Aggressive behavior in middle childhood can contribute to peer rejection, subsequently increasing risk for substance use in adolescence. However, the quality of peer relationships a child experiences can be associated with his or her genetic predisposition, a genotype–environment correlation (rGE). In addition, recent evidence indicates that psychosocial preventive interventions can buffer genetic predispositions for negative behavior. The current study examined associations between polygenic risk for aggression, aggressive behavior, and peer rejection from 8.5 to 10.5 years, and the subsequent influence of peer rejection on marijuana use in adolescence (n = 515; 256 control, 259 intervention). Associations were examined separately in control and intervention groups for children of families who participated in a randomized controlled trial of the family-based preventive intervention, the Family Check-Up . Using time-varying effect modeling (TVEM), polygenic risk for aggression was associated with peer rejection from approximately age 8.50 to 9.50 in the control group but no associations were present in the intervention group. Subsequent analyses showed peer rejection mediated the association between polygenic risk for aggression and adolescent marijuana use in the control group. The role of rGEs in middle childhood peer processes and implications for preventive intervention programs for adolescent substance use are discussed.

The current study examined whether consistency in day-to-day interactions between children and parents related to inflammatory cytokine production in youths. One hundred twenty-three parents recorded the daily quality of interactions and timing of leisure activities with their adolescent children for 2 weeks, and the degree of variability in those ratings was calculated. One year later, the production of proinflammatory cytokines in youths’ blood was measured in response to in vitro exposure to lipopolysaccharide (a bacterial product). The results indicate that greater variability in parent–child relationship quality related to greater stimulated proinflammatory cytokine production in youths, above and beyond overall relationship quality. Greater variability in the timing of parent–child leisure activities also predicted greater stimulated proinflammatory cytokine production in youths, regardless of the frequency of interactions. In sum, consistency in both the affective and temporal aspects of parent–child relationships may contribute to inflammatory processes in youth.

A wide range of developmental disorders present with characteristic psychopathologies and behaviors, with diagnoses including, inter alia, cognitive disorders and learning disabilities, epilepsies, autism, and schizophrenia. Each, to varying extent, has a genetic component to etiology and is associated with cytogenetic abnormalities. Technological developments, particularly array-based comparative genome hybridization and single nucleotide polymorphism chips, has revealed a wide range of rare recurrent and de novo copy number variants (CNVs) to be associated with disorder and psychopathology. It is surprising that many apparently similar CNVs are identified across two or more disorders hitherto considered unrelated. This article describes the characteristics of CNVs and current technological restrictions that make accurately identifying small events difficult. It summarizes the latest discoveries for individual diagnostic categories and considers the implications for a shared neurobiology. It examines likely developments in the knowledge base as well as addressing the clinical implications going forward.

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.

The Atypical Maternal Behavior Instrument for Assessment and Classification (AMBIANCE; Bronfman, Madigan, & Lyons-Ruth, 2009–2014; Bronfman, Parsons, & Lyons-Ruth, 1992–2004) is a widely used and well-validated measure for assessing disrupted forms of caregiver responsiveness within parent–child interactions. However, it requires evaluating approximately 150 behavioral items from videotape and extensive training to code, thus making its use impractical in most clinical contexts. Accordingly, the primary aim of the current study was to identify a reduced set of behavioral indicators most central to the AMBIANCE coding system using latent-trait item response theory (IRT) models. Observed mother–infant interaction data previously coded with the AMBIANCE was pooled from laboratories in both North America and Europe (N = 343). Using 2-parameter logistic IRT models, a reduced set of 45 AMBIANCE items was identified. Preliminary convergent and discriminant validity was evaluated in relation to classifications of maternal disrupted communication assigned using the full set of AMBIANCE indicators, to infant attachment disorganization, and to maternal sensitivity. The results supported the construct validity of the refined item set, opening the way for development of a brief screening measure for disrupted maternal communication. IRT models in clinical scale refinement and their potential for bridging clinical and research objectives in developmental psychopathology are discussed.

The Adult Attachment Interview (AAI) is a widely used measure in developmental science that assesses adults’ current states of mind regarding early attachment-related experiences with their primary caregivers. The standard system for coding the AAI recommends classifying individuals categorically as having an autonomous, dismissing, preoccupied, or unresolved attachment state of mind. However, previous factor and taxometric analyses suggest that: (a) adults’ attachment states of mind are captured by two weakly correlated factors reflecting adults’ dismissing and preoccupied states of mind and (b) individual differences on these factors are continuously rather than categorically distributed. The current study revisited these suggestions about the latent structure of AAI scales by leveraging individual participant data from 40 studies (N = 3,218), with a particular focus on the controversial observation from prior factor analytic work that indicators of preoccupied states of mind and indicators of unresolved states of mind about loss and trauma loaded on a common factor. Confirmatory factor analyses indicated that: (a) a 2-factor model with weakly correlated dismissing and preoccupied factors and (b) a 3-factor model that further distinguished unresolved from preoccupied states of mind were both compatible with the data. The preoccupied and unresolved factors in the 3-factor model were highly correlated. Taxometric analyses suggested that individual differences in dismissing, preoccupied, and unresolved states of mind were more consistent with a continuous than a categorical model. The importance of additional tests of predictive validity of the various models is emphasized.

This study examined the extent to which secure base script knowledge—reflected in the ability to generate narratives in which attachment-relevant events are encountered, a clear need for assistance is communicated, competent help is provided and accepted, and the problem is resolved—is associated with mothers’ electrophysiological, subjective, and observed emotional responses to an infant distress vocalization. While listening to an infant crying, mothers (N = 108, M age = 34 years) lower on secure base script knowledge exhibited smaller shifts in relative left (vs. right) frontal EEG activation from rest, reported smaller reductions in feelings of positive emotion from rest, and expressed greater levels of tension. Findings indicate that lower levels of secure base script knowledge are associated with an organization of emotional responding indicative of a less flexible and more emotionally restricted response to infant distress. Discussion focuses on the contribution of mothers’ attachment representations to their ability to effectively manage emotional responding to infant distress in a manner expected to support sensitive caregiving.

The role of genetics in relation to attachment is of continued interest to developmental psychology. Recent research has attempted to disentangle genetic main effects, environmental effects, and gene and environment (G × E) interactions in the development of attachment security/insecurity and disorganization. We systematically reviewed associations between gene markers and attachment, including G × E interactions, identifying 27 eligible studies. Inconsistent results emerged for associations between both gene effects and G × E interactions on attachment organization. Where G × E interactions used attachment as the environmental factor in the interaction, we observed more consistent results for differential susceptibility of G × E interactions on offspring behavior. Small sample size and heterogeneity in measurement of environmental factors impacted on comparability of studies. From these results, we propose that the future of research into the role of genetic effects in attachment lies in further exploration of G × E interactions, particularly where attachment acts as an environmental factor impacting on other child developmental outcomes emerging from the caregiving environment, consistent with differential susceptibility approaches to developmental psychopathology. In addition, from a methodological perspective, establishing the role of gene markers in such models will require a shift toward contemporary genomics, including genome-wide analysis (including novel genes and chromosomal loci), and epigenetic individual variations.

Numerous developmental scholars have been influenced by the research, policies, and thinking of the late Edward Zigler, who was instrumental in founding Head Start and Early Head Start. In line with the research and advocacy work of Zigler, we discuss two models that support the development of the whole child. We begin by reviewing how adverse and protective experiences “get under the skin” and affect developmental trajectories and risk and resilience processes. We then present research and examples of how experiences affect the whole child, the heart and the head (social, emotional, cognitive, and physical development), and consider development within context and across domains. We discuss examples of interventions that strengthen nurturing relationships as the mechanism of change. We offer a public health perspective on promoting optimal development through nurturing relationships and access to resources during early childhood. We end with a discussion of the myth that our current society is child-focused and argue for radical, essential change to make promoting optimal development for all children the cornerstone of our society.

Exposure to developmental risks in three domains (community, economic, and family), and relations between risks and psychosocial well-being, were examined among 918 impoverished Brazilian youth aged 14–19 (M = 15.8 years, 51.9% female) recruited in low-income neighborhoods in one city in Southern Brazil. High levels of developmental risks were reported, with levels and types of risks varying by gender, age, and (to a lesser extent) race. Associations between levels of risks in the various domains and indicators of psychological (e.g., self-esteem, negative emotionality) and behavioral (e.g., substance use) adjustment differed for male and female respondents. Findings build on prior research investigating the development of young people in conditions of pervasive urban poverty and reinforce the value of international research in this endeavor.This study was funded by grants from the World Bank and CNPq to Silvia H. Koller. Manuscript preparation was partially supported by a Faculty Development Fellowship to Marcela Raffaelli from the College of Arts and Sciences, University of Nebraska–Lincoln, and by a Visiting Fellowship at the Key Centre for Women's Health in Society, School of Population Health at the University of Melbourne. The authors acknowledge the assistance of J'aims Ribeiro in developing the questionnaire.

Maternal stress during pregnancy can cause alterations to the fetal hypothalamus–pituitary–adrenal (HPA) axis, a phenomenon known as fetal programming that may have lasting effects on offspring outcomes, including depression. Evidence suggests that these effects may vary with respect to the offspring's genetic risk. Nonetheless, few studies have examined these effects into adulthood, when risk for depression onset is highest. The present study builds upon the extant literature by examining the interaction of maternal prenatal perceived stress (MPPS) and offspring HPA-axis polygenic risk to predict offspring depression in early adulthood. A total of 381 mother–child dyads participated in a prospective, longitudinal study that spanned from pregnancy until offspring were 20 years of age. Polygenic risk was defined by a multilocus genetic profile score (MGPS) that reflected the additive risk of three HPA-axis candidate genes. The results indicated that the interaction of MPPS and HPA-axis MGPS confers risk for offspring depression at age 20, in line with the differential susceptibility model. This interaction may be specific to prenatal stress, as maternal stress during early childhood did not interact with genetic risk to predict depression. These findings provide the first evidence that genetic variants that are associated with the HPA axis may act in a polygenic, additive fashion to moderate the association between fetal programming and adult depression.

Schizophrenia is being increasingly viewed as a neurodevelopmental disorder, that is, one in which early, fixed pathology becomes manifest clinically during the normal course of maturation of the brain. Evidence for this position comes first from neuroimaging research, such as (1) studies that demonstrate morphologic brain changes (such as ventriculomegaly on CT scans) even in first break patients; and (2) a lack of correlation between these morphologic changes and duration of illness. Another source of evidence is studies of normal brain development in rodents and primates, including research that shows (1) the prefrontal cortex is a late maturing part of the brain, and (2) lesions of the prefrontal cortex may be initially silent and show delayed onset of dysfunction as the brain matures. A neurodevelopmental approach to schizophrenia, in turn, has stimulated further work into the normal development of brain regions implicated in the illness, such as the frontal cortex. Thus, the fields of neuropsychiatry and neurodevelopment have been mutually stimulated during the course of this work. In addition, viewing schizophrenia in developmental terms may have implications for the understanding of changes in cognition and behavior during normal adolescence.

A new instrument, the Why It Happened questionnaire, was developed for assessing characterological and behavior self-blame in two samples of third- through ninth-grade children (Sample 1: n = 121; sample 2: n = 322). Children's responses were very consistent within specific classes of negative events but only moderately consistent across time. Exploratory and confirmatory factor analyses of open-ended and self-rating responses, respectively, revealed that children's self-blame attributions were only moderately consistent across different classes of negative events, and that children's tendency to make characterological and behavioral attributions were unrelated for academic events and moderately correlated for social events. Multiple regression revealed that characterological self-blame about academic and social events were not significantly related to self-reported depression until ninth grade. Implications for cognitive diathesis-stress models of depression for children are discussed.

Evocative effects of child characteristics on the quality and quantity of child care were assessed in two studies using longitudinal data from the NICHD Study of Early Child Care. We focus on the influence of child characteristics on two important aspects of the child care experience: language stimulation provided by caregivers and quantity of care. In Study 1, associations between the developmental status of children aged 15 to 54 months and the language stimulation provided by their caregivers were examined using path models, and longitudinal child effects were detected across the earliest time points of the study. In Study 2, the associations among child behavior, temperament, development, and time in care were examined. Little evidence was found for such child effects on time in care. The results are discussed in terms of the effects of child care on child development and implications for developmental processes, particularly for children at greatest risk for developmental delay or psychopathology.

Little is known about the effect of natural disasters on children's neural development. Additionally, despite evidence that stress and parenting may both influence the development of neural systems underlying reward and threat processing, few studies have brought together these areas of research. The current investigation examined the effect of parenting styles and hurricane-related stress on the development of neural reactivity to reward and threat in children. Approximately 8 months before and 9 months after Hurricane Sandy, 74 children experiencing high and low levels of hurricane-related stress completed tasks that elicited the reward positivity and error-related negativity, event-related potentials indexing sensitivity to reward and threat, respectively. At the post-Hurricane assessment, children completed a self-report questionnaire to measure promotion- and prevention-focused parenting styles. Among children exposed to high levels of hurricane-related stress, lower levels of promotion-focused, but not prevention-focused, parenting were associated with a reduced post-Sandy reward positivity. In addition, in children with high stress exposure, greater prevention-focused, but not promotion-focused, parenting was associated with a larger error-related negativity after Hurricane Sandy. These findings highlight the need to consider contextual variables such as parenting when examining how exposure to stress alters the development of neural reactivity to reward and threat in children.

Affect reactivity to stress may play a role in the development of internalizing symptoms during the college transition, a critical developmental juncture for Latinx adolescents, the largest ethnic minority group on college campuses. This study examined whether affect reactivity during high school is associated with internalizing symptoms in college and explored two potential protective factors, perceived family and peer support. Participants were 209 Latinx adolescents (Mage = 18.10; 64.4% female) who completed standard surveys and four diary assessments per day over 7 days (N > 4,500 momentary observations). First, to measure affect reactivity, we assessed whether perceived stress was associated with negative affect at the momentary level during high school (senior year). Second, we tested whether affect reactivity predicted internalizing symptoms during the first year of college. Third, we tested whether perceived family or peer support buffered the negative consequences of affect reactivity. Results indicated statistically significant within- and between-person associations between stress and negative affect. Moreover, affect reactivity significantly predicted depressive, but not anxiety, symptoms. Buffering was found for family, but not peer, support. Findings extend previous research by detecting associations between momentary affect reactivity and internalizing symptoms during a sociocultural shift in Latinx adolescents’ lives and have implications for culturally appropriate programs to prevent depressive symptoms.

The current study investigated whether prosocial behavior and emotional problems, peer problems, conduct problems, and hyperactivity and inattention problems were long-term longitudinally and bidirectionally related at inter- and or intra-individual levels from early childhood through mid-adolescence. Parents in the United Kingdom reported their child’s prosocial behavior and multidimensional psychopathology at ages 3, 5, 7, 11, and 14 years (N = 16,984, 51% male, 83% White). Four random intercepts cross-lagged panel models were fitted. Higher levels of earlier prosocial behavior were associated with greater than expected decrements in psychopathology. At an intraindividual, within-person level, prosocial behavior was negatively bidirectionally associated with peer, conduct, and hyperactivity and inattention problems. Also at an intraindividual, within-person level, prosocial behavior was unidirectionally protective against emotional problems. At an interindividual level, prosocial behavior and each dimension of psychopathology were negatively associated. Therefore, engaging in prosocial behavior can reduce psychopathological symptoms over time (and vice versa), and youth who are more prosocial also tend to experience fewer psychopathological symptoms. Intraindividual associations were small while interindividual associations were moderate to large. Implications for theory, future research, and evidence-based interventions are discussed.

The current study used daily assessments of sleep to examine stability and change in sleep chronotype in adolescents and their parents. The study assessed adolescent sleep chronotype according to age, gender, and parent chronotype, and evaluated its associations with emotional and behavioral problems in youth. Participants included of 417 Mexican American adolescents (Mage = 16.0 years, Range = 13.9–20.0) and 403 caregivers, who reported bed and wake times daily for 2 consecutive weeks at two time points spaced 1 year apart. In addition, adolescents completed established self-report questionnaires of emotional and behavioral problems. Chronotype was computed as the midsleep point from bed to wake time on free days, correcting for sleep debt accumulated across scheduled days. Multilevel modeling showed a curvilinear association between adolescent age and chronotype, with a peak eveningness observed between ages 16 to 17. Adolescent and parent chronotypes were contemporaneously correlated, but each was only moderately stable over the 1-year period. Later adolescent chronotype was contemporaneously associated with more substance use in all adolescents. Individual development and the family context shape sleep chronotype in adolescents and parents. Sleep chronotype is implicated in adolescent behavioral health.

This study investigated the relationship of menarcheal timing and ego development to level of depressive symptoms in early adolescent girls. Girls who were postmenarcheal at the beginning of the sixth grade were classified as very early maturers; their premenarcheal peers were regarded as on time. Girls were further classified with the Loevinger Sentence Completion Test as relatively low or high in ego development. Depressive symptoms were assessed with the Beck Depression Inventory, short form. Results indicated a significant interaction of menarcheal timing and ego development: Very early maturing was associated with moderate levels of depressive symptoms for girls who were relatively low in ego development; very early maturing girls who were relatively advanced in ego development had the same minimal level of depressive symptoms as on time girls at either relatively low or advanced levels of ego development. The results support a proposed integration of psychoanalytic and empirically based biopsychosocial approaches to adolescent depression.

Few conditions epitomize severe and chronic stress to a greater extent than child maltreatment, which can derail development across multiple domains of functioning and throughout the life course. Furthermore, child maltreatment tends to co-occur with other adversities, such as poverty. Many individuals grow up under the stressful conditions of these adversities and exhibit developmental competence. The current study prospectively charted the developmental progression of economically disadvantaged maltreated and nonmaltreated children from childhood to emerging adulthood, and examined patterns of competence across multiple developmental domains of functioning central to the period of emerging adulthood. The study investigated childhood precursors to these patterns of adaptation and maladaptation, as well as the physiological cost of these patterns of adaptation (i.e., C-reactive protein; CRP). Latent class analysis revealed four distinct classes of functioning: multifaceted competence across domains (Multifaceted Competence); (multifaceted maladaptation across domains (Multi-Problem); (c) and two classes with mixed patterns of competence and maladaptation (Externalizing Problems and Work/School Impairment). Maltreated individuals were less likely than nonmaltreated individuals to demonstrate patterns of multifaceted competence and more likely to demonstrate aggregate maladaptation across domains. Additionally, Black men who demonstrated a pattern of multifaceted psychosocial competence also evidenced higher levels of low-grade inflammation (indexed by CRP), suggesting physiological distress was associated with adaptation in the context of stress among these individuals. Findings demonstrate the heterogenous patterns of functioning and diverse developmental outcomes that follow early adversity.