As a result of societal changes, fathers participate more actively in child care than they used to. In this article, we propose a context‐dependent biobehavioral model of emergent fatherhood in which sociocultural, behavioral, hormonal, and neural factors develop and interact during the first 1,000 days of fatherhood. Sociocultural factors, including different expectations of fathers and varying opportunities for paternal caregiving through paid paternal leave, influence paternal involvement. Levels of hormones (e.g., testosterone, vasopressin, oxytocin, cortisol) predict fathers’ parenting behaviors, and involvement in caregiving in turn affects their hormones and brain responses to infant stimuli. The birth of the first child marks the transition to fatherhood and may be a critical period in men’s lives, with a smoother transition to fatherhood predicting more optimal involvement by fathers in subsequent years. A focus on prenatal and early postnatal fathering may pave the way for developing interventions that effectively support fathering during pregnancy and in the first years of their children’s lives.

Attention-deficit and hyperactivity disorder (ADHD) is a common childhood disorder with a substantial genetic component. However, the extent to which epigenetic mechanisms play a role in the etiology of the disorder is unknown. We performed epigenome-wide association studies (EWAS) within the Pregnancy And Childhood Epigenetics (PACE) Consortium to identify DNA methylation sites associated with ADHD symptoms at two methylation assessment periods: birth and school age. We examined associations of both DNA methylation in cord blood with repeatedly assessed ADHD symptoms (age 4–15 years) in 2477 children from 5 cohorts and of DNA methylation at school age with concurrent ADHD symptoms (age 7–11 years) in 2374 children from 9 cohorts, with 3 cohorts participating at both timepoints. CpGs identified with nominal significance (p < 0.05) in either of the EWAS were correlated between timepoints (ρ = 0.30), suggesting overlap in associations; however, top signals were very different. At birth, we identified nine CpGs that predicted later ADHD symptoms (p < 1 × 10–7), including ERC2 and CREB5. Peripheral blood DNA methylation at one of these CpGs (cg01271805 in the promoter region of ERC2, which regulates neurotransmitter release) was previously associated with brain methylation. Another (cg25520701) lies within the gene body of CREB5, which previously was associated with neurite outgrowth and an ADHD diagnosis. In contrast, at school age, no CpGs were associated with ADHD with p < 1 × 10−7. In conclusion, we found evidence in this study that DNA methylation at birth is associated with ADHD. Future studies are needed to confirm the utility of methylation variation as biomarker and its involvement in causal pathways.

BackgroundInternalising and externalising problems commonly co‐occur in childhood. Yet, few developmental models describing the structure of child psychopathology appropriately account for this comorbidity. We evaluate a model of childhood psychopathology that separates the unique and shared contribution of individual psychological symptoms into specific internalising, externalising and general psychopathology factors and assess how these general and specific factors predict long‐term outcomes concerning criminal behaviour, academic achievement and affective symptoms in three independent cohorts.MethodsData were drawn from independent birth cohorts (Avon Longitudinal Study of Parents and Children (ALSPAC), N = 11,612; Generation R, N = 7,946; Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN), N = 408). Child psychopathology was assessed between 4 and 8 years using a range of diagnostic and questionnaire‐based measures, and multiple informants. First, structural equation models were used to assess the fit of hypothesised models of shared and unique components of psychopathology in all cohorts. Once the model was chosen, linear/logistic regressions were used to investigate whether these factors were associated with important outcomes such as criminal behaviour, academic achievement and well‐being from late adolescence/early adulthood.ResultsThe model that included specific factors for internalising/externalising and a general psychopathology factor capturing variance shared between symptoms regardless of their classification fits well for all of the cohorts. As hypothesised, general psychopathology factor scores were predictive of all outcomes of later functioning, while specific internalising factor scores predicted later internalising outcomes. Specific externalising factor scores, capturing variance not shared by any other psychological symptoms, were not predictive of later outcomes.ConclusionsEarly symptoms of psychopathology carry information that is syndrome‐specific as well as indicative of general vulnerability and the informant reporting on the child. The ‘general psychopathology factor' might be more relevant for long‐term outcomes than specific symptoms. These findings emphasise the importance of considering the co‐occurrence of common internalising and externalising problems in childhood when considering long‐term impact.

Institutional care has been shown to lead to insecure and disorganized attachments and indiscriminate friendliness. Some children, however, are surprisingly resilient to the adverse environment. Here the protective role of the long variant of the serotonin receptor gene (5HTT) is explored in a small hypothesis-generating study of 37 Ukrainian preschoolers reared in institutional settings or in their biological families. Attachment was observed with the Strange Situation Procedure, and indiscriminate social behavior was assessed in a semistructured interview with the caregiver. We found a moderating role of 5HTT for the association between adverse environment and attachment disorganization. Children with the ss or sl genotyope showed more attachment disorganization and less attachment security when they grew up in an institution compared to children who lived in a family, but children who were homozygous for the l allele appeared to be protected against the adverse institutional environment on attachment. We conclude that not all children may be equally vulnerable to extremely adverse rearing experiences.