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Background: Children with autism have difficulties in understanding relationships, yet little is known about the levels of autistic traits with regard to peer relationships. This study examined the association between autistic traits and peer relationships. Additionally, we examined whether the expected negative association is more pronounced in children with a lower non-verbal IQ and in those who exhibit more externalizing problems. Method: Data were collected in a large prospective birth cohort of the Generation R Study (Rotterdam, the Netherlands) for which nearly 10,000 pregnant mothers were recruited between 2002 and 2006. Follow up data collection is still currently ongoing. Information on peer relationships was collected with PEERS application, an interactive computerized task (M = 7.8 years). Autistic traits were assessed among general primary school children by using the Social Responsiveness Scale (M = 6.1 years). Information was available for 1580 children. Result: Higher levels of autistic traits predicted lower peer acceptance and higher peer rejection. The interaction of autistic traits with externalizing problems (but not with non-verbal IQ or sex) was significant: only among children with low externalizing problems, a higher level of autistic traits predicted less peer acceptance and more peer rejection. Among children exhibiting high externalizing problems, a poor peer acceptance and high level of rejection is seen independently of the level of autistic traits. Conclusion: We conclude that autistic traits—including traits that do not classify as severe enough for a clinical diagnosis—as well as externalizing problems negatively impact young children’s peer relationships. This suggests that children with these traits may benefit from careful monitoring and interventions focused at improving peer relationships.

Parenting stress of mothers has frequently been linked to negative child outcomes. According to Abidin’s stress model, this relationship may be explained by dysfunctional parenting behaviors. In this study, we scrutinized the effects of both mothers and fathers in the pathway from parenting stress through parenting behaviors to subsequent adolescent behavior problems. We expected the association between parenting stress and adolescent behavior problems to be partially mediated by maternal and paternal parenting behaviors. Further, we expected crossover effects, i.e., that parenting stress of one parent was related to the parenting behavior of the other parent. We applied a 3-wave longitudinal design using data from 441 adolescents (52% girls) and their parents (419 fathers; 436 mothers). Parents reported on parenting stress (adolescent age range = 10.9–16.3 years). Adolescents reported on perceived parental overreactivity and warmth (age range = 12.9–18.3) and their own internalizing and externalizing problems (age range = 15.9–21.3). Despite cross-sectional significant associations between parenting stress, parenting behavior, and adolescent behavior problems, we found no evidence of longitudinal linkages. One exception was maternal parenting stress, which positively predicted later adolescent externalizing problems. Consequently, the mediating role of parenting behaviors was not supported. We found no crossover effects in the pathway from parenting stress to parenting behaviors. The discrepancies between our longitudinal and cross-sectional findings raise questions about the actual impact that parents have on their children’s outcome. Though, targeting mothers’ parenting stress may help to reduce adolescent externalizing problems and its ramifications at least to some extent.

Children with Autism Spectrum Disorder (ASD) often exhibit problematic eating behaviors, an observation mostly based on male dominated, clinical ASD study samples. It is, however, important to evaluate both children with an ASD diagnosis and children with subclinical autistic traits as both often experience difficulties. Moreover, considering the suggestion of a possible girl-specific ASD phenotype, there is a need to determine whether autistic traits are related with problematic eating behaviors in girls as well. This study explores the sex-specific association between autism (both autistic traits and diagnosed ASD) and eating behavior in middle childhood in Generation R, a prospective population-based cohort from fetal life onwards. We collected parental reports of autistic traits at six years (Social Responsiveness Scale) and of eating behavior at ten years (Children's Eating Behaviour Questionnaire). In this cohort of 3559 children, autistic traits at six years were associated with more Picky Eating, Emotional Eating and Food Responsiveness in later childhood (e.g. adjusted B for Picky Eating = 0.07; 95% CI: 0.03, 0.11). Stratified analyses showed that in girls, autistic traits were associated with more Emotional Overeating and Emotional Undereating (e.g. adjusted B for Emotional Undereating = 0.12; 95% CI: 0.04, 0.20), while no associations were found for boys. Results comparing children with and without an ASD diagnosis in the cohort largely confirm these associations (e.g. in girls, adjusted B for Emotional Undereating = 0.72; 95% CI: 0.01, 1.42). Our results point to a sex-specific association between autism and eating behavior in middle childhood. Also, our study is the first study to show that autistic traits are associated with emotionally based eating problems in girls and possibly represent part of a girl-specific ASD phenotype.

Polycystic ovary syndrome (PCOS) is an endocrine condition associated with reproductive and psychiatric disorders, and with obesity. Eating disorders, such as bulimia and recurrent dieting, are also linked to PCOS. They can lead to the epigenetic dysregulation of the hypothalamic–pituitary–gonadal (HPG) axis, thereby impacting on ovarian folliculogenesis. We postulate that PCOS is induced by psychological distress and episodes of overeating and/or dieting during puberty and adolescence, when body dissatisfaction and emotional distress are often present. We propose that upregulated activation of the central HPG axis during this period can be epigenetically altered by psychological stressors and by bulimia/recurrent dieting, which are common during adolescence and which can lead to PCOS. This hypothesis is based on events that occur during a largely neglected stage of female reproductive development. To date, most research into the origins of PCOS has focused on the prenatal induction of this disorder, particularly in utero androgenization and the role of anti-Müllerian hormone. Establishing causality in our peripubertal model requires prospective cohort studies from infancy. Mechanistic studies should consider the role of the gut microbiota in addition to the epigenetic regulation of (neuro) hormones. Finally, clinicians should consider the importance of underlying chronic psychological distress and eating disorders in PCOS.

OBJECTIVE: This study examined the prospective, potentially bidirectional association of aggressive behavior with BMI and body composition across childhood in three population-based cohorts. METHODS: Repeated measures of aggression and BMI were available from the Generation R Study between ages 6 and 10 years (N = 3,974), the Netherlands Twin Register (NTR) between ages 7 and 10 years (N = 10,328), and the Swedish Twin Study of Child and Adolescent Development (TCHAD) between ages 9 and 14 years (N = 1,462). In all samples, aggression was assessed with the Child Behavior Checklist. Fat mass and fat-free mass were available in the Generation R Study. Associations were examined with cross-lagged modeling. RESULTS: Aggressive behavior at baseline was associated with higher BMI at follow-up in the Generation R Study (β = 0.02, 95% CI: 0.00 to 0.04), in NTR (β = 0.04, 95% CI: 0.02 to 0.06), and in TCHAD (β = 0.03, 95% CI: -0.02 to 0.07). Aggressive behavior was prospectively associated with higher fat mass (β = 0.03, 95% CI: 0.01 to 0.05) but not fat-free mass. There was no evidence that BMI or body composition preceded aggressive behavior. CONCLUSIONS: More aggressive behavior was prospectively associated with higher BMI and fat mass. This suggests that aggression contributes to the obesity problem, and future research should study whether these behavioral pathways to childhood obesity are modifiable., Funding Agencies:European Union Seventh Framework Program (2007-2013): Aggression in Children: Unravelling Gene-Environment Interplay to Inform Treatment and Intervention Strategies (ACTION) 602768 Dutch Diabetes Foundation 2013.81.1664 Netherlands Organization for Scientific Research (NWO) 016. VICI.170.200 Erasmus Medical Center, Rotterdam Erasmus University, Rotterdam Netherlands Organization for Health Research and Development (ZonMw) NWO NWO 480-04-004 ZonMw 912-10-020 NWO 480-15-001

Background: The association between air pollution exposure and emotional and behavioural problems in children is unclear. We aimed to assess prenatal and postnatal exposure to several air pollutants and child's depressive and anxiety symptoms, and aggressive symptoms in children of 7-11 years. Methods: We analysed data of 13182 children from 8 European population-based birth cohorts. Concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter (PM) with diameters of <= 10 mu m (PM10), <= 2.5 mu m (PM2.5), and between 10 and 2.5 mu m (PMcoarse), the absorbance of PM2.5 filters (PM(2.5)abs), and polycyclic aromatic hydrocarbons (PAHs) were estimated at residential addresses of each participant. Depressive and anxiety symptoms and aggressive symptoms were assessed at 7-11 years of age using parent reported tests. Children were classified in borderline/clinical range or clinical range using validated cut offs. Region specific models were adjusted for various socio-economic and lifestyle characteristics and then combined using random effect meta-analysis. Multiple imputation and inverse probability weighting methods were applied to correct for potential attrition bias. Results: A total of 1896 (14.4%) children were classified as having depressive and anxiety symptoms in the borderline/clinical range, and 1778 (13.4%) as having aggressive symptoms in the borderline/clinical range. Overall, 1108 (8.4%) and 870 (6.6%) children were classified as having depressive and anxiety symptoms, and aggressive symptoms in the clinical range, respectively. Prenatal exposure to air pollution was not associated with depressive and anxiety symptoms in the borderline/clinical range (e.g. OR 1.02 [95%CI 0.95 to 1.10] per 10 mu g/m(3) higher NO2) nor with aggressive symptoms in the borderline/clinical range (e.g. OR 1.04 [95%CI 0.96 to 1.12] per 10 mu g/m(3) higher NO2). Similar results were observed for the symptoms in the clinical range, and for postnatal exposures t

BACKGROUND: As an adjuvant for medication, dietary changes focused on specific nutrients have been proposed to prevent or reduce attention-deficit/hyperactivity disorder (ADHD) symptoms. However, whether an overall healthy dietary pattern is associated with ADHD symptom severity during childhood remains unclear. Furthermore, it is not clear what the direction of this association is. OBJECTIVES: We aimed to examine the association between dietary patterns and ADHD symptoms in school-aged children. In addition, we aimed to identify the temporal direction of this association-that is, whether dietary patterns predict ADHD symptoms or vice versa. METHODS: We analyzed data from 3680 children participating in the Generation R Study, a prospective cohort in Rotterdam, Netherlands. ADHD symptoms were assessed with parent-report questionnaires at ages 6 and 10 y using the Child Behavior Checklist. Dietary intake was assessed at the age of 8 y with a validated food-frequency questionnaire. We computed a diet quality score reflecting adherence to dietary guidelines. We examined bidirectional associations of diet quality with ADHD symptom scores using multivariable linear regression analysis and cross-lagged modeling. RESULTS: Linear regressions showed that more ADHD symptoms at age 6 y were associated with a lower diet quality score at age 8 y (SD score = -0.08; 95% CI: -0.11, -0.05) but that diet quality at age 8 y was not associated with ADHD symptoms at age 10 y. Cross-lagged models confirmed a unidirectional relation from ADHD symptoms to diet quality but not vice versa. Associations did not differ by overweight status or between boys and girls. CONCLUSION: Our study suggests that children with more ADHD symptoms may be at higher risk of an unhealthy diet but that overall diet quality does not affect ADHD risk.