Oct 2026· Journal of Child Psychology and Psychiatry and Allied Disciplines· 0 citations· 36 references
Medicine
TL;DR
There are likely causal effects of adolescent chronotype on mental health symptoms, but these are dependent on the dimension of mental health and period of adolescence.
Abstract
Background
This study investigated whether chronotype (biobehavioral preference for sleep and wake timing) across early adolescence impacts mental health symptoms at age 13-14. This is a relationship with growing correlational evidence but limited causal exploration.
Methods
Participants were 7,489 adolescents (aged 9-10 at baseline; 13-14 at the fifth assessment wave) from the Adolescent Brain Cognitive Development Study (ABCD). Marginal structural models with machine learning-based weight estimation were used to assess the causal impact of chronotype at ages 11-12 and 12-13, as measured by the youth-reported Munich Chronotype Questionnaire, on several dimensions of mental health symptoms at age 13-14 (parent-reported Child Behavioral Checklist internalizing and externalizing values, n = 2,668; child-reported Prodromal Psychosis Scale, n = 2,698).
Results
There was no effect of chronotype at age 11-12 on any outcome. However, later chronotype at age 12-13 was associated with slightly more severe externalizing symptoms (b = .29, p = .04) and more psychotic-like experiences at age 13-14 (b = .05, p = .02), but not with more severe internalizing symptoms. Post hoc analyses indicated the lack of relationship with internalizing held for both anxiety and depression symptoms and in both sexes.
Conclusions
There are likely causal effects of adolescent chronotype on mental health symptoms, but these are dependent on the dimension of mental health and period of adolescence. The typically reported association between later chronotype and more severe internalizing symptoms may not manifest until later adolescence (such as with the common postpubertal shift in chronotype).
Two distinct ACEs-related pathways influencing adolescent behavior through neurostructural and functional mediators, moderated by genetic risk are delineated, advances the understanding of ACEs mechanisms and highlights targets for early intervention.
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