannabis usersā€ˇobs studies of psychosis in cannabis usersā€ˇconfounders ā€ˇsocioeconomic (Philip and Johnson)ā€ˇdemographicā€ˇcommon genetic factors (Tsung)ā€ˇdysregulation of neural circuitory ā€ˇmediating drug reward and ā€ˇreinforcement (Chambers, 01)ā€ˇhypothesesā€ˇvulnerability hypothesisā€ˇUse of cannabis actually increases the ā€ˇrisk of Sā€ˇpredicts the risk of S should be higher in ā€ˇusers ā€ˇself medication hypothesisā€ˇPt with S take drugs to reduce S/S or ADRā€ˇsupportā€ˇcannabis intox leads to brief psycho ā€ˇepisode (mahters and godse)ā€ˇor recurrence of psychosis in people with ā€ˇhistory of psychosisā€ˇIV THC exacerbates +ve s/s in pt and ā€ˇinduces them in controls (D'Douza 2000)ā€ˇNEUROIMAGINGā€ˇlllar in Fn network impaired by cannabis ā€ˇand those implicated in pathogenesis of ā€ˇS (leuber, todd, 99)ā€ˇcannabinoid agonists impair cog that are ā€ˇhallmark s/s of S (Emrich, 97)ā€ˇENDOGENOUS CANNABINOIDSā€ˇ? aetiological role in Sā€ˇIncrease in CSF of S, independent of age, ā€ˇgender or Rx (Leweke, 99)ā€ˇPOST MORTEM STUDIESā€ˇIncrease binding of CRA in DLPFC of S ā€ˇindependent of recent use (Dean 01)ā€ˇIncreases binding of CRA in cingulate ā€ˇcortex of S compared with controls (ā€ˇZavitsanou)ā€ˇSweedish Conscript Cohort (Andreasson, ā€ˇ87)ā€ˇOther studiesā€ˇsubjects with high vulnerability would ā€ˇreport more perceived hostility, strange ā€ˇor unusual impressions (Amorin)ā€ˇexperience sampling (Verdoux, 03)ā€ˇacute effects of cannabis were modified ā€ˇby vulnerability of psychosisā€ˇNeuroimagingā€ˇuse before age 17 -- low % of cortical ā€ˇgrey matter (Wilson, 2000)ā€ˇMathematecal modelling studyā€ˇ- cannabis ppt psychosis in vulnerables - ā€ˇuse is more likely in S - DID NOT SUPPORT ā€ˇCAUSAL LINK (dEGENHARDT 03)ā€ˇSR & MA (Semple, Lawrie, McIntosh, 05)ā€ˇcase- contol studies (11)ā€ˇconsistent unadj OR acoss all pop group ā€ˇstudied NO BIAS, NO HETEROGENITYā€ˇMA of OR (7)ā€ˇSIMILAR fixed and random effects ORā€ˇ6 case control Studies that rated ā€ˇpsychotic S/s in users compared to non-ā€ˇuseresā€ˇHigh risk popā€ˇdid not find increased risk ; possible dose-ā€ˇresponse relationshipā€ˇgeneral pop (LARGEST CROSS-SEC ā€ˇSTUDY, dEGENHARDT 01)ā€ˇPOSSIBLE dose related effectā€ˇProsp long study (Furguson, 03)ā€ˇGreater vuln to cannabis in early ā€ˇadolescenceā€ˇFloating Topic
Note