Childhood obesity's influence on socioeconomic disparities in young adolescents' mental health.

PURPOSE: We investigated whether socioeconomic inequalities in young adolescents' mental health are partially due to the unequal distribution of childhood obesity across socioeconomic positions (SEP), i.e. differential exposure, or due to the effect of obesity on mental health being more detrimental among certain SEPs, i.e. differential impact. METHODS: We studied 4660 participants of the Generation R study, a population-based study in the Netherlands. SEP was estimated by mother's education and household income at age five of the child. We estimated the contribution of the mediating and moderating effects of high body fat percentage to the disparity in mental health. This was done through a four-way decomposition using marginal structural models with inverse probability of treatment weighting. RESULTS: Comparing children with the least to most educated mothers and the lowest to highest household income, the total disparity in emotional problems was 0.98 points (95%CI:0.35-1.63) and 1.68 points (95%CI:1.13-2.19), respectively. Of these total disparities in emotional problems, 0.50 points (95%CI:0.15-0.85) and 0.24 points (95%CI:0.09-0.46) were due to the differential exposure to obesity. Obesity did not contribute to disparities in behavioural problems. CONCLUSION: Addressing the heightened obesity prevalence among children in low SEP families may reduce inequalities in emotional problems in early adolescence.

Maternal Migration, Prenatal Stress and Child Autistic Traits: Insights From a Population-Based Cohort Study.

OBJECTIVE: There is emerging evidence for an increased prevalence of autism in children of mothers with a migration background. To date, the mechanisms underlying this relationship are poorly understood. We investigated whether prenatal stress exposure mediates the association between maternal migration and child autistic traits, assessing first- and second-generation migrant mothers in the Netherlands and their children. METHOD: The study was embedded in the prospective population-based Generation R cohort. Of the 4,727 participants, 1,773 mothers (38%) had a migration background. Prenatal stress was assessed using questionnaires related to stressful life events, family functioning, self-esteem, long-lasting difficulties, symptoms of psychopathology, social support, and perceived discrimination. Autistic traits were measured at age 6 years with the parent-reported Social Responsiveness Scale exclusively. Longitudinal multiple mediation analyses were performed. Analyses were stratified by migration origin (Europe and outside Europe) because of differences in migration characteristics. RESULTS: Maternal migration background was associated with more experienced stress and with higher child autistic trait scores (Europe: mean = 0.42, SD = 0.25; outside Europe: mean = 0.50, SD = 0.24) compared to no migration background (Netherlands: mean = 0.38, SD = 0.23; both p < .01). Prenatal stress, especially perceived discrimination and maternal psychopathology, accounted for up to half of the total effect of maternal migration, which remained after adjusting for sociodemographic factors (Bindirect = 0.035, 95% CI = 0.027, 0.043, Btotal = 0.074). CONCLUSION: Stress during pregnancy mediated the association between maternal migration status and child autistic traits. Future research should focus on early interventions to assess whether reducing prenatal stress exposure among women with a migration background can result in lower offspring autistic traits. DIVERSITY & INCLUSION STATEMENT: We worked to ensure that the study questionnaires were prepared in an inclusive way. We worked to ensure sex and gender balance in the recruitment of human participants. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. We actively worked to promote sex and gender balance in our author group. The author list of this paper includes contributors from the location and/or community where the research was conducted who participated in the data collection, design, analysis, and/or interpretation of the work.

What maternal educational mobility tells us about the mother's parenting routines, offspring school achievement and intelligence.

BACKGROUND: Educational mobility at the macro-level is a common measure of social inequality. Nonetheless, the correlates of mobility of education at the individual level are less well studied. We evaluated whether educational mobility of the second generation (compared to the first generation level) predicts differences in parenting practices of the second generation and school achievement and intelligence in the third generation. METHODS: Data from a population-based cohort of children in the Netherlands (N = 3547; 49.4% boys) were analyzed. Maternal, grandparental education and family routines, a parenting practice, were reported by the mother. Child school achievement at the end of primary school (∼12 years, with the national Dutch academic test score) and child intelligence (∼6 and 13 years) were measured in a standardized manner. Also, a child genome-wide polygenic score of academic attainment was calculated. To estimate the effect of educational mobility, inverse probability-weighted linear models and Diagonal Reference Models (DRM) were used. RESULTS: Upward maternal educational mobility was associated with better offspring school achievement, higher intelligence, and more family routines if compared to offspring of mothers with no upward mobility. However, mothers did not implement the same level of family routines as similarly educated mothers and grandfathers who already had achieved this educational level. Likewise, children of mothers with upward educational mobility had lower school achievement and intelligence than children of similarly educated mothers with no mobility. Child's genetic potential for education followed a similar association pattern with higher potential in children of upward mobile mothers. CONCLUSION: Policymakers might overlook social inequalities when focused on parental socioeconomic status. Grandparental socioeconomic status, which independently predicts child school achievement, intelligence, and parental family routines, should also be assessed. The child's genetic endowment reflects the propensity for education across generations that partly underlies mobility and some of its effect on the offspring.

Prospective associations between early childhood parental feeding practices and eating disorder symptoms and disordered eating behaviors in adolescence.

OBJECTIVE: Nonresponsive parental feeding practices are associated with poorer appetite self-regulation in children. It is unknown whether this relationship extends beyond childhood to be prospectively associated with the onset of eating disorder (ED) symptoms in adolescence. This exploratory study therefore investigated prospective associations between early childhood parental feeding practices and adolescent ED symptoms and disordered eating behaviors. METHODS: Data were from two population-based cohorts with harmonized measures: Generation R (Netherlands; n = 4900) and Gemini (UK; n = 2094). Parents self-reported their pressure to eat, restriction and instrumental feeding (i.e., using food as a reward) at child age 4-5 years. Adolescents self-reported their compensatory behaviors (e.g., fasting, purging), binge-eating symptoms, restrained eating, uncontrolled eating, and emotional eating at 12-14 years. Associations between feeding practices and ED symptoms were examined separately in each cohort using generalized linear models. RESULTS: In Gemini, pressure to eat in early childhood was associated with adolescents engaging in compensatory behaviors. In Generation R, parental restriction was associated with adolescents engaging in compensatory behaviors, restrained eating, uncontrolled eating, and emotional eating. Instrumental feeding was associated with uncontrolled eating and emotional eating in Generation R. DISCUSSION: Nonresponsive parental feeding practices were associated with a greater frequency of specific ED symptoms and disordered eating in adolescence, although effect sizes were small and findings were inconsistent between cohorts. Potentially, the cultural and developmental context in which child-parent feeding interactions occur is important for ED symptoms. Further replication studies are required to better understand parents' role in the development and maintenance of ED-related symptoms. PUBLIC SIGNIFICANCE: Prospective research examining how early childhood parental feeding practices might contribute to adolescent ED symptoms is limited. In two population-based cohorts, nonresponsive feeding practices (restriction, instrumental feeding, pressure to eat) predicted increased frequency of some ED symptoms and disordered eating behaviors in adolescence, although associations were small and further replication is required. Findings support the promotion of responsive feeding practices, which may benefit young children's developing relationship with food.

Early childhood appetitive traits and eating disorder symptoms in adolescence: a 10-year longitudinal follow-up study in the Netherlands and the UK.

BACKGROUND: Obesity and eating disorders commonly co-occur and might share common risk factors. Appetite avidity is an established neurobehavioural risk factor for obesity from early life, but the role of appetite in eating disorder susceptibility is unclear. We aimed to examine longitudinal associations between appetitive traits in early childhood and eating disorder symptoms in adolescence. METHODS: In this longitudinal cohort study, we used data from Generation R (based in Rotterdam, the Netherlands) and Gemini (based in England and Wales). Appetitive traits at age 4-5 years were measured using the parent-reported Child Eating Behaviour Questionnaire. At age 12-14 years, adolescents self-reported on overeating eating disorder symptoms (binge eating symptoms, uncontrolled eating, and emotional eating) and restrictive eating disorder symptoms (compensatory behaviours and restrained eating). Missing data on covariates were imputed using Multivariate Imputation via Chained Equations. Ordinal and binary logistic regressions were performed in each cohort separately and adjusted for confounders. Pooled results were obtained by meta-analyses. Sensitivity analyses were performed on complete cases using inverse probability weighting. FINDINGS: The final study sample included 2801 participants from Generation R and 869 participants from Gemini. Pooled findings after meta-analyses showed that higher food responsiveness in early childhood increased the odds of binge eating symptoms (odds ratio [OR]pooled 1·47, 95% CI 1·26-1·72), uncontrolled eating (1·33, 1·21-1·46), emotional eating (1·26, 1·13-1·41), restrained eating (1·16, 1·06-1·27), and compensatory behaviours (1·18, 1·08-1·30) in adolescence. Greater emotional overeating in early childhood increased the odds of compensatory behaviours (1·18, 1·06-1·33). By contrast, greater satiety responsiveness in early childhood decreased the odds of compensatory behaviours in adolescence (0·89, 0·81-0·99) and uncontrolled eating (0·86, 0·78-0·95) in adolescence. Slower eating in early childhood decreased the odds of compensatory behaviours (0·91, 0·84-0·99) and restrained eating (0·90, 0·83-0·98) in adolescence. No other associations were observed. INTERPRETATION: In this study, higher food responsiveness in early childhood was associated with a higher likelihood of self-reported eating disorder symptoms in adolescence, whereas greater satiety sensitivity and slower eating were associated with a lower likelihood of some eating disorder symptoms. Appetitive traits in children might be early neurobehavioural risk factors for, or markers of, subsequent eating disorder symptoms. FUNDING: MQ Mental Health Research, Rosetrees Trust, ZonMw.

Bidirectional associations between mental health problems and language ability across 8 years of childhood.

Research examining the development of behavior, emotions and language, and their intertwining is limited as only few studies had a longitudinal design, mostly with a short follow-up period. Moreover, most studies did not evaluate whether internalizing symptoms and externalizing symptoms are independently associated with language ability. This study examines bidirectional associations between internalizing symptoms, externalizing symptoms and language ability in childhood in a large, population-based cohort. Longitudinal data from the Millennium Cohort Study, a cohort of children in the United Kingdom followed from birth to 11 years (n = 10,878; 50.7% boys), were analyzed. Internalizing and externalizing symptoms were based on parent reports. Language ability (higher scores reflecting poorer ability) was assessed by trained interviewers at ages 3, 5, 7 and 11 years. Structural Equation Models (SEM) were performed, including random-intercept cross-lagged panel models (RI-CLPM) and cross-lagged panel models (CLPM). Internalizing symptoms, externalizing symptoms and language ability were stable over time and co-occur with each other from early life onwards. Over time, externalizing symptoms in early childhood were associated with less growth in language skills and with increases in internalizing symptoms. In late childhood, language ability was negatively associated with later internalizing and externalizing symptoms. The early start, co-occurrence and persistent nature of internalizing symptoms, externalizing symptoms and (poorer) language ability highlights the importance of comprehensive assessments in young children who present problems in one of these domains. Specifically, among children in the early grades of elementary school, those with language difficulties may benefit from careful monitoring as they are more likely to develop difficulties in behavior and emotions.

The epidemiology of acne vulgaris in a multiethnic adolescent population from Rotterdam, the Netherlands: A cross-sectional study.

BACKGROUND: Although acne is a prevalent multifactorial inflammatory skin condition, few studies were performed in multiethnic populations. OBJECTIVES: To study the prevalence and determinants of acne in a multiethnic study at the start of puberty. METHODS: This cross-sectional study is embedded in Generation R, a population-based prospective study from Rotterdam, the Netherlands. Three-dimensional facial photos at the center visit in 2016-2019 (of ∼13-year-olds) were used to grade acne severity using the Global Evaluation of the Acne Severity (GEA). Analyses were stratified by biological sex and explored through chi-square tests and multivariable ordinal logistic regression. RESULTS: A total of 4561 children (51% girls) with a median age of 13.5 (IQR 13.3-13.6) were included. The visible acne prevalence (GEA 2-5) for girls vs boys was 62% vs 45% and moderate-to-severe acne (GEA 3-5) 14% vs 9%. Higher puberty stages (adjusted odds ratios: 1.38 [1.20-1.59] and 2.16 [1.86-2.51] for girls and boys, respectively) and darker skin colors V and VI (adjusted odds ratios: 1.90 [1.17-3.08] and 2.43 [1.67-3.56]) were associated with more severe acne in both sexes, and being overweight in boys (adjusted odds ratio: 1.58 [1.15-2.17]). LIMITATIONS: Cross-sectional design. CONCLUSIONS: Acne prevalence was high at the age of 13 years and was associated with advanced puberty, darker skin color, and weight status.

Is the association between mothers' autistic traits and childhood autistic traits moderated by maternal pre-pregnancy body mass index?

BACKGROUND: Previous studies showed that there is a positive association between mothers' and children's autistic traits. We also tested if this association is more pronounced in mothers with a higher pre-pregnancy body mass index (BMI). METHOD: The study was embedded in two cohorts with information available for 4,659 participants from the Generation R and for 179 participants from the Cambridge Ultrasound Siblings and Parents Project (CUSP) cohort. In both cohorts, maternal autistic traits were assessed using the short form of the Autism Spectrum Quotient, and information about maternal height and weight before pregnancy was obtained by questionnaire. Child autistic traits were assessed with the short form of Social Responsiveness Scale in Generation R (M = 13.5 years) and with the Quantitative Checklist for Autism in Toddlers (Q-CHAT) in the CUSP cohort (M = 1.6 years). RESULT: Higher maternal autistic traits were associated with higher autistic traits in toddlerhood (CUSP cohort; ßadjusted = 0.20, p < 0.01), in early childhood (Generation R; ßadjusted = 0.19, p < 0.01), and in early adolescence (Generation R; ßadjusted = 0.16, p < 0.01). Furthermore, a higher maternal pre-pregnancy BMI was associated with higher child autistic traits, but only in Generation R (ßadjusted = 0.03, p < 0.01). There was no significant moderating effect of maternal pre-pregnancy BMI on the association between autistic traits of mothers and children, neither in Generation R nor in CUSP. In addition, child autistic traits scores were significantly higher in mothers who were underweight and in mothers who were overweight compared to mothers with a healthy weight. CONCLUSION: We confirm the association between maternal and child autistic traits in toddlerhood, early childhood, and early adolescence. Potential interacting neurobiological processes remain to be confirmed.

An epigenome-wide association study of child appetitive traits and DNA methylation.

The etiology of childhood appetitive traits is poorly understood. Early-life epigenetic processes may be involved in the developmental programming of appetite regulation in childhood. One such process is DNA methylation (DNAm), whereby a methyl group is added to a specific part of DNA, where a cytosine base is next to a guanine base, a CpG site. We meta-analyzed epigenome-wide association studies (EWASs) of cord blood DNAm and early-childhood appetitive traits. Data were from two independent cohorts: the Generation R Study (n = 1,086, Rotterdam, the Netherlands) and the Healthy Start study (n = 236, Colorado, USA). DNAm at autosomal methylation sites in cord blood was measured using the Illumina Infinium HumanMethylation450 BeadChip. Parents reported on their child's food responsiveness, emotional undereating, satiety responsiveness and food fussiness using the Children's Eating Behaviour Questionnaire at age 4-5 years. Multiple regression models were used to examine the association of DNAm (predictor) at the individual site- and regional-level (using DMRff) with each appetitive trait (outcome), adjusting for covariates. Bonferroni-correction was applied to adjust for multiple testing. There were no associations of DNAm and any appetitive trait when examining individual CpG-sites. However, when examining multiple CpGs jointly in so-called differentially methylated regions, we identified 45 associations of DNAm with food responsiveness, 7 associations of DNAm with emotional undereating, 13 associations of DNAm with satiety responsiveness, and 9 associations of DNAm with food fussiness. This study shows that DNAm in the newborn may partially explain variation in appetitive traits expressed in early childhood and provides preliminary support for early programming of child appetitive traits through DNAm. Investigating differential DNAm associated with appetitive traits could be an important first step in identifying biological pathways underlying the development of these behaviors.

An epigenome-wide association study of child appetitive traits and DNA methylation.

Childhood appetitive traits are consistently associated with obesity risk, and yet their etiology is poorly understood. Appetitive traits are complex phenotypes which are hypothesized to be influenced by both genetic and environmental factors, as well as their interactions. Early-life epigenetic processes, such as DNA methylation (DNAm), may be involved in the developmental programming of appetite regulation in childhood. In the current study, we meta-analyzed epigenome-wide association studies (EWASs) of cord blood DNAm and early-childhood appetitive traits. Data were from two independent cohorts: the Generation R Study (n=1,086, Rotterdam, the Netherlands) and the Healthy Start study (n=236, Colorado, USA). DNAm at autosomal methylation sites in cord blood was measured using the Illumina Infinium HumanMethylation450 BeadChip. Parents reported on their child's food responsiveness, emotional undereating, satiety responsiveness and food fussiness using the Children's Eating Behaviour Questionnaire at age 4-5 years. Multiple regression models were used to examine the association of DNAm (predictor) at the individual site- and regional-level (using DMRff) with each appetitive trait (outcome), adjusting for covariates. Bonferroni-correction was applied to adjust for multiple testing. There were no associations of DNAm and any appetitive trait at the individual site-level. However, at the regional level, we identified 45 associations of DNAm with food responsiveness, 7 associations of DNAm with emotional undereating, 13 associations of DNAm with satiety responsiveness, and 9 associations of DNAm with food fussiness. This study shows that DNAm in the newborn may partially explain variation in appetitive traits expressed in early childhood and provides preliminary support for early programming of child appetitive traits through DNAm. Investigating differential DNAm associated with appetitive traits could be an important first step in identifying biological pathways underlying the development of these behaviors.

A Longitudinal Study of Stress During Pregnancy, Children's Sleep and Polygenic Risk for Poor Sleep in the General Pediatric Population.

Early life stress is robustly associated with poor sleep across life. Preliminary studies suggest that these associations may begin already in utero. Here, we study the longitudinal associations of prenatal psychosocial stress with sleep across childhood, and assess whether prenatal stress interacts with genetic liability for poor sleep.The study is embedded in the Generation R population-based birth cohort. Caregivers reported on prenatal psychosocial stress (life events, contextual, parental or interpersonal stressors) and on children's sleep at ages 2 months, 1.5, 2, 3 and 6 years. The study sample consisted of 4,930 children; polygenic risk scores for sleep traits were available in 2,063.Prenatal stress was consistently associated with more sleep problems across assessments. Effect sizes ranged from small (B = 0.21, 95%CI: 0.14;0.27) at 2 months to medium (B = 0.45, 95%CI: 0.38;0.53) at 2 years. Prenatal stress was moreover associated with shorter sleep duration at 2 months (Bhrs = -0.22, 95%CI: -0.32;-0.12) and at 2 years (Bhrs = -0.04, 95%CI -0.07; -0.001), but not at 3 years (Bhrs = 0.02, 95%CI: -0.02;0.06). Prenatal negative life events interacted with polygenic risk for insomnia to exacerbate sleep problems at 6 years (Binteraction = 0.07, 95%CI: 0.02;0.13).Psychosocial stress during pregnancy has negative associations with children's sleep that persist across childhood, and are exacerbated by genetic liability for insomnia. Associations with sleep duration were more pronounced in infancy and seem to attenuate with age. These findings highlight the role of the prenatal environment for developing sleep regulation, and could inform early intervention programs targeting sleep in children from high-risk pregnancies.

Dietary patterns, brain morphology and cognitive performance in children: Results from a prospective population-based study.

Dietary patterns in childhood have been associated with child neurodevelopment and cognitive performance, while the underlying neurobiological pathway is unclear. We aimed to examine associations of dietary patterns in infancy and mid-childhood with pre-adolescent brain morphology, and whether diet-related differences in brain morphology mediate the relation with cognition. We included 1888 and 2326 children with dietary data at age one or eight years, respectively, and structural neuroimaging at age 10 years in the Generation R Study. Measures of brain morphology were obtained using magnetic resonance imaging. Dietary intake was assessed using food-frequency questionnaires, from which we derived diet quality scores based on dietary guidelines and dietary patterns using principal component analyses. Full scale IQ was estimated using the Wechsler Intelligence Scale for Children-Fifth Edition at age 13 years. Children with higher adherence to a dietary pattern labeled as 'Snack, processed foods and sugar' at age one year had smaller cerebral white matter volume at age 10 (B = -4.3, 95%CI -6.9, -1.7). At age eight years, higher adherence to a 'Whole grains, soft fats and dairy' pattern was associated with a larger total brain (B = 8.9, 95%CI 4.5, 13.3), and larger cerebral gray matter volumes at age 10 (B = 5.2, 95%CI 2.9, 7.5). Children with higher diet quality and better adherence to a 'Whole grains, soft fats and dairy' dietary pattern at age eight showed greater brain gyrification and larger surface area, clustered primarily in the dorsolateral prefrontal cortex. These observed differences in brain morphology mediated associations between dietary patterns and IQ. In conclusion, dietary patterns in early- and mid-childhood are associated with differences in brain morphology which may explain the relation between dietary patterns and neurodevelopment in children.

Children with Autism Spectrum Disorder in Times of COVID-19: Examining Emotional and Behavioral Problems, Parental Well-Being, and Resilience.

This longitudinal study assessed the impact of the COVID-19 pandemic on children with autism spectrum disorder (ASD; n = 62; Mage = 13 years) by measuring emotional and behavioral problems before and during the pandemic, and by comparing this change to a matched sample of children without ASD (n = 213; Mage = 16 years). Moreover, we examined whether indicators of parental well-being promoted resilience of children with ASD. Results showed that the mean change in problems did not differ between children with and without ASD. Importantly, some children showed an increase in problems, while others showed resilience. Parental well-being indicators were not related to resilience among children with ASD. The interindividual variability in responses, particularly among children with ASD, highlights the need for personalized support.

Interrelated development of autism spectrum disorder symptoms and eating problems in childhood: a population-based cohort.

Eating problems, such as food selectivity or picky eating, are thought to be an epiphenomenon of autism spectrum disorders (ASD). Yet eating problems are also common in the general pediatric population and overlap with ASD symptoms. However, the temporal association between ASD symptoms and eating problems is poorly understood. This study examines the bidirectional association between ASD symptoms and eating problems across child development, and investigates whether these associations differ by child sex. Participants (N = 4,930) were from the population-based Generation R Study. Parents reported their child's ASD symptoms and eating problems using the Child Behavior Checklist at 5 assessments from toddlerhood to adolescence (1.5 to 14 years, 50% girls). A Random Intercept Cross-Lagged Panel Model was used to examine the lagged associations between ASD symptoms and eating problems at the within-person level, controlling for stable, trait-like differences at the between-person level. At the between-person level, there was a strong correlation between ASD symptoms and eating problems (ß = .48, 95% CI: 0.38 to 0.57). Controlling for these between-person effects, there was limited evidence for consistent, predictive effects of ASD symptoms and eating problems at the within-person level. Associations did not differ by child sex. Findings suggest that ASD symptoms and eating problems may represent a cluster of traits that are highly stable from early childhood to adolescence, which have a minimal reciprocal effect at the individual-level. Future research could focus on these trait-like qualities to inform the development of supportive, family-focused interventions.

Sleep, 24-hour activity rhythms, and cardiometabolic risk factors in school-age children.

STUDY OBJECTIVES: Disturbed sleep and 24-hour activity rhythms are linked to adverse cardiometabolic profiles in adults and adolescents, and these associations may originate in early life. We aimed to study associations of sleep and 24-hour rhythms with cardiometabolic risk factors in school-age children. METHODS: This cross-sectional population-based study comprised 894 children aged 8-11 years from the Generation R Study. Sleep (duration, efficiency, number of awakenings, and time awake after sleep onset) and 24-hour activity rhythms (social jet lag, interdaily stability, and intradaily variability) were assessed using triaxial wrist actigraphy for 9 consecutive nights. Cardiometabolic risk factors included adiposity (body mass index Z-score, fat mass index using dual-energy X-ray absorptiometry, and visceral fat mass and liver fat fraction using magnetic resonance imaging), blood pressure, and blood markers (glucose, insulin, and lipids). We adjusted for season, age, sociodemographics, and lifestyle factors. RESULTS: Each increase in interquartile range of nightly awakenings (2 times) was associated with -0.12 standard deviation (95% confidence interval: -0.21, -0.04) lower body mass index and 0.15 mmol/L (0.10, 0.21) higher glucose. Among boys, an increase in interquartile range of intradaily variability (0.12) was associated with higher fat mass index (+0.07 kg/m2; 95% confidence interval: 0.03, 0.11) and visceral FM (+0.08 g; 95% confidence interval: 0.02, 0.15). We observed no associations with blood pressure or clustering of cardiometabolic risk factors. CONCLUSIONS: Already at school age, greater fragmentation of the 24-hour activity rhythm is associated with general and organ adiposity. In contrast, more nightly awakenings were associated with lower body mass index. Future research should bring clarity to these disparate observations in order to create potential targets for obesity prevention programs. CITATION: Beunders VAA, Koopman-Verhoeff ME, Vermeulen MJ, et al. Sleep, 24-hour activity rhythms, and cardiometabolic risk factors in school-age children. J Clin Sleep Med. 2023;19(7):1219-1229.

Neurobiological, Psychosocial, and Behavioral Mechanisms Mediating Associations Between Physical Activity and Psychiatric Symptoms in Youth in the Netherlands.

Importance: Understanding the mechanisms by which physical activity is associated with a lower risk of psychiatric symptoms may stimulate the identification of cost-efficient strategies for preventing and treating mental illness at early life stages. Objective: To examine neurobiological, psychosocial, and behavioral mechanisms that mediate associations of physical activity with psychiatric symptoms in youth by testing an integrated model. Design, setting, and participants: Generation R is an ongoing prospective population-based cohort study collecting data from fetal life until young adulthood in a multiethnic urban population in the Netherlands. Pregnant women living in Rotterdam with an expected delivery date between April 2002 and January 2006 were eligible for participation along with their children born during this time. Data were collected at a single research center in the Erasmus Medical Center Sophia Children's Hospital. For the current study, data were analyzed from 4216 children with complete data on both exposure and outcome at ages 6, 10, and 13 years. Data were analyzed from January 2021 to November 2022. Exposures: Physical activity was ascertained at age 6 years (visit 1) via parent report and included weekly frequency and duration of walking or cycling to or from school, physical education at school, outdoor play, swimming, and sports participation. Main Outcomes and Measures: Psychiatric symptoms (internalizing and externalizing symptoms) were assessed at age 6 years (visit 1) and at age 13 years (visit 3) using the Child Behavior Checklist. Several mechanisms were explored as mediators, measured at age 10 years (visit 2). Neurobiological mechanisms included total brain volume, white matter microstructure, and resting-state connectivity assessed using a 3-T magnetic resonance imaging scanner. Psychosocial mechanisms included self-esteem, body image, and friendship. Behavioral mechanisms included sleep quality, diet quality, and recreational screen time. Pearson correlations between physical activity measures and psychiatric symptoms were calculated, with false discovery rate correction applied to account for the number of tests performed. Mediation analyses were performed when a correlation (defined as false discovery rate P < .05) between exposure and outcome was observed and were adjusted for confounders. Results: Among the 4216 children included in this study, the mean (SD) age was 6.0 (0.4) years at visit 1, and 2115 participants (50.2%) were girls. More sports participation was associated with fewer internalizing symptoms (ß for direct effect, -0.025; SE, 0.078; P = .03) but not externalizing symptoms. Self-esteem mediated the association between sports participation and internalizing symptoms (ß for indirect effect, -0.009; SE, 0.018; P = .002). No evidence was found for associations between any other neurobiological, psychosocial, or behavioral variables. No association was found between other types of physical activity and psychiatric symptoms at these ages. Conclusions and Relevance: The integrated model presented in this cohort study evaluated potential mechanisms mediating associations between physical activity and psychiatric symptoms in youth. Self-esteem mediated an association between sports participation in childhood and internalizing symptoms in adolescence; other significant mediations were not observed. Further studies might explore whether larger effects are present in certain subgroups (eg, children at high risk of developing psychiatric symptoms), different ages, or structured sport-based physical activity interventions.

Poverty from fetal life onward and child brain morphology.

Poverty is a risk factor for impaired child development, an association possibly mediated by brain morphology. Previous studies lacked prospective poverty assessments during pregnancy and did not stratify by majority/minority status. We investigated the association of household poverty from fetal life forward with brain morphological differences at age 10 years, in 2166 mother-child dyads. Overall, the results showed no associations between any poverty exposure early in life and brain volumes. However, there was the evidence of timing effects: children exposed to poverty in utero had smaller amygdala volumes (B = - 0.18, 95%CI - 0.30; - 0.07, pFDR-adjusted = 0.009). There were also differences in associations by majority/minority status (cerebral white matter: p for interaction = 0.04). Dutch children exposed to childhood poverty showed smaller cerebral white matter volumes than their control (B = - 0.26, 95%CI - 0.45; - 0.06, pFDR-adjusted = 0.035). This association was not observed in the minority population (B = - 0.05, 95%CI - 0.23; 0.12, pFDR-adjusted = 0.542). The smaller cerebral white matter volume mediated the association between childhood poverty and poorer school performance in Dutch children. Our findings point to the importance of poverty exposure in the fetal period and suggest different mechanisms and vulnerabilities across majority/minority groups.

Fetal and infant growth patterns, sleep, and 24-h activity rhythms: a population-based prospective cohort study in school-age children.

The study objective was to explore associations of fetal and infant weight patterns and preterm birth with sleep and 24-h activity rhythm parameters at school-age. In our prospective population-based study, 1327 children were followed from birth to age 10-15 years. Fetal weight was estimated using ultrasound in the second and third trimester of pregnancy. Birth weight and gestational age were available from midwife registries. Infant weight was measured at 6, 12 and 24 months. Fetal and infant weight acceleration or deceleration were defined as a change of >0.67 standard deviation between the corresponding age intervals. At school-age, sleep duration, sleep efficiency, wake after sleep onset, social jetlag, inter-daily stability, and intra-daily variability were assessed using tri-axial wrist actigraphy for 9 consecutive nights. We observed that low birth weight (<2500 g) was associated with 0.24 standard deviation (95% confidence interval [CI] 0.04; 0.43) longer sleep duration compared to normal weight. Compared to normal growth, growth deceleration in fetal life and infancy was associated with 0.40 standard deviation (95% CI 0.07; 0.73) longer sleep duration, 0.44 standard deviation (95% CI 0.14; 0.73) higher sleep efficiency, and -0.41 standard deviation (95% CI -0.76; -0.07) shorter wake after sleep onset. A pattern of normal fetal growth followed by infant growth acceleration was associated with -0.40 standard deviation (95% CI -0.61; -0.19) lower inter-daily stability. Preterm birth was not associated with any sleep or 24-h rhythm parameters. Our findings showed that children with fetal and infant growth restriction had longer and more efficient sleep at school-age, which may be indicative of an increased need for sleep for maturational processes and development after a difficult start in life.

Maternal sensitivity in early childhood and body mass index in adolescence: A population-based study on the role of self-regulation as a mediator.

Maternal sensitivity has been implicated in various aspects of child health and development, including overweight. However, long-term effects, the role of paternal sensitivity and the explanatory pathways are unclear. This study examined whether maternal sensitivity in early childhood is prospectively associated with adolescent body mass index and whether children's self-regulation mediates this relation. Data from 540 children and their mothers were available from a large cohort study in the Netherlands. Maternal sensitivity was assessed at child ages 1, 3, and at 4 years paternal sensitivity was also included. Children's self-regulation skills were observed at age 3, eating behaviour was assessed at 10 years, and child BMI was measured at 13 years. Longitudinal structural equation modelling was applied. The cross-sectional association between maternal sensitivity and child self-regulation was significant, while lower levels of self-regulation and higher levels of food responsiveness and restrained eating predicted a higher child BMI at 13 years. Furthermore, a direct association of paternal sensitivity at 4 years with BMI at 13 years was found, but only in girls. Maternal sensitivity was not directly associated with child BMI after adjusting for covariates. Our findings showed the importance of self-regulation in the early years for subsequent weight development. Nevertheless, as self-regulation could not explain the relationship between parenting and child weight, research should focus on the contribution of other contextual factors, such as feeding styles and the social environment, to this relationship.