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CHILDHOOD SEPARATION ANXIETY DISORDER AND ADULT ONSET PANIC ATTACKS SHARE A COMMON GENETIC DIATHESIS
Author(s) -
RobersonNay Roxann,
Eaves Lindon J.,
Hettema John M.,
Kendler Kenneth S.,
Silberg Judy L.
Publication year - 2012
Publication title -
depression and anxiety
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.634
H-Index - 129
eISSN - 1520-6394
pISSN - 1091-4269
DOI - 10.1002/da.21931
Subject(s) - diathesis , psychology , panic disorder , separation anxiety disorder , twin study , anxiety , clinical psychology , dizygotic twin , anxiety disorder , conduct disorder , psychiatry , generalized anxiety disorder , medicine , heritability , genetics , biology , immunology
Background 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. Methods Participants included parents and their monozygotic or dizygotic twins (n = 1,437 twin pairs) participating in the V irginia T win S tudy of A dolescent B ehavioral D evelopment and those twins who later completed the Y oung A dult F ollow‐ U p ( YAFU ). The C hild and A dolescent P sychiatric A ssessment was completed at three waves during childhood/adolescence followed by the S tructured C linical I nterview for DSM ‐ III ‐ R at the YAFU . Two separate, bivariate C holesky models were fit to childhood diagnoses of SAD and overanxious disorder ( OAD ), respectively, and their relation with AOPA ; a trivariate C holesky model also examined the collective influence of childhood SAD and OAD on AOPA . Results 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 C holesky reaffirmed outcomes of bivariate models . Conclusions 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 .