This White Paper addresses the current gaps in knowledge, as well as opportunities for future studies in pediatric sleep. The Sleep Research Society’s Pipeline Development Committee assembled a panel of experts tasked to provide information to those interested in learning more about the field of pediatric sleep, including trainees. We cover the scope of pediatric sleep, including epidemiological studies and the development of sleep and circadian rhythms in early childhood and adolescence. Additionally, we discuss current knowledge of insufficient sleep and circadian disruption, addressing the neuropsychological impact (affective functioning) and cardiometabolic consequences. A significant portion of this White Paper explores pediatric sleep disorders (including circadian rhythm disorders, insomnia, restless leg and periodic limb movement disorder, narcolepsy, and sleep apnea), as well as sleep and neurodevelopment disorders (e.g. autism and attention deficit hyperactivity disorder). Finally, we end with a discussion on sleep and public health policy. Although we have made strides in our knowledge of pediatric sleep, it is imperative that we address the gaps to the best of our knowledge and the pitfalls of our methodologies. For example, more work needs to be done to assess pediatric sleep using objective methodologies (i.e. actigraphy and polysomnography), to explore sleep disparities, to improve accessibility to evidence-based treatments, and to identify potential risks and protective markers of disorders in children. Expanding trainee exposure to pediatric sleep and elucidating future directions for study will significantly improve the future of the field.

Context People characterized as late chronotype have elevated type 2 diabetes and cardiovascular disease risk compared to early chronotype. It is unclear how chronotype is associated with insulin sensitivity, metabolic flexibility, or plasma TCA cycle intermediates concentration, amino acids (AA), and/or beta-oxidation. Objective This study examined these metabolic associations with chronotype. Methods The Morningness-Eveningness Questionnaire (MEQ) was used to classify adults with metabolic syndrome (ATP III criteria) as either early (n = 15 [13F], MEQ = 64.7 ± 1.4) or late (n = 19 [16F], MEQ = 45.5 ± 1.3) chronotype. Fasting bloods determined hepatic (HOMA-IR) and adipose insulin resistance (Adipose-IR) while a 120-minute euglycemic clamp (40 mU/m²/min, 5 mmoL/L) was performed to test peripheral insulin sensitivity (glucose infusion rate). Carbohydrate (CHO_OX) and fat oxidation (F_OX), as well as nonoxidative glucose disposal (NOGD), were also estimated (indirect calorimetry). Plasma tricarboxylic acid cycle (TCA) intermediates, AA, and acyl-carnitines were measured along with VO₂max and body composition (DXA). Results There were no statistical differences in age, BMI, fat-free mass, VO₂max, or ATP III criteria between groups. Early chronotype, however, had higher peripheral insulin sensitivity (P = 0.009) and lower HOMA-IR (P = 0.02) and Adipose-IR (P = 0.05) compared with late chronotype. Further, early chronotype had higher NOGD (P = 0.008) and greater insulin-stimulated CHO_OX (P = 0.02). While fasting lactate (P = 0.01), TCA intermediates (isocitrate, α-ketoglutarate, succinate, fumarate, malate; all P ≤ 0.04) and some AA (proline, isoleucine; P = 0.003-0.05) were lower in early chronotype, other AA (threonine, histidine, arginine; all P ≤ 0.05) and most acyl-carnitines were higher (P ≤ 0.05) compared with late chronotype. Conclusion Greater insulin sensitivity and metabolic flexibility relates to plasma TCA concentration in early chronotype.

To examine demographic, psychosocial, and behavioral determinants of postpartum sleep duration and sleep efficiency among a cohort of black and Latina women. Data were from 148 women (67% black, 32% Latina) at 5 months postpartum, recruited from an academic medical center in Philadelphia. Relevant demographic, psychosocial and behavioral predictors were assessed via questionnaire. Nocturnal sleep was objectively measured for 1 week using wrist actigraphy. Sleep duration was examined as a continuous variable and in categories (<7 versus ≥7 h per night); sleep efficiency was examined as a continuous variable. Independent multiple linear regression models were built to evaluate significant determinants of sleep. Adjusted models revealed that breastfeeding, having a bedtime after midnight, and being employed were associated with shorter sleep duration (–25–33 min, all p < 0.05). Multiparity, being unmarried, being employed, breastfeeding, having a bedtime after midnight, bedsharing, and responding to infant awakenings by getting up immediately rather than waiting a few minutes to see if the infant fell back asleep, were all significant determinants of sleeping <7 h per night (OR varying: 2.29–4.59, all p < 0.05). Bedsharing was the only variable identified from the multiple regression model that associated with poorer sleep efficiency (–3.8%, p < 0.05). Findings may inform interventions for improving postpartum sleep in socioeconomically disadvantaged, racial/ethnic minority postpartum women.

Insulin resistance is a key etiological factor in promoting not only type 2 diabetes mellitus but also cardiovascular disease (CVD). Exercise is a first-line therapy for combating chronic disease by improving insulin action through, in part, reducing hepatic glucose production and lipolysis as well as increasing skeletal muscle glucose uptake and vasodilation. Just like a pharmaceutical agent, exercise can be viewed as a “drug” such that identifying an optimal prescription requires a determination of mode, intensity, and timing as well as consideration of how much exercise is done relative to sitting for prolonged periods (e.g., desk job at work). Furthermore, proximal nutrition (nutrient timing, carbohydrate intake, etc.), sleep (or lack thereof), as well as alcohol consumption are likely important considerations for enhancing adaptations to exercise. Thus, identifying the maximal exercise “drug” for reducing insulin resistance will require a multi-health behavior approach to optimize type 2 diabetes and CVD care.