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Original Investigation
September 2014

Consistent Etiology of Severe, Frequent Psychotic Experiences and Milder, Less Frequent Manifestations: A Twin Study of Specific Psychotic Experiences in Adolescence

Author Affiliations
  • 1Medical Research Council Social, Genetic and Developmental Psychiatry Centre, King’s College London, Institute of Psychiatry, London, England
  • 2Department of Psychiatry, University of Oxford, Oxford, England
  • 3Department of Psychology, University of Warwick, Coventry, England
  • 4Institute of Psychiatry, King’s College London, London, England
  • 5Academic Unit of Psychiatry and Behavioural Sciences, University of Leeds, Leeds, England
  • 6Centre for Brain and Cognitive Development, Birkbeck, University of London, London, England
JAMA Psychiatry. 2014;71(9):1049-1057. doi:10.1001/jamapsychiatry.2014.994
Abstract

Importance  The onset of psychosis is usually preceded by psychotic experiences (PE). Little is known about the etiology of PE and whether the degree of genetic and environmental influences varies across different levels of severity. A recognized challenge is to identify individuals at high risk of developing psychotic disorders prior to disease onset.

Objectives  To investigate the degree of genetic and environmental influences on specific PE, assessed dimensionally, in adolescents in the community and in those who have many, frequent experiences (defined using quantitative cutoffs). We also assessed the degree of overlap in etiological influences between specific PE.

Design, Setting, and Participants  Structural equation model-fitting, including univariate and bivariate twin models, liability threshold models, DeFries-Fulker extremes analysis, and the Cherny method, was used to analyze a representative community sample of 5059 adolescent twin pairs (mean [SD] age, 16.31 [0.68] years) from England and Wales.

Main Outcomes and Measures  Psychotic experiences assessed as quantitative traits (self-rated paranoia, hallucinations, cognitive disorganization, grandiosity, and anhedonia, as well as parent-rated negative symptoms).

Results  Genetic influences were apparent for all PE (15%-59%), with modest shared environment for hallucinations and negative symptoms (17%-24%) and significant nonshared environment (49%-64%) for the self-rated scales and 17% for parent-rated negative symptoms. Three empirical approaches converged to suggest that the etiology in extreme-scoring groups (most extreme scoring: 5%, 10%, and 15%) did not differ significantly from that of the whole distribution. There was no linear change in heritability across the distribution of PE, with the exception of a modest increase in heritability for increasing severity of parent-rated negative symptoms. Of the PE that showed covariation, this appeared to be due to shared genetic influences (bivariate heritabilities, 0.54-0.71).

Conclusions and Relevance  These findings are consistent with the concept of a psychosis continuum, suggesting that the same genetic and environmental factors influence both extreme, frequent PE and milder, less frequent manifestations in adolescents. Individual PE in adolescence, assessed quantitatively, have lower heritability estimates and higher estimates of nonshared environment than those for the liability to schizophrenia. Heritability varies by type of PE, being highest for paranoia and parent-rated negative symptoms and lowest for hallucinations.

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