There can be many different reasons why a kid or a teenager doesn’t sleep well, but a new twin-study suggests that there are probably partial genetic influences, but the specific genetic factors may change with age. And it doesn’t mean there is nothing you can do.
From the press release:
Results show that clinically significant insomnia was moderately heritable at all stages of the longitudinal study. Genetic factors contributed to 33 to 38 percent of the insomnia ratings at the first two stages of the study, when participants had an average age of 8 to 10 years. The heritability of insomnia was 14 to 24 percent at the third and fourth follow-up points, when the average age of participants was 14 to 15 years. The remaining source of variance in the insomnia ratings was the non-shared environment, with no influence of shared, family-wide factors. Further analysis found that genetic influences around age 8 contributed to insomnia at all subsequent stages of development, and that new genetic influences came into play around the age of 10 years.
“Insomnia in youth is moderately related to genetic factors, but the specific genetic factors may change with age,” said study author Philip Gehrman, PhD, assistant professor in the Department of Psychology at the University of Pennsylvania in Philadelphia. “We were most surprised by the fact that the genetic factors were not stable over time, so the influence of genes depends on the developmental stage of the child.”
Study results are published in the January issue of the journal Sleep.
Insomnia involves difficulty initiating or maintaining sleep, or waking up earlier than desired, according to the American Academy of Sleep Medicine. Children with insomnia may resist going to bed on an appropriate schedule or have difficulty sleeping without intervention by a parent or caregiver. An insomnia disorder results in daytime symptoms such as fatigue, irritability or behavioral problems.
According to the authors, the results suggest that genes controlling the sleep-wake system play a role in childhood insomnia. Therefore, molecular genetic studies are needed to identify this genetic mechanism, which could facilitate the development of targeted treatments.
“These results are important because the causes of insomnia may be different in teens and children, so they may need different treatment approaches,” said Gehrman.
The study group comprised 1,412 twin pairs who were between the ages of 8 and 18 years: 739 monozygotic pairs, 672 dizygotic pairs and one pair with unknown zygosity. Participants were followed up at three additional time points. Average ages at each of the four waves of the study were 8, 10, 14 and 15 years. Results were interpreted in terms of the progression across time, rather than differences between discrete age groups. Clinical ratings of insomnia symptoms were assessed by trained clinicians using the Child and Adolescent Psychiatric Assessment and rated according to the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition.
Abstract of the research:
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).
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.