Sleep Duration, Quality, and Timing as Modifiable Determinants of Growth and Endocrine Health in Children and Adolescents: A Critical Narrative Review

Abstract

Adequate sleep is increasingly recognised as a modifiable determinant of somatic growth and endocrine function during childhood and adolescence, yet the strength and consistency of this relationship across different sleep dimensions remain incompletely resolved. This critical narrative review synthesises evidence on how sleep duration, sleep quality, and sleep timing relate to linear growth, pubertal maturation, and metabolic-endocrine regulation in paediatric populations. Literature was drawn from peer-reviewed biomedical and life-science sources, general and specialist scholarly indexes, and citation tracking of recent reviews, covering mechanistic, cohort, cross-sectional, and intervention studies published predominantly since 2000, with foundational older work retained where historically necessary. The relationship between slow-wave sleep and pulsatile growth hormone release is well established physiologically, but its translation into measurable differences in childhood height remains inconsistent across cohort studies, with nighttime sleep duration showing more reproducible associations with linear growth than total sleep time. Evidence linking sleep quality, particularly obstructive sleep-disordered breathing, to growth faltering and post-surgical catch-up growth is comparatively robust. The association between sleep duration and pubertal timing is bidirectional and modest in magnitude, with genetic and observational data suggesting that later menarche modestly lengthens habitual sleep, while shorter sleep in mid-childhood may be associated with earlier pubertal onset in some age windows. Sleep curtailment is consistently associated with unfavourable leptin, ghrelin, and insulin-sensitivity profiles, although effect sizes vary by measurement method, pubertal stage, and adiposity status. Sleep timing and circadian misalignment, including social jetlag, appear to influence cardiometabolic risk independently of sleep duration, particularly in female adolescents. Cortisol regulation is sensitive to both sleep duration and sleep architecture in children, although the direction of causation is difficult to establish from existing designs. Across domains, methodological heterogeneity, reliance on subjective sleep measures, and a scarcity of studies spanning the pubertal transition limit the strength of causal inference that can currently be drawn. Priorities for future research include objectively measured, longitudinal cohorts extending across puberty, mechanistic paediatric studies of appetite-regulating hormones, and trials of sleep extension or circadian realignment with endocrine and growth endpoints.