Among children exposed to elevated maternal depression symptoms (MDS), recent studies have demonstrated reduced internalizing and externalizing problems for those who have attended formal childcare (i.e., center-based, family-based childcare). However, these studies did not consider whether childcare attendance is associated with benefits for the child only or also with reduced MDS. Using a four-wave longitudinal cross-lagged model, we evaluated whether formal childcare attendance was associated with MDS or child behavior problems and whether it moderated longitudinal associations between MDS and child behavior problems and between child behavior problems and MDS. The sample was drawn from a population-based cohort study and consisted of 908 biologically related mother–child dyads, followed from 5 months to 5 years. Attending formal childcare was not associated with MDS or child behavior problems but moderated the association between MDS at 3.5 years and child internalizing and externalizing problems at 5 years as well as between girls’ externalizing problems at 3.5 years and MDS at 5 years. No other moderation of formal childcare was found. Findings suggest that attending formal childcare reduces the risks of behavior problems in the context of MDS but also the risk of MDS in the context of girls’ externalizing problems.

The pregnancy period represents a unique window of opportunity to identify risks to both the fetus and mother and to deter the intergenerational transmission of adversity and mental health problems. Although the maternal–fetal dyad is especially vulnerable to the effects of stress during pregnancy, less is known about how the dyad is also receptive to salutary, resilience-promoting influences. The present review adopts life span and intergenerational perspectives to review four key areas of research. The first part describes how pregnancy is a sensitive period for both the mother and fetus. In the second part, the focus is on antecedents of maternal prenatal risks pertaining to prenatal stress response systems and mental health. The third part then turns to elucidating how these alterations in prenatal stress physiology and mental health problems may affect infant and child outcomes. The fourth part underscores how pregnancy is also a time of heightened fetal receptivity to maternal and environmental signals, with profound implications for adaptation. This section also reviews empirical evidence of promotive and protective factors that buffer the mother and fetus from developmental and adaptational problems and covers a sample of rigorous evidence-based prenatal interventions that prevent maladaptation in the maternal–fetal dyad before babies are born. Finally, recommendations elaborate on how to further strengthen understanding of pregnancy as a period of multilevel risk and resilience, enhance comprehensive prenatal screening, and expand on prenatal interventions to promote maternal–fetal adaptation before birth.

This study explores the conceptualization of mother–infant cortisol attunement both theoretically and empirically, and its association with mother–infant attachment disorganization. In a community sample (N = 256), disorganization and cortisol were assessed during the Strange Situation Procedure (SSP) at infant age 17 months. Salivary cortisol was collected at baseline, and 20 and 40 min after the SSP. We utilized three statistical approaches: correlated growth modeling (probing a simultaneous conceptualization of attunement), cross-lagged modeling (probing a lagged, reciprocal conceptualization of attunement), and a multilevel model difference score analysis (to examine the pattern of discrepancies in mother–infant cortisol values). Correlated growth modeling revealed that disorganized, relative to organized, dyads had significant magnitude of change over time, such that, among disorganized dyads, as mothers had greater declines in cortisol, infants had greater increases. The difference score analysis revealed that disorganized, relative to organized, dyads had a greater divergence between maternal and infant cortisol values, such that maternal values were lower than infant values. Disorganized attachment status was not significantly associated with attunement when conceptualized as reciprocal and lagged in the cross-lagged model. Findings suggest that mother–infant dyads in disorganized attachment relationships, who are by definition behaviorally misattuned, are also misattuned in their adrenocortical responses.

Infant siblings of children with autism spectrum disorder (ASD) exhibit greater heterogeneity in behavioral presentation and outcomes relative to infants at low familial risk (LR), yet there is limited understanding of the diverse developmental profiles that characterize these infants. We applied a hierarchical agglomerative cluster analysis approach to parse developmental heterogeneity in 420 toddlers with heightened (HR) and low (LR) familial risk for ASD using measures of four dimensions of development: language, social, play, and restricted and repetitive behaviors (RRB). Results revealed a two-cluster solution. Comparisons of clusters revealed significantly lower language, social, and play performance, and higher levels of restricted and repetitive behaviors in Cluster 1 relative to Cluster 2. In Cluster 1, 25% of children were later diagnosed with ASD compared to 8% in Cluster 2. Comparisons within Cluster 1 between subgroups of toddlers having ASD+ versus ASD− 36-month outcomes revealed significantly lower functioning in the ASD+ subgroup across cognitive, motor, social, language, symbolic, and speech dimensions. Findings suggest profiles of early development associated with resiliency and vulnerability to later ASD diagnosis, with multidimensional developmental lags signaling vulnerability to ASD diagnosis.

Although shyness is a ubiquitous phenomenon with early developmental origins, little research has examined the influence of prenatal exposures on the developmental trajectory of shyness. Here, we examined trajectories of shyness from childhood to adulthood in three groups (N = 254), with varying degrees of prenatal adversity as indicated by the number of stressful exposures: extremely low birth weight (ELBW; <1000 g) survivors prenatally exposed to exogenous corticosteroids (ELBW+S, n = 56); ELBW survivors not prenatally exposed to exogenous corticosteroids (ELBW+NS, n = 56); and normal birth weight (NBW, n = 142) controls. Multilevel modeling revealed that the ELBW+S individuals exhibited the highest levels of childhood shyness, which remained stable into adulthood. The ELBW+NS and NBW controls had comparably low levels of childhood shyness; however, the ELBW+NS individuals experienced patterns of increasing shyness, while NBW controls displayed decreases in shyness into adulthood. We speculate that individuals exposed to multiple prenatal stressors (i.e., ELBW+S) may be developmentally programmed to be more sensitive to detecting social threat, with one manifestation being early developing, stable shyness, while increasing shyness among ELBW+NS individuals may reflect a later developing shyness influenced by postnatal context. We discuss the implications of these findings for understanding the developmental origins and developmental course of human shyness from childhood through adulthood.

Research showing that risk for schizophrenia, bipolar disorder with psychosis, and other psychosis-spectrum diagnoses in adulthood is multidetermined has underscored the necessity of studying the additive and interactive factors in childhood that precede and predict future disorders. In this study, risk for the development of psychosis-spectrum disorders was examined in a 2-generation, 30-year prospective longitudinal study of 3,905 urban families against a sociocultural backdrop of changing economic and social conditions. Peer nominations of aggression, withdrawal, and likeability and national census information on neighborhood-level socioeconomic disadvantage in childhood, as well as changes in neighborhood socioeconomic conditions over the lifespan, were examined as predictors of diagnoses of schizophrenia, bipolar disorder, and other psychosis-spectrum disorders in adulthood relative to developing only nonpsychotic disorders or no psychiatric disorders. Individuals who were both highly aggressive and highly withdrawn were at greater risk for other psychosis-spectrum diagnoses when they experienced greater neighborhood disadvantage in childhood or worsening neighborhood conditions over maturation. Males who were highly aggressive but low on withdrawal were at greater risk for schizophrenia diagnoses. Childhood neighborhood disadvantage predicted both schizophrenia and bipolar diagnoses, regardless of childhood social behavior. Results provided strong support for multiple-domain models of psychopathology, and suggest that universal preventive interventions and social policies aimed at improving neighborhood conditions may be particularly important for decreasing the prevalence of psychosis-spectrum diagnoses in the future.

Parents play an essential role in supporting child development by providing a safe home, proper nutrition, and rich educational opportunities. In this article we focus on the role of caregiver speech in supporting development of young children with autism spectrum disorder (ASD). We review studies from typically developing children and children with autism showing that rich and responsive caregiver speech supports language development. Autism intervention studies that target caregiver speech are reviewed as are recent scientific advances from studies of typical development. The strengths and weakness of different techniques for collecting language data from caregivers and children are reviewed, and natural language samples are recommended as best practice for language research in autism. We conclude that caregivers play a powerful role in shaping their children's development and encourage researchers to adapt parent-mediated intervention studies to acknowledge individual differences in parents by using a personalized medicine approach.

This study examined effects of risk factors in multiple domains measured in preschool and kindergarten on age 6 depression symptoms, and on changes in symptom levels between ages 4 and 6. Two models were examined in a large, diverse (N = 796) community sample of children and parents. Risk variables included SES, stress, conflict, parental depression, parental hostility, support, scaffolding, child negative affect (NA), effortful control (EC), sensory regulation (SR), and attachment security. Model 1 included effects of risk factors at ages 4 and 5 on child depression symptoms at age 6. Model 2 also included depression symptoms at all three ages to examine changes in these symptoms. Model 1 revealed that age 4 and 5 parental depression, NA, EC, and SR predicted age 6 child depression levels, Several age 4 variables had indirect pathways to age 6 depression via age 5 EC. Model 2 revealed that preschool depression was the only age 4 variable, and EC and SR were the only age 5 variables that significantly predicted increases in age 6 depression. These findings highlight the role of self-regulation in child depression and suggest that targeting self-regulation may be an effective prevention and intervention strategy.

Hypertensive disorders of pregnancy (HDP) may increase the risk of offspring depression in childhood. Low birth weight is also associated with increased risk of mental health problems, including depression. This study sought to investigate (a) whether there is an association between HDP and the risk of depression in childhood and (b) whether low birth weight mediates this association. The current study is based on the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective, population-based study that has followed a cohort of offspring since their mothers were pregnant (n = 6,739). Depression at the age of 7 years was diagnosed using parent reports via the Development and Well-Being Assessment (DAWBA). Log-binomial regression and mediation analyses were used. Children exposed to HDP were 2.3 times more likely to have a depression diagnosis compared with nonexposed children, adjusted Risk Ratio [RR], 2.31; 95% CI, [1.20, 4.47]. Low birth weight was a weak mediator of this association. Results were adjusted for confounding variables including antenatal depression and anxiety during pregnancy.This study suggests that fetal exposure to maternal hypertensive disorders of pregnancy increased the risk of childhood depression. The study adds to the evidence suggesting that the uterine environment is a critical determinant of neurodevelopmental and psychiatric outcomes.

Nearly 1 in 5 children in the United States lives in a household whose income is below the official federal poverty line, and more than 40% of children live in poor or near-poor households. Research on the effects of poverty on children's development has been a focus of study for many decades and is now increasing as we accumulate more evidence about the implications of poverty. The American Academy of Pediatrics recently added “Poverty and Child Health” to its Agenda for Children to recognize what has now been established as broad and enduring effects of poverty on child development. A recent addition to the field has been the application of neuroscience-based methods. Various techniques including neuroimaging, neuroendocrinology, cognitive psychophysiology, and epigenetics are beginning to document ways in which early experiences of living in poverty affect infant brain development. We discuss whether there are truly worthwhile reasons for adding neuroscience and related biological methods to study child poverty, and how might these perspectives help guide developmentally based and targeted interventions and policies for these children and their families.

Atypical communication characteristics (ACCs), such as speech delay, odd pitch, and pragmatic difficulties, are common features of autism spectrum disorder (ASD) as are the symptoms of a wide range of psychiatric disorders. Using a simple retrospective method, this study aimed to better understand the relation and stability of ACCs with a broad range of psychiatric symptoms among large, well-characterized samples of clinic-referred children and adolescents with and without ASD. Youth with ASD had higher rates and a more variable pattern of developmental change in ACCs than the non-ASD diagnostic group. Latent class analysis yielded three ACC stability subgroups within ASD: Stable ACCs, Mostly Current-Only ACCs, and Little Professors. Subgroups exhibited differences in severity of ASD symptomatology, co-occurring psychiatric symptoms, and other correlates. Our findings provide support for the clinical utility of characterizing caregiver-perceived changes in ACCs in identifying children at risk for co-occurring psychopathology and other clinically relevant variables.

Currently, two main approaches exist to distinguish differential susceptibility from diathesis-stress and vantage sensitivity in Genotype × Environment interaction (G × E) research: regions of significance (RoS) and competitive-confirmatory approaches. Each is limited by its single-gene/single-environment foci given that most phenotypes are the product of multiple interacting genetic and environmental factors. We thus addressed these two concerns in a recently developed R package (LEGIT) for constructing G × E interaction models with latent genetic and environmental scores using alternating optimization. Herein we test, by means of computer simulation, diverse G × E models in the context of both single and multiple genes and environments. Results indicate that the RoS and competitive-confirmatory approaches were highly accurate when the sample size was large, whereas the latter performed better in small samples and for small effect sizes. The competitive-confirmatory approach generally had good accuracy (a) when effect size was moderate and N ≥ 500 and (b) when effect size was large and N ≥ 250, whereas RoS performed poorly. Computational tools to determine the type of G × E of multiple genes and environments are provided as extensions in our LEGIT R package.

Early life adversity (ELA) has been associated with inflammation and immunosenescence, as well as hyporeactivity of the HPA axis. Because the immune system and the HPA axis are tightly intertwined around the glucocorticoid receptor (GR), we examined peripheral GR functionality in the EpiPath cohort among participants who either had been exposed to ELA (separation from parents and/or institutionalization followed by adoption; n = 40) or had been reared by their biological parents (n = 72).

Expression of the strict GR target genes FKBP5 and GILZ as well as total and 1F and 1H GR transcripts were similar between groups. Furthermore, there were no differences in GR sensitivity, examined by the effects of dexamethasone on IL6 production in LPS-stimulated whole blood. Although we did not find differences in methylation at the GR 1F exon or promoter region, we identified a region of the GR 1H promoter (CpG 1-9) that showed lower methylation levels in ELA.

Our results suggest that peripheral GR signaling was unperturbed in our cohort and the observed immune phenotype does not appear to be secondary to an altered GR response to the perturbed HPA axis and glucocorticoid (GC) profile, although we are limited in our measures of GR activity and time points.

The objective was to determine the longitudinal associations between callous-unemotional (CU) and oppositional defiant (OD) behaviors from the first to fourth grades for Spanish children. Four possible outcomes were evaluated: (a) CU behaviors in the first grade predict increases in OD behaviors in the fourth grade, controlling for OD behaviors in the first grade; (b) OD behaviors in the first grade predict increases in CU behaviors in the fourth grade, controlling for CU behaviors in the first grade; (c) both unique effects are significant; and (d) neither unique effect is significant. A longitudinal panel model with two latent variables (CU and OD behaviors), three sources (mothers, fathers, teachers), and two occasions (spring of the first and fourth grades) was used to evaluate the four possibilities among 758 (54% boys) first grade and 469 (53% boys) fourth grade Spanish children. For mother-, father-, and teacher-reports, OD behaviors in the first grade predicted increases in CU behaviors in the fourth grade, after controlling for CU behaviors in the first grade, whereas CU behaviors in the first grade did not predict increases in OD behaviors in the fourth grade, after controlling for OD behaviors in the first grade. OD behaviors thus conferred independent vulnerability to increases in CU behaviors 3 years later among young children.

Children who have been adopted internationally commonly experience institutional care and other forms of adversity prior to adoption that can alter the functioning of the hypothalamic–pituitary–adrenal (HPA) axis. In particular, internationally adopted children tend to have blunted diurnal declines compared to children raised in their birth families. The Attachment and Biobehavioral Catch-Up (ABC) intervention was developed to enhance young children's biological and behavioral regulation by promoting sensitive parenting. The current study used a randomized controlled trial to assess whether ABC improved the diurnal functioning of the HPA axis among 85 children who had been adopted internationally when they were between the ages of 4 and 33 months (M = 16.12). Prior to the intervention, there were no significant differences in diurnal cortisol production between children whose parents were randomly assigned to receive ABC and children whose parents were randomly assigned to receive a control intervention. After the intervention, children whose parents had received the ABC intervention exhibited steeper declines in cortisol levels throughout the day than children whose parents had received the control intervention. These results indicate that the ABC intervention is effective in enhancing a healthy pattern of diurnal HPA axis regulation for young children who have been adopted internationally.

Research suggests that childhood adversity (CA) is associated with a wide range of repercussions, including an increased likelihood of interpersonal stress generation. This may be particularly true following interpersonal childhood adversity (ICA) and for youth with high hypothalamic-pituitary-adrenal (HPA) axis-related genetic risk. In the current study, we applied a multilocus genetic profile score (MGPS) approach to measuring HPA axis-related genetic variation and examined its interaction with ICA to predict interpersonal stress generation in a sample of adolescents aged 14–17 (N = 241, Caucasian subsample n = 192). MGPSs were computed using 10 single nucleotide polymorphisms from HPA axis-related genes (CRHR1, NRC31, NRC32, and FKBP5). ICA significantly predicted greater adolescent interpersonal dependent stress. Additionally, MGPS predicted a stronger association between ICA and interpersonal dependent (but not independent or noninterpersonal dependent) stress. No gene–environment interaction (G×E) effects were found for noninterpersonal CA and MGPS in predicting adolescent interpersonal dependent stress. Effects remained after controlling for current depressive symptoms and following stratification by race. Findings extend existing G×E research on stress generation to HPA axis-related genetic variation and demonstrate effects specific to the interpersonal domain.

This paper reviews and synthesizes key areas of research related to the etiology, development, and maintenance of internalizing symptoms in children, adolescents, and adults with autism spectrum disorder (ASD). In developing an integrated conceptual model, we draw from current conceptual models of internalizing symptoms in ASD and extend the model to include factors related to internalizing within other populations (e.g., children that have experienced early life stress, children with other neurodevelopmental conditions, typically developing children) that have not been systematically examined in ASD. Our review highlights the need for more research to understand the developmental course of internalizing symptoms, potential moderators, and the interplay between early risk and protective factors. Longitudinal studies incorporating multiple methods and both environmental and biological factors will be important in order to elucidate these mechanisms.

Social-communication skills emerge within the context of rich social interactions, facilitated by an infant's capacity to attend to people and objects in the environment. Disruption in this early neurobehavioral process may decrease the frequency and quality of social interactions and learning opportunities, potentially leading to downstream deleterious effects on social development. This study examined early attention in infant siblings of children with autism spectrum disorder (ASD) who are at risk for social and communication delays. Visual and auditory attention was mapped from age 1 week to 5 months in infants at familial risk for ASD (high risk; N = 41) and low-risk typically developing infants (low risk; N = 39). At 12 months, a subset of participants (N = 40) was administered assessments of social communication and nonverbal cognitive skills. Results revealed that high-risk infants performed lower on attention tasks at 2 and 3 months of age compared to low-risk infants. A significant association between overall attention at 3 months and developmental outcome at 12 months was observed for both groups. These results provide evidence for early vulnerabilities in visual attention for infants at risk for ASD during a period of important neurodevelopmental transition (between 2 and 3 months) when attention has significant implications for social communication and cognitive development.

We review evidence of racial discrimination as a critical and understudied form of adversity that has the potential to impact stress biology, particularly hypothalamic–pituitary–adrenal (HPA) axis activity. We highlight ethnic racial identity (ERI) as a positive regulatory influence on HPA axis activity, as indexed by levels of salivary cortisol. In past research by our group, Black individuals with high adolescent discrimination had low adult cortisol levels (hypocortisolism). Here, we present new analyses showing that ERI, measured prospectively from ages 12 through 32 in 112 Black and white individuals, is related to better-regulated cortisol levels in adulthood, particularly for Black participants. We also describe ongoing research that explores whether the promotion of ERI during adolescence can reduce ethnic–racial disparities in stress biology and in emotional health and academic outcomes.

This study investigated the longitudinal associations among prenatal substance use, socioeconomic adversity, parenting (maternal warmth, sensitivity, and harshness), children's self-regulation (internalization of rules and conscience), and conduct problems from infancy to middle childhood (Grade 2). Three competing conceptual models including cascade (indirect or mediated), additive (cumulative), and transactional (bidirectional) effects were tested and compared. The sample consisted of 216 low-income families (primary caretaker and children; 51% girls; 74% African American). Using a repeated-measures, multimethod, multi-informant design, a series of full panel models were specified. Findings primarily supported a developmental cascade model, and there was some support for additive effects. More specifically, maternal prenatal substance use and socioeconomic adversity in infancy were prospectively associated with lower levels of maternal sensitivity. Subsequently, lower maternal sensitivity was associated with decreases in children's conscience in early childhood, and in turn, lower conscience predicted increases in teacher-reported conduct problems in middle childhood. There was also a second pathway from sustained maternal depression (in infancy and toddlerhood) to early childhood conduct problems. These findings demonstrated how processes of risk and resilience collectively contributed to children's early onset conduct problems.