Biological and behavioral pathways from prenatal depression to offspring cardiometabolic risk: Testing the developmental origins of health and disease hypothesis.

Given prior literature focused on the Developmental Origins of Health and Disease framework, there is strong rationale to hypothesize that reducing depression in the prenatal period will cause improvements in offspring cardiometabolic health. The current review outlines evidence that prenatal depression is associated with offspring cardiometabolic risk and health behaviors. We review evidence of these associations in humans and in nonhuman animals at multiple developmental periods, from the prenatal period (maternal preeclampsia, gestational diabetes), neonatal period (preterm birth, small size at birth), infancy (rapid weight gain), childhood and adolescence (high blood pressure, impaired glucose-insulin homeostasis, unfavorable lipid profiles, abdominal obesity), and into adulthood (diabetes, cardiovascular disease). In addition to these cardiometabolic outcomes, we focus on health behaviors associated with cardiometabolic risk, such as child eating behaviors, diet, physical activity, and sleep health. Our review focuses on child behaviors (e.g., emotional eating, preference for highly palatable foods, short sleep duration) and parenting behaviors (e.g., pressuring child to eat, modeling of health behaviors). These changes in health behaviors may be detected before changes to cardiometabolic outcomes, which may allow for early identification of and prevention for children at risk for poor adult cardiometabolic outcomes. We also discuss the methods of the ongoing Care Project, which is a randomized clinical trial to test whether reducing prenatal maternal depression improves offspring's cardiometabolic health and health behaviors in preschool. The goal of this review and the Care Project are to inform future research, interventions, and policies that support prenatal mental health and offspring cardiometabolic health. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Understanding risk and causal mechanisms for developing obesity in infants and young children: A National Institutes of Health workshop.

Obesity in children remains a major public health problem, with the current prevalence in youth ages 2-19 years estimated to be 19.7%. Despite progress in identifying risk factors, current models do not accurately predict development of obesity in early childhood. There is also substantial individual variability in response to a given intervention that is not well understood. On April 29-30, 2021, the National Institutes of Health convened a virtual workshop on "Understanding Risk and Causal Mechanisms for Developing Obesity in Infants and Young Children." The workshop brought together scientists from diverse disciplines to discuss (1) what is known regarding epidemiology and underlying biological and behavioral mechanisms for rapid weight gain and development of obesity and (2) what new approaches can improve risk prediction and gain novel insights into causes of obesity in early life. Participants identified gaps and opportunities for future research to advance understanding of risk and underlying mechanisms for development of obesity in early life. It was emphasized that future studies will require multi-disciplinary efforts across basic, behavioral, and clinical sciences. An exposome framework is needed to elucidate how behavioral, biological, and environmental risk factors interact. Use of novel statistical methods may provide greater insights into causal mechanisms.

Characteristics of Melatonin Use Among US Children and Adolescents.

This survey study describes parent-reported sleep practices, such as prevalence, frequency, and timing of melatonin use, among young people aged 1 to 13 years.

Factors contributing to U.S. parents' decisions to administer melatonin to children.

OBJECTIVE: Pediatric melatonin use is increasingly prevalent in the U.S. despite limited research on its efficacy and long-term safety. The current study investigated factors contributing to parents' decisions whether to give children melatonin. METHODS: Parents of children 1.0-13.9 years completed an online questionnaire on children's health, sleep, and melatonin use. Parents who reported giving melatonin to their child were asked open-ended follow-up questions on why their child takes melatonin and why they stopped (if applicable). Responses were assigned to categories through thematic coding. RESULTS: Data were analyzed on 212 children who either consumed melatonin in the past 30 days (n = 131) or took melatonin previously (n = 81). Among children who recently took melatonin, 51.1 % exhibited bedtime resistance and 46.2 % had trouble falling asleep. Parents most commonly gave children melatonin to: help them fall asleep (49.3 %), wind down before bedtime (22.7 %), facilitate changes in their sleep routine (17.5 %), and/or change their circadian rhythm (11.4 %). Parents stopped giving melatonin because their child did not need it anymore (32.0 %), experienced negative side effects (9.3 %), and/or concerns about health and safety (13.3 %). Finally, parents initiated melatonin use on their own (50.0 %), were encouraged by a friend or family member (27.4 %), and/or followed the recommendation of a health provider (48.1 %). CONCLUSIONS: Parents administered melatonin to children for a number of reasons and discontinued melatonin based on their own observations of a variety of effects. Parents frequently initiated use without the recommendation of a medical professional. Further research on indications and efficacy of melatonin and wider dissemination of guidelines are needed to help parents make informed decisions regarding children's sleep health.

Differences in the Pupillary Responses to Evening Light between Children and Adolescents.

Purpose: To assess differences in the pupillary light responses (PLRs) to blue and red evening lights between children and adolescents. Methods: Forty healthy participants (8-9 years, n=21; 15-16 years, n=19) completed a PLR assessment 1 h before their habitual bedtime. After a 1 h dim-light adaptation period (<1 lux), baseline pupil diameter was measured in darkness for 30 s, followed by a 10 s exposure to 3.0×1013 photons/cm2/s of either red (627 nm) or blue (459 nm) light, and a 40 s recovery in darkness to assess pupillary re-dilation. Subsequently, participants underwent 7 min of dim-light re-adaptation followed by an exposure to the other light condition. Lights were counterbalanced across participants. Results: Across both age groups, maximum pupil constriction was significantly greater (p< 0.001, ηp2=0.48) and more sustained (p< 0.001, ηp2=0.41) during exposure to blue compared to red light. For adolescents, the post-illumination pupillary response (PIPR), a hallmark of melanopsin function, was larger after blue compared with red light (p= 0.02, d=0.60). This difference was not observed in children. Across light exposures, children had larger phasic (p< 0.01, ηp2=0.20) and maximal (p< 0.01, ηp2=0.22) pupil constrictions compared to adolescents. Conclusions: Blue light elicited a greater and more sustained pupillary response than red light across participants. However, the overall amplitude of the rod/cone-driven phasic response was greater in children than in adolescents. Our findings using the PLR highlight a higher sensitivity to evening light in children compared to adolescents, and continued maturation of the human non-visual photoreception/system throughout development.

Sleep Health at the Genomic Level: Six Distinct Factors and Their Relationships With Psychopathology.

Background: Poor sleep is associated with many negative health outcomes, including multiple dimensions of psychopathology. In the past decade, sleep researchers have advocated for focusing on the concept of sleep health as a modifiable health behavior to mitigate or prevent these outcomes. Sleep health dimensions often include sleep efficiency, duration, satisfaction, regularity, timing, and daytime alertness. However, there is no consensus on how to best operationalize sleep health at the phenotypic and genetic levels. In some studies, specific sleep health domains were examined individually, while in others, sleep health domains were examined together (e.g., with an aggregate sleep health score). Methods: Here, we compared alternative sleep health factor models using genomic structural equation modeling on summary statistics from previously published genome-wide association studies of self-reported and actigraphic sleep measures with effective sample sizes up to 452,633. Results: Our best-fitting sleep health model had 6 correlated genetic factors pertaining to 6 sleep health domains: circadian preference, efficiency, alertness, duration, noninsomnia, and regularity. All sleep health factors were significantly correlated (|rgs| = 0.11-0.51), except for the circadian preference factor with duration and noninsomnia. Better sleep health was generally significantly associated with lower genetic liability for psychopathology (|rgs| = 0.05-0.48), yet the 6 sleep health factors showed divergent patterns of associations with different psychopathology factors, especially when controlling for covariance among the sleep health factors. Conclusions: These results provide evidence for genetic separability of sleep health constructs and their differentiation with respect to associations with mental health.

Modeling the Effects of Napping and Non-napping Patterns of Light Exposure on the Human Circadian Oscillator.

In early childhood, consolidation of sleep from a biphasic to a monophasic sleep-wake pattern, that is, the transition from sleeping during an afternoon nap and at night to sleeping only during the night, represents a major developmental milestone. Reduced napping behavior is associated with an advance in the timing of the circadian system; however, it is unknown if this advance represents a standard response of the circadian clock to altered patterns of light exposure or if it additionally reflects features of the developing circadian system. Using a mathematical model of the human circadian pacemaker, we investigated the impact of napping and non-napping patterns of light exposure on entrained circadian phases. Simulated light schedules were based on published data from 20 children (34.2 ± 2.0 months) with habitual napping or non-napping sleep patterns (15 nappers). We found the model predicted different circadian phases for napping and non-napping light patterns: both the decrease in afternoon light during the nap and the increase in evening light associated with napping toddlers' later bedtimes contributed to the observed circadian phase difference produced between napping and non-napping light schedules. We systematically quantified the effects on phase shifting of nap duration, timing, and light intensity, finding larger phase delays occurred for longer and earlier naps. In addition, we simulated phase response curves to a 1-h light pulse and 1-h dark pulse to predict phase and intensity dependence of these changes in light exposure. We found the light pulse produced larger shifts compared with the dark pulse, and we analyzed the model dynamics to identify the features contributing to this asymmetry. These findings suggest that napping status affects circadian timing due to altered patterns of light exposure, with the dynamics of the circadian clock and light processing mediating the effects of the dark pulse associated with a daytime nap.

Pediatric sleep: current knowledge, gaps, and opportunities for the future.

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.

Creating the Cave: Conducting Circadian Science in Early Childhood.

In humans, physiological outputs of the body's internal clock (i.e., saliva, serum, and temperature) can be collected to quantify the timing of the circadian system. In-lab assessment of salivary melatonin in a dimly lit environment is a common approach for adolescents and adults; however, the reliable measurement of melatonin onset in toddlers and preschoolers requires a modification of laboratory methods. For > 15 years, we have successfully collected data from ~250 in-home dim light melatonin onset (DLMO) assessments of children aged 2-5 years. Although in-home studies of circadian physiology may introduce a host of challenges and may increase the risk of incomplete data (e.g., accidental light exposure), in-home studies afford more comfort (e.g., less arousal in children) and flexibility for families. Here, we provide effective tools and strategies to assess children's DLMO, a reliable marker of circadian timing, through a rigorous in-home protocol. We first describe our basic approach, including the study protocol, collection of actigraphy data, and strategies for training child participants to complete procedures. Next, we detail how to convert the home into a "cave", or dim-light environment, and present guidelines for timing the salivary data collection. Lastly, we provide helpful tips to increase participants' compliance based upon behavioral and developmental science tenets.

Evidence of circalunar rhythmicity in young children's evening melatonin levels.

In adults, recent evidence demonstrates that sleep and circadian physiology change across lunar phases, including findings that endogenous melatonin levels are lower near the full moon compared to the new moon. Here, we extend these results to early childhood by examining circalunar fluctuations in children's evening melatonin levels. We analysed extant data on young children's circadian rhythms (n = 46, aged 3.0-5.9 years, 59% female). After following a strict sleep schedule for 5-7 days, children completed an in-home, dim-light circadian assessment (<10 lux). Salivary melatonin was assessed at regular 20- to 30-min intervals until 1 h past each child's scheduled bedtime. Melatonin levels varied significantly across lunar phases, such that melatonin was lower in participants assessed near the full moon as compared to near the new moon. Significant differences were observed at 50 min (meanfull  = 2.5 pg/ml; meannew  = 5.4 pg/ml) and 10 min (meanfull  = 7.3 pg/ml; meannew  = 15.8 pg/ml) before children's scheduled bedtime, as well as at 20 min (meanfull  = 15.5 pg/ml; meannew  = 26.1 pg/ml) and 50 min (meanfull  = 19.9 pg/ml; meannew  = 34.3 pg/ml) after bedtime. To our knowledge, these are the first data demonstrating that melatonin secretion, a process regulated by the human circadian system, is sensitive to changes in lunar phase at an early age. Future research is needed to understand the mechanisms underlying this association (e.g., an endogenous circalunar rhythm) and its potential influence on children's sleep and circadian health.

Impact of the COVID-19 pandemic on children's sleep habits: an ECHO study.

BACKGROUND: Sleep in childhood is affected by behavioral, environmental, and parental factors. We propose that these factors were altered during the COVID-19 pandemic. This study investigates sleep habit changes during the pandemic in 528 children 4-12 years old in the US, leveraging data from the Environmental Influences on Child Health Outcomes (ECHO) Program. METHODS: Data collection occurred in July 2019-March 2020 (pre-pandemic) and two pandemic periods: December 2020-April 2021 and May-August 2021. Qualitative interviews were performed in 38 participants. RESULTS: We found no changes in sleep duration, but a shift to later sleep midpoint during the pandemic periods. There was an increase in latency at the first pandemic collection period but no increase in the frequency of bedtime resistance, and a reduced frequency of naps during the pandemic. Qualitative interviews revealed that parents prioritized routines to maintain sleep duration but were more flexible regarding timing. Children from racial/ethnic minoritized communities slept less at night, had later sleep midpoint, and napped more frequently across all collection periods, warranting in-depth investigation to examine and address root causes. CONCLUSIONS: The COVID-19 pandemic significantly impacted children sleep, but parental knowledge of the importance of sleep might have played a significant protective role. IMPACT: During the COVID-19 pandemic, US children changed their sleep habits, going to bed and waking up later, but their sleep duration did not change. Sleep latency was longer. Parental knowledge of sleep importance might have played a protective role. Regardless of data collection periods, children from racial/ethnic minoritized communities slept less and went to bed later. This is one of the first study on this topic in the US, including prospective pre-pandemic qualitative and quantitative data on sleep habits. Our findings highlight the pandemic long-term impact on childhood sleep. Results warrants further investigations on implications for overall childhood health.

Evening Light Intensity and Phase Delay of the Circadian Clock in Early Childhood.

Late sleep timing is prevalent in early childhood and a risk factor for poor behavioral and health outcomes. Sleep timing is influenced by the phase of the circadian clock, with later circadian timing linked to delayed sleep onset in young children. Light is the strongest zeitgeber of circadian timing and, in adults, evening light produces circadian phase delay in an intensity-dependent manner. The intensity-dependent circadian phase-shifting response to evening light in children, however, is currently unknown. In the present study, 33 healthy, good-sleeping children aged 3.0 to 4.9 years (M = 4.14 years, 39% male) completed a 10-day between-subjects protocol. Following 7 days of a stable sleep schedule, an in-home dim-light circadian assessment was performed. Children remained in dim-light across 3 days (55 h), with salivary melatonin collected in regular intervals throughout each evening. Phase-shifting effects of light exposure were determined via changes in the timing of the dim-light melatonin onset (DLMO) prior to (Day 8) and following (Day 10) a light exposure stimulus. On Day 9, children were exposed to a 1 h light stimulus in the hour before their habitual bedtime. Each child was randomly assigned to one intensity between 5 and 5000 lux (4.5-3276 melanopic EDI). Across light intensities, children showed significant circadian phase delays, with an average phase delay of 56.1 min (SD = 33.6 min), and large inter-individual variability. No relationship between light intensity and magnitude of the phase shift was observed. However, a greater percentage of melatonin suppression during the light exposure was associated with a greater phase delay (r = -0.73, p < 0.01). These findings demonstrate that some young children may be highly sensitive to light exposure in the hour before bedtime and suggest that the home lighting environment and its impact on circadian timing should be considered a possible contributor to behavioral sleep difficulties.

Keeping an eye on circadian time in clinical research and medicine.

BACKGROUND: Daily rhythms are observed in humans and almost all other organisms. Most of these observed rhythms reflect both underlying endogenous circadian rhythms and evoked responses from behaviours such as sleep/wake, eating/fasting, rest/activity, posture changes and exercise. For many research and clinical purposes, it is important to understand the contribution of the endogenous circadian component to these observed rhythms. CONTENT: The goal of this manuscript is to provide guidance on best practices in measuring metrics of endogenous circadian rhythms in humans and promote the inclusion of circadian rhythms assessments in studies of health and disease. Circadian rhythms affect all aspects of physiology. By specifying minimal experimental conditions for studies, we aim to improve the quality, reliability and interpretability of research into circadian and daily (i.e., time-of-day) rhythms and facilitate the interpretation of clinical and translational findings within the context of human circadian rhythms. We describe protocols, variables and analyses commonly used for studying human daily rhythms, including how to assess the relative contributions of the endogenous circadian system and other daily patterns in behaviours or the environment. We conclude with recommendations for protocols, variables, analyses, definitions and examples of circadian terminology. CONCLUSION: Although circadian rhythms and daily effects on health outcomes can be challenging to distinguish in practice, this distinction may be important in many clinical settings. Identifying and targeting the appropriate underlying (patho)physiology is a medical goal. This review provides methods for identifying circadian effects to aid in the interpretation of published work and the inclusion of circadian factors in clinical research and practice.

Development of the circadian system in early life: maternal and environmental factors.

In humans, an adaptable internal biological system generates circadian rhythms that maintain synchronicity of behavior and physiology with the changing demands of the 24-h environment. Development of the circadian system begins in utero and continues throughout the first few years of life. Maturation of the clock can be measured through sleep/wake patterns and hormone secretion. Circadian rhythms, by definition, can persist in the absence of environmental input; however, their ability to adjust to external time cues is vital for adaptation and entrainment to the environment. The significance of these external factors that influence the emergence of a stable circadian clock in the first years of life remain poorly understood. Infants raised in our post-modern world face adverse external circadian signals, such as artificial light and mistimed hormonal cues via breast milk, which may increase interference with the physiological mechanisms that promote circadian synchronization. This review describes the very early developmental stages of the clock and common circadian misalignment scenarios that make the developing circadian system more susceptible to conflicting time cues and temporal disorder between the maternal, fetal, infant, and peripheral clocks.

High sensitivity of melatonin suppression response to evening light in preschool-aged children.

Light at night in adults suppresses melatonin in a nonlinear intensity-dependent manner. In children, bright light of a single intensity before bedtime has a robust melatonin suppressing effect. To our knowledge, whether evening light of different intensities is related to melatonin suppression in young children is unknown. Healthy, good-sleeping children (n = 36; 3.0-4.9 years; 39% male) maintained a stable sleep schedule for 7 days followed by a 29.5-h in-home dim-light circadian assessment (~1.5 lux). On the final night of the protocol, children received a 1-h light exposure (randomized to one of 15 light levels, ranging 5-5000 lux, with ≥2 participants assigned to each light level) in the hour before habitual bedtime. Salivary melatonin was measured to calculate the magnitude of melatonin suppression during light exposure compared with baseline levels from the previous evening, as well as the degree of melatonin recovery 50 min after the end of light exposure. Melatonin levels were suppressed between 69.4% and 98.7% (M = 85.4 ± 7.2%) during light exposure across the full range of intensities examined. Overall, we did not observe a light intensity-dependent melatonin suppression response; however, children exposed to the lowest quartile of light intensities (5-40 lux) had an average melatonin suppression (77.5 ± 7.0%) which was significantly lower than that observed at each of the three higher quartiles of light intensities (86.4 ± 5.6%, 89.2 ± 6.3%, and 87.1 ± 5.0%, respectively). We further found that melatonin levels remained below 50% baseline for at least 50 min after the end of light exposure for the majority (62%) of participants, and recovery was not influenced by light intensity. These findings indicate that preschool-aged children are highly sensitive to light exposure in the hour before bedtime and suggest the lighting environment may play a crucial role in the development and the maintenance of behavioral sleep problems through impacts on the circadian timing system.

Better sleep, better life? How sleep quality influences children's life satisfaction.

PURPOSE: To assess the association between children's sleep quality and life satisfaction; and to evaluate the underlying mechanisms of this relationship. METHODS: Three pediatric cohorts in the National Institutes of Health (NIH) Environmental influences on Child Health (ECHO) Research Program administered Patient-Reported Outcome Measurement Information System (PROMIS®) parent-proxy measures to caregivers (n = 1111) who reported on their 5- to 9-year-old children's (n = 1251) sleep quality, psychological stress, general health, and life satisfaction; extant sociodemographic data were harmonized across cohorts. Bootstrapped path modeling of individual patient data meta-analysis was used to determine whether and to what extent stress and general health mediate the relationship between children's sleep quality and life satisfaction. RESULTS: Nonparametric bootstrapped path analyses with 1000 replications suggested children's sleep quality was associated with lower levels of stress and better general health, which, in turn, predicted higher levels of life satisfaction. Family environmental factors (i.e., income and maternal mental health) moderated these relationships. CONCLUSION: Children who sleep well have happier lives than those with more disturbed sleep. Given the modifiable nature of children's sleep quality, this study offers evidence to inform future interventional studies on specific mechanisms to improve children's well-being.

Spatio-temporal properties of sleep slow waves and implications for development.

Objective sleep quality can be measured by electroencephalography (EEG), a non-invasive technique to quantify electrical activity generated by the brain. With EEG, sleep depth is measured by appearance and an increase in slow wave activity (scalp-SWA). EEG slow waves (scalp-SW) are the manifestation of underlying synchronous membrane potential transitions between silent (DOWN) and active (UP) states. This bistable periodic rhythm is defined as slow oscillation (SO). During its "silent state" cortical neurons are hyperpolarized and appear inactive, while during its "active state" cortical neurons are depolarized, fire spikes and exhibit continuous synaptic activity, excitatory and inhibitory. In adults, data from high-density EEG revealed that scalp-SW propagate across the cortical mantle in complex patterns. However, scalp-SW propagation undergoes modifications across development. We present novel data from children, indicating that scalp-SW originate centro-parietally, and emerge more frontally by adolescence. Based on the concept that SO and SW could actively modify neuronal connectivity, we discuss whether they fulfill a key purpose in brain development by actively conveying modifications of the maturing brain.

Many naps, one nap, none: A systematic review and meta-analysis of napping patterns in children 0-12 years.

The onset of monophasic sleep, in which napping ceases and sleep consolidates into a single night period, is a key developmental milestone of childhood. Yet to date, there is little consensus regarding the timing of cessation of napping in children. The aim of the current study is to examine global evidence regarding napping patterns in childhood, and, through meta-analysis, describe patterns of napping cessation and duration observed in children aged 0-12 y. A systematic search of all published, original research articles reporting children's napping patterns, by age, was conducted. The quality of studies was assessed, and meta-analysis of eligible studies undertaken. Risk of bias and heterogeneity of measurement was high. Current evidence indicates that less than 2.5% of children cease napping prior to age 2, while 94% cease napping by age 5. The preschool period (3-5 y; 36-60 mo) represents a particularly dynamic period in napping cessation, with large variation in rates of napping across studies evidencing potential ecological effects. Future studies should focus on understanding of the underlying mechanisms explaining individual variations in napping patterns and the extent to which patterns of napping may represent a marker of child development.

A simple sleep EEG marker in childhood predicts brain myelin 3.5 years later.

Epidemiological research reveals that insufficient sleep in children has negative cognitive and emotional consequences; however, the physiological underpinnings of these observations remain understudied. We tested the hypothesis that the topographical distribution of deep sleep slow wave activity during the childhood predicts brain white matter microstructure (myelin) 3.5 y later. Healthy children underwent sleep high-density EEG at baseline (n = 13; ages 2.4-8.0 y) and follow-up (n = 14; ages 5.5-12.2 y). At follow-up, myelin (myelin water fraction) and cortical morphology were also quantified. Our investigation revealed 3 main findings. (1) The Frontal/Occipital (F/O)-ratio at baseline strongly predicted whole brain myelin at follow-up. (2) At follow-up, the F/O-ratio was only minimally (negatively) linked to brain myelin. (3) Cortical morphology was not related to the F/O-ratio, neither at baseline nor at follow-up. Our results support the hypothesis that during child development EEG markers during sleep longitudinally predict brain myelin content. Data extend previous findings reporting a link between EEG markers of sleep need and cortical morphology, by supporting the hypothesis that sleep is a necessary component to underlying processes of brain, and specifically myelin, maturation. In line with the overarching theory that sleep contributes to neurodevelopmental processes, it remains to be investigated whether chronic sleep loss negatively affects white matter myelin microstructure growth during sensitive periods of development.

Parenting and toddler self-regulation in low-income families: What does sleep have to do with it?

Toddlerhood is a sensitive period in the development of self-regulation, a set of adaptive skills that are fundamental to mental health and partly shaped by parenting. Healthy sleep is known to be critical for self-regulation; yet, the degree to which child sleep alters interactive child-parent processes remains understudied. This study examines associations between observed parenting and toddler self-regulation, with toddler sleep as a moderator of this association. Toddlers in low-income families (N = 171) and their mothers were videotaped during free play and a self-regulation challenge task; videos were coded for mothers' behavior and affect (free play) and toddlers' self-regulation (challenge task). Mothers reported their child's nighttime sleep duration via questionnaire. Results revealed significant Sleep × Maternal Negative Affect and Sleep × Maternal Negative Control interactions. Children who did not experience negative parenting had good self-regulation regardless of their nighttime sleep duration. For children who did experience negative parenting, self-regulation was intact among those who obtained more nighttime sleep, but significantly poorer among children who were getting less nighttime sleep. Thus, among children who were reported to obtain less nighttime sleep, there were more robust associations between negative parenting and poorer self-regulation than among toddlers who were reported to obtain more sleep.

Los primeros años de la niñez son un período sensible en el desarrollo de la auto-regulación, un grupo de habilidades adaptables que son fundamentales para la salud mental y a las que en parte les da forma la crianza. Es sabido que el dormir bien es esencial para la auto-regulación y, aun así, el nivel al que el sueño del niño altera los procesos interactivos entre progenitor y niño permanece poco estudiado. Este estudio examina las asociaciones entre la crianza observada y la auto-regulación del niño pequeño, tomando como moderador de tal asociación el proceso de dormir del niño pequeño. Se grabó en video a niños pequeños de familias de bajos ingresos (N=171) y sus madres durante una sesión de juego libre y una tarea de auto-regulación que suponía un reto; los videos fueron codificados en cuanto al comportamiento y afecto de las madres (juego libre) y la auto-regulación de los niños pequeños (tarea que suponía reto). Las madres reportaron acerca del sueño nocturno de sus niños por medio de un cuestionario. Los resultados revelaron interacciones significativas en cuanto al dormir y el negativo afecto materno, así como el dormir y el negativo control materno. Los niños que no experimentaron una crianza negativa tenían una buena auto-regulación independientemente de la duración de su sueño nocturno. En el caso de los niños que experimentaron una crianza negativa, la auto-regulación quedó intacta en aquellos que lograban más tiempo nocturno de dormir, pero fue significativamente más pobre en los niños que tenían menos tiempo de sueño nocturno. Por tanto, en el caso de los niños indicados en el reporte con menos tiempo de dormir nocturno, se dieron asociaciones más robustas entre la crianza negativa y una más pobre auto-regulación que entre los niños pequeños indicados en el reporte con más tiempo de dormir.

La petite enfance est une période sensible dans le développement de l'auto-régulation, un ensemble de compétences qui sont fondamentales pour la santé mentale et en partie formées par le parentage. L'on sait qu'un sommeil sain est critique pour l'auto-régulation et pourtant la mesure dans laquelle le sommeil de l'enfant altère les processus interactifs enfant-parent demeure peu étudiée. Cette étude examine les liens entre le parentage observé et l'auto-régulation du petit enfant, le sommeil de l'enfant ayant un effet modérateur dans ce lien. Des jeunes enfants de familles issues de milieux défavorisés (N=171) et leurs mères ont été filmés durant un jeu libre et un exercice de défi d'auto-régulation. Les vidéos ont été codées pour le comportement des mères et l'affect (jeu libre) et l'auto-régulation des jeunes enfants (exercice de défi). Les mères ont fait état de la durée de sommeil nocturne de leur enfant au moyen d'un questionnaire. Les résultats ont révélé que : sommeil significatif x l'affect négatif maternel et le sommeil x négatif maternel contrôle les interactions. Les enfants qui n'avaient pas fait l'expérience d'un parentage négatif avaient une bonne auto-régulation quelle qu'ait été la durée du sommeil nocturne. Pour les enfants ayant fait l'expérience d'une parentage négatif, l'auto-régulation était intacte chez ceux ayant plus dormi, mais bien moindre chez les enfants qui avaient moins dormi. Donc, chez les enfants ayant moins de sommeil nocturne les liens bien plus robustes ont été découverts entre le parentage négatif et une moindre auto-régulation que chez les petits enfants dormant plus durant la nuit.