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Published on: October 11, 2018
Multifactorial influences on childhood insomnia: Genetic, socioeconomic, brain development and psychopathology
Xiaolong Zhang1, Yuqing Sun2, Meng Wang2
1Department of Physiology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, China.
Insights
Genetic and socioeconomic factors combined increase childhood insomnia risk, impacting brain development and mental health. Early interventions targeting these combined risks are crucial for affected children.
Area of Science:
- Neuroscience
- Genetics
- Child Psychology
Background:
- Childhood insomnia is a prevalent sleep disturbance with significant negative consequences.
- Its complex etiology involves biological, neurodevelopmental, social-environmental, and behavioral factors.
- Current understanding and interventions for childhood insomnia remain insufficient.
Purpose of the Study:
- To investigate the multifactorial origins of childhood insomnia.
- To examine the interplay of genetic architecture, social-environmental variables, and neural mechanisms.
- To explore the relationship between childhood insomnia and mental health outcomes.
Main Methods:
- Utilized data from 4340 participants at baseline and 2717 at follow-up from the Adolescent Brain Cognitive Development (ABCD) Study.
- Assessed joint effects of polygenic risk score (PRS) and socioeconomic status (SES) on insomnia symptoms.
- Employed structural equation modeling (SEM) to analyze directional relationships and mediation pathways.
Main Results:
- SES and PRS independently and additively influenced children's insomnia symptoms.
- Inferior precentral sulcus deviation mediated the relationship between SES/PRS and insomnia.
- Insomnia, precentral development, and accumulated SES-PRS risks significantly predicted psychopathology symptoms.
Conclusions:
- Childhood insomnia arises from the additive effects of genetic and socioenvironmental factors.
- Precentral development is a key neural pathway mediating these effects.
- Findings suggest potential targets for early detection and intervention in childhood insomnia.
Abstract:
Insomnia is the most prevalent sleep disturbance during childhood and can result in extensively detrimental effects. Children's insomnia involves a complex interplay of biological, neurodevelopmental, social-environmental, and behavioral variables, yet remains insufficiently addressed. This study aimed to investigate the multifactorial etiology of childhood insomnia from its genetic architecture and social-environmental variables to its neural instantiation and the relationship to mental health. This cohort study uses 4340 participants at baseline and 2717 participants at 2-year follow-up from the Adolescent Brain Cognitive Development (ABCD) Study. We assessed the joint effects of polygenic risk score (PRS) and socioeconomic status (SES) on insomnia symptoms and then investigated the underlying neurodevelopmental mechanisms. Structural equation model (SEM) was applied to investigate the directional relationships among these variables. SES and PRS affected children's insomnia symptoms independently and additively (SES: β = -0.089, P = 1.91 × 10-8; PRS: β = 0.041, P = 0.008), which was further indirectly mediated by the deviation of inferior precentral sulcus (β = 0.0027, P = 0.0071). SEM revealed that insomnia (β = 0.457, P < 0.001) and precentral development (β = -0.039, P = 0.009) significantly mediated the effect of SES_PRS (accumulated risks of PRS and SES) on psychopathology symptoms. Furthermore, baseline insomnia symptoms, SES_PRS, and precentral deviation significantly predicted individual total psychopathology syndromes (r = 0.346, P < 0.001). These findings suggest the additive effects of genetic and socioenvironmental factors on childhood insomnia via precentral development and highlight potential targets in early detection and intervention for childhood insomnia.
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