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The genetic epidemiology of schizotypal personality disorder

Kendler, Kenneth S. ; Ohlsson, Henrik LU ; Sundquist, Jan LU and Sundquist, Kristina LU (2024) In Psychological Medicine
Abstract

Background. The concept of schizotypal personality disorder (SPD) emerged from observations of personality characteristics common in relatives of schizophrenic patients. While often studied in family designs, few studies and none with genetic measures, have examined SPD in epidemiological samples. Methods. We studied individuals born in Sweden 1940–2000 with an ICD-10 diagnosis of SPD with no prior schizophrenia (SZ) diagnosis (n = 2292). Demographic features, patterns of comorbidity, and Family Genetic Risk Scores (FGRS) were assessed from multiple Swedish registries. Prediction of progression to SZ was assessed by Cox models. Results. SPD was rare, with a prevalence of 0.044%, and had high levels of comorbidity with autism spectrum... (More)

Background. The concept of schizotypal personality disorder (SPD) emerged from observations of personality characteristics common in relatives of schizophrenic patients. While often studied in family designs, few studies and none with genetic measures, have examined SPD in epidemiological samples. Methods. We studied individuals born in Sweden 1940–2000 with an ICD-10 diagnosis of SPD with no prior schizophrenia (SZ) diagnosis (n = 2292). Demographic features, patterns of comorbidity, and Family Genetic Risk Scores (FGRS) were assessed from multiple Swedish registries. Prediction of progression to SZ was assessed by Cox models. Results. SPD was rare, with a prevalence of 0.044%, and had high levels of comorbidity with autism spectrum disorder (ASD), OCD, ADHD, and major depression (MD), and increased rates of being single, unemployed and in receipt of welfare. Affected individuals had elevated levels of FGRS for SZ (+0.42), ASD (+0.30), MD (+0.29), and ADHD (+0.20). Compared to cases of schizophrenia, they had significantly lower rates of FGRSSZ, but significantly elevated rates of genetic risk for ASD, MD, and ADHD. Over a mean follow-up of 8.7 years, 14.6% of SPD cases received a first diagnosis of SZ, the risk for which was significantly increased by levels of FGRSSZ, male sex, young age at SPD diagnosis and an in-patient SPD diagnosis and significantly decreased by comorbidity with MD, ASD, and ADHD. Conclusions. Our results not only support the designation of SPD as a schizophrenia spectrum disorder but also suggest potentially important etiologic links between SPD and ASD and, to a lesser extent, ADHD, OCD, and MD.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
epub
subject
keywords
comorbidity, conversion to schizophrenia, genetic risk, Schizotypal personality disorder, Sweden
in
Psychological Medicine
publisher
Cambridge University Press
external identifiers
  • pmid:38362845
  • scopus:85186255661
ISSN
0033-2917
DOI
10.1017/S0033291724000230
language
English
LU publication?
yes
id
d43330d3-16da-49ec-a64d-7b0375cfa521
date added to LUP
2024-03-27 10:43:43
date last changed
2024-04-24 14:37:54
@article{d43330d3-16da-49ec-a64d-7b0375cfa521,
  abstract     = {{<p>Background. The concept of schizotypal personality disorder (SPD) emerged from observations of personality characteristics common in relatives of schizophrenic patients. While often studied in family designs, few studies and none with genetic measures, have examined SPD in epidemiological samples. Methods. We studied individuals born in Sweden 1940–2000 with an ICD-10 diagnosis of SPD with no prior schizophrenia (SZ) diagnosis (n = 2292). Demographic features, patterns of comorbidity, and Family Genetic Risk Scores (FGRS) were assessed from multiple Swedish registries. Prediction of progression to SZ was assessed by Cox models. Results. SPD was rare, with a prevalence of 0.044%, and had high levels of comorbidity with autism spectrum disorder (ASD), OCD, ADHD, and major depression (MD), and increased rates of being single, unemployed and in receipt of welfare. Affected individuals had elevated levels of FGRS for SZ (+0.42), ASD (+0.30), MD (+0.29), and ADHD (+0.20). Compared to cases of schizophrenia, they had significantly lower rates of FGRS<sub>SZ</sub>, but significantly elevated rates of genetic risk for ASD, MD, and ADHD. Over a mean follow-up of 8.7 years, 14.6% of SPD cases received a first diagnosis of SZ, the risk for which was significantly increased by levels of FGRS<sub>SZ</sub>, male sex, young age at SPD diagnosis and an in-patient SPD diagnosis and significantly decreased by comorbidity with MD, ASD, and ADHD. Conclusions. Our results not only support the designation of SPD as a schizophrenia spectrum disorder but also suggest potentially important etiologic links between SPD and ASD and, to a lesser extent, ADHD, OCD, and MD.</p>}},
  author       = {{Kendler, Kenneth S. and Ohlsson, Henrik and Sundquist, Jan and Sundquist, Kristina}},
  issn         = {{0033-2917}},
  keywords     = {{comorbidity; conversion to schizophrenia; genetic risk; Schizotypal personality disorder; Sweden}},
  language     = {{eng}},
  publisher    = {{Cambridge University Press}},
  series       = {{Psychological Medicine}},
  title        = {{The genetic epidemiology of schizotypal personality disorder}},
  url          = {{http://dx.doi.org/10.1017/S0033291724000230}},
  doi          = {{10.1017/S0033291724000230}},
  year         = {{2024}},
}