Onset of clinical psychosis in relation to baseline psychotic experiences, alcohol-cannabis use, stressful events and familial risk in a 6 years prospective population-based cohort study

INTRODUCTION: Psychosis, both clinical and subclinical forms, is probably a consequence of underlying genetic and environmental interactions. Psychosis proneness is considered to express in the form of psychotic experiences in early stages. OBJECTİVES: Defining differential impact of environmental/familial risk factors and psychotic experiences across the onset of clinical psychosis METHODS: A representative sample of the urban adult population of İzmir covering 11 districts and 302 neighbourhoods was visited at baseline (T1) and 6 years after (T2). Psychotic experiences were screened with Composite International Diagnostic Interview 2.1 and probable cases were clinically re-interviewed. Associations between independent variables (sociodemographic and socioeconomic properties, alcohol and cannabis use, stressful life events, family history of psychiatric disorders, subclinical psychotic experiences/symptoms in T1) and newly onset clinical psychosis were analysed. Logistic regression yielding odds ratios [ORs] and 95% CIs was used to examine associations adjusted for sociodemographic and properties regression models adjusted for sociodemographic and socioeconomic properties. RESULTS: Of the sample interviewed T1 (n: 4011), 2566 individuals (65.1%) were contacted and 2142 were re-interviewed. Of subclinical psychotic symptoms at T1, 6.4% transitioned to clinical psychosis. Of newly onset clinical psychosis at T2, 63% had psychotic experiences at T1. Sociodemographic and socioeconomic properties, psychotic experiences at T1 (χ²= 93.6, p<0,01), risky alcohol consumption for the last six years (OR: 4.8, %95 CI: 1.8-12.6, p<0,01), at least 5 times cannabis use (OR: 24.5, %95 CI: 2.2-275.4, p<0,01), number of stressful life events exposed (β=7.75; %95 CI: 0.01-0.02; p<0,01), history of forensic events (OR: 3.1, % 95 CI: 1.1-8.4, p<0.05), family history of depression/anxiety disorder (OR:7.3, %95 CI:3.0-17.7, p<0.01), family history of plausible psychosis (OR: 12.0, %95CI: 3.8-37.7, p<0.01) were significantly associated with onset of clinical psychosis. Cannabis use was associated with psychosis risk in dose-response manner. Although quitting cannabis decreased psychosis risk, significant proportion of the risk remained. CONCLUSIONS: Most of familial and environmental risk factors associated with psychotic experiences at T1 were also associated with clinical psychotic outcome at T2. This finding suggests an etiological continuum between psychotic experiences and clinical psychosis. Most of newly onset clinical psychosis was preceded by psychotic experiences in early stages. Therefore, a significant proportion of clinical psychosis may be conceptualized as the rare poor outcome of psychotic experiences.