Hostname: page-component-586b7cd67f-dsjbd Total loading time: 0 Render date: 2024-11-25T11:37:58.881Z Has data issue: false hasContentIssue false

Phenotypic and Genetic Analyses of a Short Measure of Psychosis-proneness in a Large-scale Australian Twin Study

Published online by Cambridge University Press:  21 February 2012

David A. Hay*
Affiliation:
School of Psychology, Curtin University of Technology and Mental Health Research Institute of Victoria. [email protected]
Nicholas G. Martin
Affiliation:
Queensland Institute of Medical Research and Joint Genetics Program, The University of Queensland.
Debra Foley
Affiliation:
Department of Psychiatry, Medical College of Virginia.
Susan A. Treloar
Affiliation:
Queensland Institute of Medical Research and Joint Genetics Program, The University of Queensland.
Katherine M. Kirk
Affiliation:
Queensland Institute of Medical Research and Joint Genetics Program, The University of Queensland.
Andrew C. Heath
Affiliation:
Department of Psychiatry, Washington University School of Medicine.
*
*Address for Correspondence: Professor David A. Hay, School of Psychology, Curtin University of Technology, GPO Box U 1987, Perth WA 6845, Australia.

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Previous genetic analyses of psychosis proneness have been limited by their small sample size. For the purposes of large-scale screening, a 12-item questionnaire was developed through a two-stage process of reduction from the full Chapman and Chapman scales. 3685 individuals (including 1438 complete twin pairs) aged 18–25 years and enrolled in the volunteer Australian Twin Registry returned a mail questionnaire which included this psychosis proneness scale and the Eysenck Personality Questionnaire. Despite the brevity of the questionnaire, item and factor analysis identified four unambiguous and essentially uncorrelated scales. There were (1) Perceptual Aberration – Magical Ideation; (2) Hypomania – Impulsivity/Nonconformity; (3) Social Anhedonia and (4) Physical Anhedonia. Model-fitting analyses showed additive genetic and specific environmental factors were sufficient for three of the four scales, with the Social Anhedonia scale requiring also a parameter for genetic dominance. There was no evidence for the previously hypothesised sex differences in the genetic determination of psychosis-proneness. The potential value of multivariate genetic analysis to examine the relationship between these four scales and dimensions of personality is discussed. The growing body of longitudinal evidence on psychosis-proneness suggests the value of incorporating this brief measure into developmental twin studies.

Type
Articles
Copyright
Copyright © Cambridge University Press 2001