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Delineating factors associated with vulnerability to psychosis in young people Open Access


Other title
obstetric complication
cannabis use
adverse childhood experience
psychosis vulnerability
psychosis proneness
prenatal maternal stressor
Type of item
Degree grantor
University of Alberta
Author or creator
Roper, Leslie J
Supervisor and department
Purdon, Scot E. (Psychiatry)
Aitchison, Katherine J. (Psychiatry and Medical Genetics)
Examining committee member and department
Baker, Glen B. (Psychiatry)
Purdon, Scot E. (Psychiatry)
Aitchison, Katherine J. (Psychiatry and Medical Genetics)
Colman, Ian (Epidemiology, Public Health and Preventive Medicine)
Department of Psychiatry

Date accepted
Graduation date
Master of Science
Degree level
Introduction: The etiology of psychosis is complex and appears to be the result of the confluence of several predisposing influences, such as obstetric complications, prenatal life events, life adversity and/or trauma and substance use, in particular cannabis use, operating on top of genetic risk. We sought to assess a group of local adolescents to see if their experience of these predisposing influences might predict their scores on scales of psychosis proneness. Methods: Participants were high school students from Edmonton and the surrounding area (n = 221). Psychosis proneness was assessed using the Magical Ideation Scale (MIS), a measure of positive schizotypy, and the Social Anhedonia Scale (SAS), a measure of negative schizotypy. Predisposing factors were assessed by a measure of adverse events (AEs) and a questionnaire on cannabis use. In addition, 73 participants agreed to have their mothers complete a questionnaire regarding obstetric complications (OCs) and prenatal life events or maternal stressors (PNMS). Results: AEs were common, with 91% endorsing at least one and 69% endorsing multiple events. AEs were associated with scores on the MIS (standardized β = 0.32, p < 0.001), but not on the SAS. Fifty-four percent of mothers endorsed at least one OC and 59% endorsed at least one PNMS. No association was found between OCs or PNMS and MIS or SAS score. Thirty-four percent of participants endorsed cannabis use at least once in their lifetime, and 17% endorsed having used in the past 30 days. Cannabis use at least once in lifetime was associated with MIS score (standardized β = 0.18, p = 0.006), but not with SAS score. AEs were also associated with cannabis use (standardized β = 0.26, p < 0.001). In combining predisposing factors to attempt to augment the association, AEs combined with PNMS resulted in an adjusted R2 of 0.12 for an association with MIS, an increase over the adjusted R2 for AEs alone (R2 = 0.10). Similarly, when AEs were combined with OCs, the adjusted R2 was 0.12 for association with MIS. Discussion: AEs and cannabis use were highly associated with scores on the MIS, linking positive schizotypy to life adversity and cannabis use, as anticipated. However, AEs were also associated with cannabis use, suggesting perhaps the cannabis link is mediated by AEs. However, it is important to note both associations as both have individually been linked to psychosis, particularly when cannabis use is begun earlier in life. As the evidence for a link of OCs and PNMS with psychosis is strong, the lack of results here was unanticipated. However, when added to AEs, they improved the predictive model for MIS score, and therefore may be acting as additional life stressors. No risk factor was found to be associated with SAS. It is possible that the MIS is more sensitive to environmental influences of psychosis proneness, whereas the SAS might be more sensitive to a genetic predisposition. Of note, AEs were very highly endorsed in this study compared to global and recent local analyses. This may indicate a problem with data collection in our study, over-endorsement by the participants, or possibly an indication that other measures are not capturing full endorsement in their assessments. Further research should consider the associations of each of these risk factors and how interactions are affecting the proneness model. Biological and psychological mechanisms whereby these vulnerabilities affect proneness should be considered.
Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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