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VOLUME 38, ISSUE 01

HERITABILITY OF INSOMNIA PROGRESSION DURING CHILDHOOD/ADOLESCENCE
The Heritability of Insomnia Progression during Childhood/Adolescence: Results from a Longitudinal Twin Study

http://dx.doi.org/10.5665/sleep.4334

Nicola L. Barclay, PhD1; Philip R. Gehrman, PhD2; Alice M. Gregory, PhD3; Lindon J. Eaves, PhD4; Judy L. Silberg, PhD5

1Northumbria Centre for Sleep Research, Department of Psychology, Northumbria University, UK; 2Department of Psychiatry and Penn Sleep Centre, University of Pennsylvania, Philadelphia, PA; 3Department of Psychology, Goldsmiths, University of London, UK; 4Virginia Institute for Psychiatric and Behavioral Genetics, Richmond, VA; 5Virginia Commonwealth University School of Medicine, Richmond, VA



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Study Objectives:

To determine prevalence and heritability of insomnia during middle/late childhood and adolescence; examine longitudinal associations in insomnia over time; and assess the extent to which genetic and environmental factors on insomnia remain stable, or whether new factors come into play, across this developmental period.

Design:

Longitudinal twin study.

Setting:

Academic medical center.

Patients or Participants:

There were 739 complete monozygotic twin pairs (52%) and 672 complete dizygotic twin pairs (48%) initially enrolled and were followed up at three additional time points (waves). Mode ages at each wave were 8, 10, 14, and 15 y (ages ranged from 8–18 y).

Interventions:

None.

Measurements and Results:

Clinical ratings of insomnia symptoms were assessed using the Child and Adolescent Psychiatric Assessment (CAPA) by trained clinicians, and rated according to Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition—Revised criteria for presence of “clinically significant insomnia,” over four sequential waves. Insomnia symptoms were prevalent but significantly decreased across the four waves (ranging from 16.6% to 31.2%). “Clinically significant insomnia” was moderately heritable at all waves (h2 range = 14% to 38%), and the remaining source of variance was the nonshared environment. Multivariate models indicated that genetic influences at wave 1 contributed to insomnia at all subsequent waves, and that new genetic influences came into play at wave 2, which further contributed to stability of symptoms. Nonshared environmental influences were time-specific.

Conclusion:

Insomnia is prevalent in childhood and adolescence, and is moderately heritable. The progression of insomnia across this developmental time period is influenced by stable as well as new genetic factors that come into play at wave 2 (modal age 10 y). Molecular genetic studies should now identify genes related to insomnia progression during childhood and adolescence.

Citation:

Barclay NL, Gehrman PR, Gregory AM, Eaves LJ, Silberg JL. The heritability of insomnia progression during childhood/adolescence: results from a longitudinal twin study. SLEEP 2015;38(1):109–118.

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