Childhood adversity is associated with higher adult weight, but few investigations prospectively test mechanisms accounting for this association. Using two socioeconomically high-risk prospective longitudinal investigations, the Minnesota Longitudinal Study of Risk and Adaptation (MLSRA; N = 267; 45.3% female) and the Fragile Families and Child Wellbeing Study (FFCWS; n = 2,587; 48.5% female), pathways between childhood adversity and later body mass index (BMI) were tested using impulsivity, emotion dysregulation, and overeating as mediators. Childhood adversity from 0 to 5 years included four types of adversities: greater unpredictability, threat/abuse, deprivation/neglect, and low socioeconomic status. Parents reported on child impulsivity, emotion dysregulation, and overeating. Height and weight were self-reported and measured at 32 and 37 years in MLSRA and at 15 years in FFCWS. FFCWS results indicated that threat, deprivation, and low socioeconomic status predicted greater impulsivity and emotion dysregulation at 5 years, which in turn predicted greater overeating at 9 years and higher BMI z-score at 15 years. Early unpredictability in FFCWS predicted higher BMI through greater impulsivity but not emotion dysregulation at age 5. MLSRA regression results replicated the threat/abuse → emotion dysregulation → overeating → higher BMI pathway. These findings suggest that different dimensions of early adversity may follow both similar and unique pathways to predict BMI.

This study compared the structure and quality of emotion language in adolescents with externalizing disorders (N = 21), internalizing disorders (N = 18), and without a behavioral or emotional disorder (N = 16). Emotion language was elicited in response to vignette material prototypical for anger/sadness and fear, to autobiographical experiences, and to an actual emotional challenge. The findings reveal different emphases in the emotion language of internalizing and externalizing youth rather than a relative weakness for externalizing adolescents. Overall, clinical adolescents used fewer emotion terms that were semantically specific for anger, sad, or fear than typical adolescents. The results also show that emotion language is affected differentially for externalizing and internalizing adolescents depending on the emotion domain. Internalizing youth's emotion language to anger/sad events used inner-directed terms, situational references, and reduced intensity while their representation of emotions in response to salient threatening material was dominated by terms with a cognitive focus. Externalizing adolescents' emotion language responses to anger/sad events were more outer directed and intense, and their emotion language in a salient threat situation more orientated to direct affective terms. The results suggest that examining emotion language for specific emotion domains in adolescents with specific disorders will better clarify the role of emotion language in the regulation of emotions than approaches that globalize emotion language competencies or deficits.

Using a genetic moderation approach, this study examines how an experimental prime of religion impacts self-control in a social context, and whether this effect differs depending on the genotype of an oxytocin receptor gene (OXTR) polymorphism (rs53576). People with different genotypes of OXTR seem to have different genetic orientations toward sociality, which may have consequences for the way they respond to religious cues in the environment. In order to determine whether the influence of religion priming on self-control is socially motivated, we examine whether this effect is stronger for people who have OXTR genotypes that should be linked to greater rather than less social sensitivity (i.e., GG vs. AA/AG genotypes). The results showed that experimentally priming religion increased self-control behaviors for people with GG genotypes more so than people with AA/AG genotypes. Furthermore, this Gene × Religion interaction emerged in a social context, when people were interacting face to face with another person. This research integrates genetic moderation and social psychological approaches to address a novel question about religion's influence on self-control behavior, which has implications for coping with distress and psychopathology. These findings also highlight the importance of the social context for understanding genetic moderation of psychological effects.

Internalizing symptoms during adolescence and beyond is a major public health concern, particularly because severe symptoms can lead to the diagnosis of a number of serious psychiatric conditions. This study utilizes a unique sample with a complex statistical method in order to explore Gene × Environment interactions found in internalizing symptoms during adolescence. Data for this study were drawn from a longitudinal prevention intervention study (n = 798) of Baltimore city school children. Internalizing symptom data were collected using self-report and blood or saliva samples genotyped using Affymetrix 6.0 microarrays. A major depression polygenic score was created for each individual using information from the major depressive disorder Psychiatric Genetics Consortium and used as a predictor in a latent trait–state–occasion model. The major depressive disorder polygenic score was a significant predictor of the stable latent trait variable, which captures time-independent phenotypic variability. In addition, an early childhood stressor of death or divorce was a significant predictor of occasion-specific variables. A Gene × Environment interaction was not a significant predictor of the latent trait or occasion variables. These findings support the importance of genetics on the stable latent trait portion of internalizing symptoms across adolescence.

There is a great need for discovery of biological markers that could be used diagnostically for pediatric onset disorders, particularly those with potentially confusing phenomenology such as pediatric-onset bipolar disorder (BD). Obtaining these markers would help overcome current subjective diagnostic techniques of relying on parent and child interview and symptomatic history. Brain imaging may be the most logical choice for a diagnostic tool, and certain neurobiological abnormalities have already been found in pediatric BD. However, much work remains to be done before neuroimaging can be used reliably to diagnose this disorder, and because of the nature of BD and the limitations of imaging technology and technique, neuroimaging will likely at most be only a diagnostic aide in the near future. In this paper we discuss the characteristics of pediatric BD that complicate the use of biological markers as diagnostic tools, how neuroimaging techniques have been used to study pediatric BD so far, and the limitations and potential of such techniques for future diagnostic use.This work was supported in part by NIH Grant MH64460-01 (to K.C.).

Children with both a language impairment and a learning disability are at risk for poor social competence. Yet the processes that place these children at risk remain unclear. A developmental–organizational perspective was used to explore processes underlying risk for poor social competence among language learning disabled children. To this end, the relative influences of language learning disability and social discourse skills on social competence were examined in 50 language learning disabled (LLD) and 50 control (non-LLD) children aged 8–12 years. Findings indicated that social discourse skills mediated the relation between LLD status and children's social competence. Specifically, a domain of social discourse, figurative language, was the strongest mediator of the effect of LLD status on social competence. Additionally, differences were confirmed between the LLD and non-LLD group in two domains of social discourse, recreating sentences and figurative language, as well as social competence. Two other domains of social discourse, understanding ambiguous sentences and making inferences, did not discriminate the groups. The findings emphasize the importance of analyzing interrelations among domains to identify critical factors related to developmental outcomes.

The current study examined the prospective association between child maltreatment and the development of substance use disorder in adolescence with the aim of investigating pathways underlying this relation, as well as genetic moderation of these developmental mechanisms. Specifically, we tested whether youth who experienced maltreatment prior to age 8 were at risk for the development of marijuana dependence in adolescence by way of a childhood externalizing pathway and a childhood internalizing pathway. Moreover, we tested whether variation in FK506 binding protein 5 gene (FKBP5) CATT haplotype moderated these pathways. The participants were 326 children (n =179 maltreated; n = 147 nonmaltreated) assessed across two waves of data collection (childhood: ages 7–9 and adolescence: ages 15–18). Results indicated that higher levels of child externalizing symptoms significantly mediated the effect of child maltreatment on adolescent marijuana dependence symptoms for individuals with one or two copies of the FKBP5 CATT haplotype only. We did not find support for an internalizing pathway from child maltreatment to adolescent marijuana dependence, nor did we find evidence of moderation of the internalizing pathway by FKBP5 haplotype variation. Findings extend previous research by demonstrating that whether a maltreated child will traverse an externalizing pathway toward substance use disorder in adolescence is dependent on FKBP5 genetic variation.

Copy number variants (CNVs) are submicroscopic deletions and duplications of genomic material that were previously thought to be rare phenomena. They have now been robustly associated with a variety of disorders such as autism, schizophrenia, and attention-deficit/hyperactivity disorder through an emerging research base in affective disorders. A complex picture is emerging of a polygenic, heterogeneous model of disease, with CNVs conferring broad susceptibility to a variety of neurodevelopmental disorders, rather than specific disorders per se. Although the insights gleaned thus far only represent a small piece of a much larger puzzle, progress has been rapid and new technologies promise even more insights into these hitherto opaque brain disorders. We will discuss CNVs, the current state of evidence for their role in the pathogenesis of classical psychiatric disorders, and the application of such knowledge in clinical settings.

Research on proactive and reactive aggression has identified covariates unique to each function of aggression, but hypothesized correlates have often not been tested with consideration of developmental changes in or the overlap between the types of aggression. The present study examines the unique developmental trajectories of proactive and reactive aggression over adolescence and young adulthood and tests these trajectories’ associations with key covariates: callous–unemotional (CU) traits, impulsivity, and internalizing emotions. In a sample of 1,211 justice-involved males (ages 15–22), quadratic growth models (i.e., intercepts, linear slopes, and quadratic slopes) of each type of aggression were regressed onto quadratic growth models of the covariates while controlling for the other type of aggression. After accounting for the level of reactive aggression, the level of proactive aggression was predicted by the level of CU traits. However, change in proactive aggression over time was not related to the change in any covariates. After accounting for proactive aggression, reactive aggression was predicted by impulsivity, both at the initial level and in change over time. Results support that proactive and reactive aggression are unique constructs with separate developmental trajectories and distinct covariates.

The generalist genes specialist environment model, when applied to developmental psychopathology, predicts that genetic influences should explain variance that is shared across internalizing and externalizing problems, whereas environmental influences should explain variance that distinguishes the two overarching problem types. The present study is a direct test of this hypothesis, leveraging a sample of 708 twins and siblings (aged 10–18 years, 93% White) from the United States. Measures of severity of symptoms, regardless of type, and of directionality of symptoms – whether the adolescent tended to exhibit more externalizing or internalizing problems – were subjected to genetic (A), shared environmental (C), and nonshared environmental (E) (ACE) variance decompositions. As expected, severity of problems was under substantial genetic influence, but there were also significant shared and nonshared environmental influences. Contrary to the generalist genes specialist environment model, directionality of problem type was also under considerable genetic influence, with modest nonshared environmental influence. Findings corroborate existing evidence from other designs highlighting the role of familial influences (including generalist genes) in comorbidity of adolescent internalizing and externalizing problems, but suggest that the specialist environments hypothesis may not be the key factor in distinguishing problem type.

This study evaluated whether children with higher adverse childhood experiences (ACE) scores had alterations in immune cell gene expression profiles. RNA sequencing was conducted on dried blood spot samples from 37 generally healthy English-speaking children (age 5–11) who were recruited from well-child visits at a university-affiliated pediatric practice. The Whole Child Assessment was used to assess ACE exposure. Primary analyses examined an a priori-specified composite of 19 pro-inflammatory gene transcripts. Secondary analyses examined a 34-gene composite assessing Type I interferon response, and used Transcript Origin Analyses to identify cellular mechanisms. After controlling for age, body mass index percentile, sex, race/ethnicity, current insurance status, and household smoking exposure, pro-inflammatory gene expression was elevated by 0.094 log2 RNA expression units with each Child-ACE total score point (p = .019). Type I interferon gene expression was similarly upregulated (0.103; p = .008). Transcript origin analyses implicated CD8+ T cell as the primary sources of gene transcripts upregulated, and nonclassical (CD16+) monocytes as sources of downregulated transcripts. These preliminary analyses suggest that parent-reported ACE exposures are associated with increased expression of both inflammatory and interferon gene transcripts in children's circulating blood cells.

The current study examined whether social status and social integration, two related but distinct indicators of an adolescent's standing within a peer network, mediate the association between risky symptoms (depressive symptoms and deviant behavior) and substance use across adolescence. The sample of 6,776 adolescents participated in up to seven waves of data collection spanning 6th to 12th grades. Scores indexing social status and integration were derived from a social network analysis of six schools and subsequent psychometric modeling. Results of latent growth models showed that social integration and status mediated the relation between risky symptoms and substance use and that risky symptoms mediated the relation between social standing and substance use during the high school transition. Before this transition, pathways involving deviant behavior led to high social integration and status and in turn to substance use. After this transition, both deviant behavior and depressive symptoms led to low social integration and status and in turn greater substance use. These findings suggest that the high school transition is a risky time for substance use related to the interplay of increases in depressive symptoms and deviant behavior on the one hand and decreases in social status and integration on the other.

Growing research has documented distinct developmental sequelae in insecure and secure parent–child relationships, supporting a model of early attachment as moderating future developmental processes rather than, or in addition to, a source of direct effects. We explored maladaptive developmental implications of infants’ anger proneness in 102 community families. Anger was assessed in infancy through observations in the Car Seat episode and parents’ ratings. Children's security with parents was assessed in the Strange Situation paradigm at 15 months. At preschool age, child negativity (defiance and negative affect) was observed in interactions with the parent, and at early school age, oppositionality was rated by parents and teachers. Security was unrelated to infant anger; however, it moderated associations between infant anger and future maladaptive outcomes, such that highly angry infants embarked on a negative trajectory in insecure, but not in secure, parent–child dyads. For insecure, but not secure, mother–child dyads, infants’ mother-rated anger predicted negativity at preschool age. For insecure, but not secure, father–child dyads, infants’ anger in the Car Seat predicted father- and teacher-rated oppositional behavior at early school age. Results highlight the developmentally complex nature of the impact of attachment, depending on the relationship with mother versus father, type of measure, and timing of effects.

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.

It is argued that personality pathology represents the final emergent product of a complex interaction of underlying neurobehavioral systems as well as environment inputs. A number of factors may be involved in the developmental pathway and a cascading of effects is plausible, although a unifying cascade for all personality disorders is not likely. The present study suggests a possible cascade relevant to one personality disorder: schizoid personality disorder in emerging adulthood. In brief, it is hypothesized that the absence of a relationship characterized by a rich degree of psychological proximal process in early childhood, which is associated with nurturance and the facilitation of more complex development, predicts impairment in the actualization of the affiliation system (i.e., that system that facilitates interpersonal connectedness and social bonds in human beings and is under substantial genetic influence), and this impairment in the affiliation system predicts the appearance of schizoid personality disorder symptoms in emerging adulthood (late teens/early 20s), which persists over time into emerging adulthood. The impairment in the affiliation system is argued to proceed through childhood sociality as reflected in temperament on through adult personality as reflected in communal positive emotion. Furthermore, it is also hypothesized that the relationship between proximal processes and the affiliation system maintains irrespective of other childhood temperament factors that might adversely impact early parent/caregiver and child relations. The data for a preliminary illustration of this possible cascade are drawn from The Longitudinal Study of Personality Disorders, which is a prospective, multiwave study of personality disorders, personality, and temperament in a large sample of adults drawn from a nonclinical population.

As approximately one-third of peer-victimized children evidence heightened aggression (Schwartz, Proctor, & Chien, 2001), it is imperative to identify the circumstances under which victimization and aggression co-develop. The current study explored two potential moderators of victimization–aggression linkages: (a) attentional bias toward cues signaling threat and (b) attentional bais toward cues communicating interpersonal support. Seventy-two fifth- and sixth-grade children (34 boys; Mage = 11.67) were eye tracked while watching video clips of bullying. Each scene included a bully, a victim, a reinforcer, and a defender. Children's victimization was measured using peer, parent, and teacher reports. Aggression was measured using peer reports of overt and relational aggression and teacher reports of aggression. Victimization was associated with greater aggression at high levels of attention to the bully. Victimization was also associated with greater aggression at low attention to the defender for boys, but at high attention to the defender for girls. Attention to the victim was negatively correlated with aggression regardless of victimization history. Thus, attentional biases to social cues integral to the bullying context differentiate whether victimization is linked to aggression, necessitating future research on the development of these biases and concurrent trajectories of sociobehavioral development.

Previous studies have documented the serotonin transporter linked polymorphic region (5-HTTLPR) as a genetic susceptibility variant that contributes to variability in outcomes related to affective psychopathology, with the short allele associated with negative affectivity and the long allele associated with positive affectivity. In a separate but related line of research, extensive evidence suggests that frontal electroencephalography (EEG) hemispheric asymmetry in the alpha band is also associated with risk for affective psychopathologies, with leftward asymmetry associated with approach-related behavior patterns and rightward frontal EEG asymmetry associated with withdrawn behavioral tendencies. We examined frontal EEG hemispheric asymmetries in relation to 5-HTTLPR genotyping in 70 children between 4 and 6 years of age. Analyses revealed that frontal EEG lateralization interacted with genotype such that children homozygous for the short allele exhibited rightward frontal EEG asymmetries, children who were homozygous for the long allele consistently exhibited a positive pattern of leftward asymmetry, and heterozygotes exhibited equivalent left and right frontal activity. These findings suggest that the 5-HTTLPR short allele may provide a degree of susceptibility for later affective psychopathology in adolescence and adulthood, through mediation of frontal brain activity that is associated with cognitive–behavioral withdrawal tendencies and negative affectivity.

In the last decade, an abundance of research has utilized the National Institute of Mental Health (NIMH) research domain criteria (RDoC) framework to examine mechanisms underlying anxiety and depression in youth. However, relatively little work has examined how these mechanistic intrapersonal processes intersect with context during childhood and adolescence. The current paper covers reviews and meta-analyses that have linked RDoC-relevant constructs to ecological systems in internalizing problems in youth. Specifically, cognitive, biological, and affective factors within the RDoC framework were examined. Based on these reviews and some of the original empirical research they cover, we highlight the integral role of ecological factors to the RDoC framework in predicting onset and maintenance of internalizing problems in youth. Specific recommendations are provided for researchers using the RDoC framework to inform future research integrating ecological systems and development. We advocate for future research and research funding to focus on better integration of the environment and development into the RDoC framework.

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.