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Psychotic experiences, alcohol–cannabis abuse, stressful events and familial risk is associated with onset of clinical psychosis: Evidence from a 6-year longitudinal population-based cohort
Published online by Cambridge University Press: 23 March 2020
Abstract
Both clinical and subclinical psychosis is probably a consequence of underlying genetic and environmental interactions.
Defining differential impact of environmental/familial risk factors and psychotic experiences across the onset of clinical psychosis.
To assess mental health outcomes in a 6-year follow-up of a representative general population sample with a special focus on extended psychosis phenotype.
Addresses were contacted in multistage clustered area probability sampling frame covering 9 districts and 302 neighbourhoods (n: 4011) at baseline (T1) and 6 years after (n: 2142) (T2). Psychotic experiences were screened with Composite International Diagnostic Interview and probable cases were re-interviewed with SCID-I. Relations were tested using logistic regression models.
Of subclinical psychotic symptoms at baseline, 6.4% transitioned to clinical psychosis; 44.4% persisted, 90.2% transitioned to any DSM disorder. Of newly onset clinical psychosis at T2, 62.8% had subclinical psychotic expressions at baseline. The risk of developing clinical psychosis was greater in those with baseline subclinical psychotic experiences, alcohol–cannabis abuse, stressful-forensic event history and family history of mental disorders. Most of risk factors associated with psychosis proneness at T1 were also associated with clinical psychotic outcome at T2 (Table 1).
Psychotic experiences takes attention for the risk to develop psychosis due to underlying genetic and environmental interactions; also may be an important risk factor to develop any mental disorder.
The authors have not supplied their declaration of competing interest.
- Type
- EW408
- Information
- European Psychiatry , Volume 33 , Issue S1: Abstracts of the 24th European Congress of Psychiatry , March 2016 , pp. S216 - S217
- Copyright
- Copyright © European Psychiatric Association 2016
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