Evidence for genetic influences common and specific to symptoms of generalized anxiety and panic

被引:85
作者
Scherrer, JF [1 ]
True, WR
Xian, H
Lyons, MJ
Eisen, SA
Goldberg, J
Lin, N
Tsuang, MT
机构
[1] St Louis Univ, Hlth Sci Ctr, Sch Publ Hlth, St Louis, MO 63103 USA
[2] St Louis VAMC 151JC, Res & Med Serv, St Louis, MO 63106 USA
[3] Washington Univ, Dept Med, Div Gen Med Sci, St Louis, MO USA
[4] Dept Vet Affairs, Hlth Serv Res & Dev Serv, Hines, IL USA
[5] Univ Illinois, Sch Publ Hlth, Program Epidemiol, Chicago, IL USA
[6] Boston Univ, Dept Psychol, Boston, MA 02215 USA
[7] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA
[8] Brockton W Roxbury VA, Boston, MA 02115 USA
[9] Harvard Univ, Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA
[10] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Mental Hlth Ctr, Boston, MA 02115 USA
关键词
twins; generalized anxiety; panic; males;
D O I
10.1016/S0165-0327(99)00031-2
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Generalized anxiety disorder (GAD) and panic disorder (PD) often co-occur and have been shown to be heritable. Researchers have debated the validity of the distinction between GAD and PD. To test for distinction between disorders, we estimated the genetic and environmental contributions which were specific and common to GAD and PD in a cohort of male-male twin pairs. Methods: Data were obtained from a telephone interview performed in 1992 utilizing the Diagnostic Interview Schedule Version 3-Revised. Interviews were administered to 6724 male-male monozygotic and dizygotic twin pair members of the Vietnam Era Twin Registry. We defined lifetime GAD by the report of six or more DSM-III-R symptoms and lifetime PD by the report of four or more DSM-III-R symptoms. Results: The lifetime co-occurrence of GAD and PD was best explained by a model which did not include family environmental influences. The variance in risk for GAD was due to a 37.9% influence from additive genetic factors with the remainder due to unique environmental influences. The variance in risk for PD was due to a 22.6% additive genetic contribution which was common with GAD and a 21.2% non-additive genetic contribution specific to PD with the remainder of variance in risk for PD due to unique environmental influences. Limitations: Results may be limited to middle aged males. Model fitting with full diagnostic criteria was not possible due to low prevalences. Conclusions: Our data suggest a distinction in liability for GAD versus PD. The common genetic influence to GAD and PD may partially account for the risk of the co-occurrence of these disorders in a lifetime. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:25 / 35
页数:11
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