Relationships Among Avoidant Personality Disorder, Social Anxiety Disorder, and Normative Personality Traits: A Twin Study

2019 ◽  
Vol 33 (3) ◽  
pp. 289-309 ◽  
Author(s):  
Audun Welander-Vatn ◽  
Fartein Ask Torvik ◽  
Nikolai Czajkowski ◽  
Kenneth S. Kendler ◽  
Ted Reichborn-Kjennerud ◽  
...  

Avoidant personality disorder (AvPD) and social anxiety disorder (SAD) share risk factors to a substantial degree, and both are characterized by the experience of anxiety in social situations. The authors investigated whether these disorders are differentially related to the Big Five personality traits. They also examined the underlying genetic and environmental influences on these associations. A population-based sample of 1,761 female twins was interviewed at baseline, and 1,471 of these were re-interviewed 10 years later. Associations between AvPD, SAD, and personality traits were investigated with multivariate biometric analyses. The authors found that AvPD and SAD are differentially related to several personality traits at the phenotypic, genetic, and environmental level. The genetic and environmental liability to AvPD could be fully accounted for by the genetic and environmental factors influencing SAD and personality. The findings may increase current etiological understanding of these disorders and inform future classification and treatment efforts.

2014 ◽  
Vol 45 (8) ◽  
pp. 1581-1589 ◽  
Author(s):  
K. Isomura ◽  
M. Boman ◽  
C. Rück ◽  
E. Serlachius ◽  
H. Larsson ◽  
...  

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


PLoS ONE ◽  
2017 ◽  
Vol 12 (11) ◽  
pp. e0188024 ◽  
Author(s):  
Michael M. Havranek ◽  
Fleur Volkart ◽  
Bianca Bolliger ◽  
Sophie Roos ◽  
Maximilian Buschner ◽  
...  

2012 ◽  
Vol 26 (6) ◽  
pp. 665-672 ◽  
Author(s):  
Luana Marques ◽  
Eliora Porter ◽  
Aparna Keshaviah ◽  
Mark H. Pollack ◽  
Michael Van Ameringen ◽  
...  

2016 ◽  
Vol 125 (1) ◽  
pp. 114-124 ◽  
Author(s):  
Fartein Ask Torvik ◽  
Audun Welander-Vatn ◽  
Eivind Ystrom ◽  
Gun Peggy Knudsen ◽  
Nikolai Czajkowski ◽  
...  

2019 ◽  
Vol 93 (1) ◽  
pp. 88-104 ◽  
Author(s):  
Frederik Weischer Frandsen ◽  
Sebastian Simonsen ◽  
Stig Poulsen ◽  
Per Sørensen ◽  
Marianne Engelbrecht Lau

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ariane Wiegand ◽  
Benjamin Kreifelts ◽  
Matthias H. J. Munk ◽  
Nadja Geiselhart ◽  
Katia E. Ramadori ◽  
...  

AbstractSocial anxiety disorder (SAD) is a psychiatric disorder characterized by extensive fear in social situations. Multiple genetic and environmental factors are known to contribute to its pathogenesis. One of the main environmental risk factors is early life adversity (ELA). Evidence is emerging that epigenetic mechanisms such as DNA methylation might play an important role in the biological mechanisms underlying SAD and ELA. To investigate the relationship between ELA, DNA methylation, and SAD, we performed an epigenome-wide association study for SAD and ELA examining DNA from whole blood of a cohort of 143 individuals using DNA methylation arrays. We identified two differentially methylated regions (DMRs) associated with SAD located within the genes SLC43A2 and TNXB. As this was the first epigenome-wide association study for SAD, it is worth noting that both genes have previously been associated with panic disorder. Further, we identified two DMRs associated with ELA within the SLC17A3 promoter region and the SIAH3 gene and several DMRs that were associated with the interaction of SAD and ELA. Of these, the regions within C2CD2L and MRPL28 showed the largest difference in DNA methylation. Lastly, we found that two DMRs were associated with both the severity of social anxiety and ELA, however, neither of them was found to mediate the contribution of ELA to SAD later in life. Future studies are needed to replicate our findings in independent cohorts and to investigate the biological pathways underlying these effects.


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