SLEEP DURATION, OBESITY, AND INSULIN RESISTANCE IN CHILDREN AND ADOLESCENTS

Abstract

Introduction: Insufficient sleep, delayed sleep timing, and night-to-night irregularity are common during childhood and adolescence. These exposures coincide with critical periods of adiposity gain, pubertal insulin resistance, circadian reorganization, and increasing autonomy over food, activity, and digital-media use. Short sleep is consistently associated with obesity, but the independent relationship with insulin resistance and the reversibility of metabolic risk remain less certain.   Objective: To critically synthesize evidence linking sleep duration with obesity and insulin resistance in children and adolescents, distinguish duration from timing and regularity, quantify the principal observational and experimental effects, and translate the evidence into clinically useful assessment and management.   Methods: A structured narrative review of PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library was conducted through August 31, 2026. Pediatric systematic reviews, meta-analyses, prospective cohorts, objective sleep studies, randomized sleep-manipulation experiments, and sleep-focused obesity-prevention or treatment trials were prioritized. Total and central adiposity were analyzed separately from fasting insulin, homeostatic model assessment of insulin resistance, oral-glucose-tolerance-test indices, and incident insulin resistance.   Results and Discussion: Prospective meta-analyses consistently associate short sleep with later overweight or obesity, with pooled relative risks generally between 1.30 and 1.58 and a stronger signal in school-aged children than in adolescents. Experimental restriction increases energy-dense food intake, dietary glycemic load, and eating in the absence of hunger, providing a plausible behavioral pathway. Sleep-extension trials reliably increase sleep, but effects on body mass index are small, heterogeneous, and frequently absent in intention-to-treat analyses. Evidence concerning insulin resistance is more complex: cross-sectional associations often attenuate after adjustment for adiposity and puberty, whereas a two-year actigraphy cohort found that sleeping at least one hour below age recommendations was associated with 2.74-fold higher odds of developing insulin resistance. In a randomized crossover trial of adolescents with obesity and type 2 diabetes risk, one week of sleep extension increased oral-glucose-tolerance-test-derived insulin sensitivity by 20% compared with habitual and restricted sleep.   Conclusion: Adequate and regular sleep should be considered a fundamental component of pediatric metabolic health, but not a stand-alone obesity treatment. Evidence supports a modest prospective contribution to obesity and a potentially reversible effect on insulin sensitivity in high-risk adolescents. Clinical care should assess sleep duration, timing, variability, obstructive sleep apnea, pubertal stage, and adiposity together, while future trials should evaluate sustained metabolic effects using objective sleep measurements and robust glucose phenotyping.