An examination of the etiologic overlap between the genetic and environmental influences on insomnia and common psychopathology. Issue 5 (16th January 2017)

• Record Type: Journal Article
• Authors: Lind, Mackenzie J.; Hawn, Sage E.; Sheerin, Christina M.; Aggen, Steven H.; Kirkpatrick, Robert M.; Kendler, Kenneth S.; Amstadter, Ananda B.
• Is Part Of: Depression and anxiety. Volume 34:Issue 5(2017)
• Page Start: 453
• Page End: 462
• Publication Date: 2017-01-16
• Subjects: alcoholism/alcohol use disorders -- depression -- GAD/generalized anxiety disorder -- genetics -- sleep disorders -- twin studies; Anxiety -- Periodicals; Depression, Mental -- Periodicals; Depression -- Periodicals; Anxiety -- Periodicals; Anxiety Disorders -- Periodicals; 616.8527005
• DOI: 10.1002/da.22587
• Languages: English
• ISSNs: 1091-4269

Abstract

Abstract : Background: Insomnia is comorbid with internalizing and externalizing psychiatric disorders. However, the extent to which the etiologic influences on insomnia and common psychopathology overlap is unclear. There are limited genetically informed studies of insomnia and internalizing disorders and few studies of overlap exist with externalizing disorders. Methods: We utilized twin data from the Virginia Adult Twin Studies of Psychiatric and Substance Use Disorders (total n = 7, 500). Insomnia, internalizing disorders (major depressive disorder [MDD], generalized anxiety disorder [GAD]), and alcohol abuse or dependence (AAD) were assessed at two time points, while antisocial personality disorder (ASPD) was assessed once. Cholesky decompositions were performed in OpenMx and longitudinal measurement models were run on available phenotypes to reduce measurement error. Results: The latent additive genetic influences on insomnia overlapped significantly (56% for females, 74% for males) with MDD and were shared completely (100%) with GAD. There was significant overlap of latent unique environmental influences, with overlap ranging from 38 to 100% across disorders. In contrast, there was less genetic overlap between insomnia and externalizing disorders, with 18% of insomnia's heritability shared with AAD and 23% with ASPD. Latent unique environmental overlap between insomnia and both externalizing disorders was negligible. Conclusions: The evidence for substantial genetic overlap between insomnia and stable aspects of both internalizing disorders suggests that there may be few insomnia‐specific genes and investigation into unique environmental factors is important for understanding insomnia development. The modest overlap between insomnia and externalizing disorders indicates that these disorders are genetically related, but largely etiologically distinct.