A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness–persistence–impairment model of psychotic disorder
2008/07/08 by Jim van Os, J. van Os, Richard J. Linscott +7 · 2,379 citations
Medicine · Psychology · #Bipolar Disorder and Treatment #Clinical psychology #Environmental health #Incidence (geometry) #Internal medicine #Medicine #Meta-analysis #Obsessive-Compulsive Spectrum Disorders #Persistence (discontinuity) #Population #Psychiatry #Psychology #Psychosis #Schizophrenia (object-oriented programming) #Schizophrenia research and treatment #Subclinical infection
paper · open access · doi:10.1017/s0033291708003814
published in Psychological Medicine 39(2), 179-195 (Cambridge University Press)
openalex publication_date 2008/07/08 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
Abstract
A systematic review of all reported incidence and prevalence studies of population rates of subclinical psychotic experiences reveals a median prevalence rate of around 5% and a median incidence rate of around 3%. A meta-analysis of risk factors reveals associations with developmental stage, child and adult social adversity, psychoactive drug use, and also male sex and migrant status. The small difference between prevalence and incidence rates, together with data from follow-up studies, indicates that approximately 75-90% of developmental psychotic experiences are transitory and disappear over time. There is evidence, however, that transitory developmental expression of psychosis (psychosis proneness) may become abnormally persistent (persistence) and subsequently clinically relevant (impairment), depending on the degree of environmental risk the person is additionally exposed to. The psychosis proneness-persistence-impairment model considers genetic background factors impacting on a broadly distributed and transitory population expression of psychosis during development, poor prognosis of which, in terms of persistence and clinical need, is predicted by environmental exposure interacting with genetic risk.
Citations
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