The role of sleep deficiency in the relationship between adverse childhood experiences and early adolescent pain outcomes

• DOI: 10.1002/jcv2.70011
• Publication Date: 2025-03-24T05:08:23Z
• Authors: Thea Senger‐Carpe...; Anao Zhang; Monica Ordway; Sarah A. Stoddard; Terri Voepel‐Lewis

AbstractBackgroundSleep deficiency is common among youth exposed to adverse childhood experiences (ACEs) and may contribute towards persistent/recurrent pain (PRP). This study tested the hypotheses that sleep deficiency mediates the effect of ACEs on PRP and moderates the effect of ACEs on PRP exerted through anxiety and depression symptoms.MethodsWe used 4 years of Adolescent Brain Cognitive Development Study® data to test our hypotheses. Annual assessments of sleep duration and quality (from the Sleep Disturbances Scale for Children), pain, anxiety, and depression (from the Child Behavior Checklist) were used to derive our measures. Structural equation modeling and sleep subgroup comparisons estimated effects of early childhood ACEs (measured with parent/youth surveys) on PRP (defined as pain reported for 3 or 4 years) via sleep duration and quality, accounting for effects of anxiety/depression symptoms. Results are presented as standardized adjusted odds ratios with 95% confidence intervals (adj. OR [95% CI]).ResultsData from 7912 youth were included, nearly one third of whom (n = 2527) were classified with PRP by age 12–13. The effect of early childhood ACEs on adolescent PRP was mediated, in part, through insufficient sleep duration (adj. OR 1.01 [95% CI 1.01, 1.02]) and higher sleep quality (adj. OR 0.99 [ 95% CI 0.97, 0.99]). The direct effect of ACEs on PRP was significant only for the subgroup of youth with both insufficient duration and low quality sleep (adj. OR 1.43 [95% CI 1.05, 1.95]). Mediation effects of depression and anxiety were supported across all sleep subgroups with one exception, and sleep did not moderate these associations.ConclusionSleep deficiency may underlie the effect of early ACEs on PRP, though anxiety and depression are likely important to these pathways regardless of sleep. Further investigation into the potentially mechanistic role of sleep deficiency in ACEs/pain associations is warranted.