J Affect Disord. 2024 Dec 9:S0165-0327(24)02017-2. doi: 10.1016/j.jad.2024.12.031. Online ahead of print.
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.
PMID:39662779 | DOI:10.1016/j.jad.2024.12.031
