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Population-based, multi-generational family clustering study of social anxiety disorder and avoidant personality disorder

Published online by Cambridge University Press:  12 September 2014

K. Isomura
Affiliation:
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
M. Boman
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
C. Rück
Affiliation:
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
E. Serlachius
Affiliation:
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
H. Larsson
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
P. Lichtenstein
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
D. Mataix-Cols*
Affiliation:
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
*
*Address for correspondence: Professor D. Mataix-Cols, Ph.D., Department of Clinical Neuroscience, Karolinska Institutet, Child and Adolescent Psychiatry Research Center, Gävlegatan 22 (Entré B), floor 8 SE-11330 Stockholm, Sweden. (Email: david.mataix.cols@ki.se)

Abstract

Background

We aimed to provide unbiased estimates of familial risk and heritability of social anxiety disorder (SAD) and avoidant personality disorder (AVPD).

Method

We identified 18 399 individuals diagnosed with SAD and 2673 with AVPD in the Swedish National Patient Register between 1997 and 2009. Risks (odds ratios; OR) for SAD in all biological and non-biological relatives of probands, compared to relatives of unaffected individuals were calculated. We also estimated the risks for AVPD in relatives of probands with SAD.

Results

The risk for SAD among relatives of SAD probands increased proportionally to the degree of genetic relatedness. The risks for first-degree relatives [OR 4.74, 95% confidence interval (CI) 4.28–5.25] were significantly higher than for second-degree and third-degree relatives. Second-degree relatives (OR 2.30, 95% CI 2.01–2.63) had significantly higher risk than third-degree relatives (OR 1.72, 95% CI 1.52–1.94). Relatives at similar genetic distances had similar risks for SAD, despite different degrees of shared environment. Heritability was estimated to be approximately 56%. There were no significant sex differences in the familial patterns. The risk of AVPD in relatives of SAD probands was significantly elevated, even after excluding individuals with both diagnoses (first-degree OR 3.54, second-degree OR 2.20, third-degree OR 1.62). Non-biological relatives (spouses/partners) also had elevated risks for both SAD (OR 4.01) and AVPD (OR 3.85).

Conclusions

SAD clusters in families primarily due to genetic factors. SAD and AVPD are aetiologically related and may represent different expressions of the same vulnerability. The strong marital concordance observed in SAD/AVPD may indicate assortative mating but the exact mechanisms and implications require further investigation.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2014 

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