Klein Award Winner
CHILDHOOD SEPARATION ANXIETY DISORDER AND ADULT ONSET PANIC ATTACKS SHARE A COMMON GENETIC DIATHESIS
Article first published online: 27 MAR 2012
© 2012 Wiley Periodicals, Inc.
Depression and Anxiety
Volume 29, Issue 4, pages 320–327, April 2012
How to Cite
Roberson-Nay, R., Eaves, L. J., Hettema, J. M., Kendler, K. S. and Silberg, J. L. (2012), CHILDHOOD SEPARATION ANXIETY DISORDER AND ADULT ONSET PANIC ATTACKS SHARE A COMMON GENETIC DIATHESIS. Depress. Anxiety, 29: 320–327. doi: 10.1002/da.21931
- Issue published online: 17 APR 2012
- Article first published online: 27 MAR 2012
- Manuscript Accepted: 3 FEB 2012
- Manuscript Received: 2 FEB 2012
- separation anxiety disorder;
- panic attacks;
- twins; genetic;
Childhood separation anxiety disorder (SAD) is hypothesized to share etiologic roots with panic disorder. The aim of this study was to estimate the genetic and environmental sources of covariance between childhood SAD and adult onset panic attacks (AOPA), with the primary goal to determine whether these two phenotypes share a common genetic diathesis.
Participants included parents and their monozygotic or dizygotic twins (n = 1,437 twin pairs) participating in the Virginia Twin Study of Adolescent Behavioral Development and those twins who later completed the Young Adult Follow-Up (YAFU). The Child and Adolescent Psychiatric Assessment was completed at three waves during childhood/adolescence followed by the Structured Clinical Interview for DSM-III-R at the YAFU. Two separate, bivariate Cholesky models were fit to childhood diagnoses of SAD and overanxious disorder (OAD), respectively, and their relation with AOPA; a trivariate Cholesky model also examined the collective influence of childhood SAD and OAD on AOPA.
In the best-fitting bivariate model, the covariation between SAD and AOPA was accounted for by genetic and unique environmental factors only, with the genetic factor associated with childhood SAD explaining significant variance in AOPA. Environmental risk factors were not significantly shared between SAD and AOPA. By contrast, the genetic factor associated with childhood OAD did not contribute significantly to AOPA. Results of the trivariate Cholesky reaffirmed outcomes of bivariate models.
These data indicate that childhood SAD and AOPA share a common genetic diathesis that is not observed for childhood OAD, strongly supporting the hypothesis of a specific genetic etiologic link between the two phenotypes.