We investigated the antecedents and consequences of chronic victimization by bullies across a school transition using a genetically sensitive longitudinal design. Data were from the Environmental Risk Longitudinal Twin Study (E-Risk), an epidemiological cohort of 2,232 children. We used mothers' and children's reports of bullying victimization during primary school and early secondary school. Children who experienced frequent victimization at both time points were classed as “chronic victims” and were found to have an increased risk for mental health problems and academic difficulties compared to children who were bullied only in primary school, children bullied for the first time in secondary school, and never-bullied children. Biometric analyses revealed that stability in victimization over this period was influenced primarily by genetic and shared environmental factors. Regression analyses showed that children's early characteristics such as preexistent adjustment difficulties and IQ predicted chronic versus transitory victimization. Family risk factors for chronic victimization included socioeconomic disadvantage, low maternal warmth, and maltreatment. Our results suggest that bullying intervention programs should consider the role of the victims' behaviors and family background in increasing vulnerability to chronic victimization. Our study highlights the importance of widening antibullying interventions to include families to reduce the likelihood of children entering a pathway toward chronic victimization.

Biological parents pass on genotypes to their children, as well as provide home environments that correlate with their genotypes; thus, the association between the home environment and children's temperament can be genetically (i.e., passive gene–environment correlation) or environmentally mediated. Furthermore, family environments may suppress or facilitate the heritability of children's temperament (i.e., gene–environment interaction). The sample comprised 807 twin pairs (mean age = 7.93 years) from the longitudinal Wisconsin Twin Project. Important passive gene–environment correlations emerged, such that home environments were less chaotic for children with high effortful control, and this association was genetically mediated. Children with high extraversion/surgency experienced more chaotic home environments, and this correlation was also genetically mediated. In addition, heritability of children's temperament was moderated by home environments, such that effortful control and extraversion/surgency were more heritable in chaotic homes, and negative affectivity was more heritable under crowded or unsafe home conditions. Modeling multiple types of gene–environment interplay uncovered the complex role of genetic factors and the hidden importance of the family environment for children's temperament and development more generally.

We provide a theoretical and empirical basis for the claim that individual differences exist in developmental plasticity and that phenotypic plasticity should be a subject of study in its own right. To advance this argument, we begin by highlighting challenges that evolutionary thinking poses for a science of development and psychopathology, including for the diathesis–stress framework that has (fruitfully) guided so much empirical inquiry on developmental risk, resilience, and dysregulation. With this foundation laid, we raise a series of issues that the differential-susceptibility hypothesis calls attention to, while highlighting findings that have emerged over just the past several years and are pertinent to some of the questions posed. Even though it is clear that this new perspective on Person × Environment interaction is stimulating research and influencing how hypotheses are framed and data interpreted, a great many topics remain that need empirical attention. Our intention is to encourage students of development and psychopathology to treat phenotypic plasticity as an individual-difference construct while exploring unknowns in the differential-susceptibility equation.

Children in foster care have often encountered a range of adverse experiences, including neglectful and/or abusive care and multiple caregiver transitions. Prior research findings suggest that such experiences negatively affect inhibitory control and the underlying neural circuitry. In the current study, event-related functional magnetic resonance imaging was employed during a go/no go task that assesses inhibitory control to compare the behavioral performance and brain activation of foster children and nonmaltreated children. The sample included two groups of 9- to 12-year-old children: 11 maltreated foster children and 11 nonmaltreated children living with their biological parents. There were no significant group differences on behavioral performance on the task. In contrast, patterns of brain activation differed by group. The nonmaltreated children demonstrated stronger activation than did the foster children across several regions, including the right anterior cingulate cortex, the middle frontal gyrus, and the right lingual gyrus, during correct no go trials, whereas the foster children displayed stronger activation than the nonmaltreated children in the left inferior parietal lobule and the right superior occipital cortex, including the lingual gyrus and cuneus, during incorrect no go trials. These results provide preliminary evidence that the early adversity experienced by foster children impacts the neural substrates of inhibitory control.

Alterations in hypothalamic–pituitary–adrenal (HPA) axis functioning have been associated with major depression disorder (MDD) and some anxiety disorders. Few researchers have tested the possibility that high levels of recent life stress or elevations in negative emotion may partially account for the HPA axis alterations observed in these disorders. In a sample of 300 adolescents from the Youth Emotion Project, we examined associations between MDD and anxiety disorders, dimensional measures of internalizing symptomatology, life stress, mood on the days of cortisol testing, and HPA axis functioning. Adolescents with a past MDD episode and those with a recent MDD episode comorbid with an anxiety disorder had flatter diurnal cortisol slopes than adolescents without a history of internalizing disorders. Higher reports of general distress, a dimension of internalizing symptomatology, were also associated with flatter slopes. Negative emotion, specifically sadness and loneliness, was associated with flatter slopes and partially accounted for the associations between comorbid MDD and anxiety disorders and cortisol. The associations between past MDD and cortisol slopes were not accounted for by negative emotion, dimensional variation in internalizing symptomatology, or levels of life stress, indicating that flatter cortisol slopes may also be a “scar” marker of past experiences of MDD.

The current study examined biomarkers of stress in war-exposed young children and addressed maternal and child factors that may correlate with children's stress response. Participants were 232 Israeli children aged 1.5–5 years, including 148 children exposed to continuous war. Similarly, 56 were diagnosed with posttraumatic stress disorder (PTSD) and 92 were defined as exposed-no-PTSD. Child cortisol (CT) and salivary alpha amylase (sAA), biomarkers of the hypothalamic–pituitary–adrenal and sympathetic–adrenal–medullary arms of the stress response, were measured at baseline, following challenge, and at recovery. Maternal CT and sAA, PTSD symptoms, and reciprocal parenting, and child negative emotionality and regulatory strategies were assessed. Differences between war-exposed children and controls emerged, but these were related to child PTSD status. Children with PTSD exhibited consistently low CT and sAA, exposed-no-PTSD displayed consistently high CT and sAA, and controls showed increase in CT following challenge and decrease at recovery and low sAA. Exposed children showed higher negative emotionality; however, whereas exposed-no-PTSD children employed comfort-seeking strategies, children with PTSD used withdrawal. Predictors of child CT included maternal CT, PTSD symptoms, low reciprocity, and negative emotionality. Findings suggest that high physiological arousal combined with approach strategies may be associated with greater resilience in the context of early trauma.

Married men engage in significantly less antisocial behavior than unmarried men, but it is not clear whether this reflects a causal relationship. Instead, the relationship could reflect selection into marriage whereby the men who are most likely to marry (men in steady employment with high levels of education) are the least likely to engage in antisocial behavior. The relationship could also be the result of reverse causation, whereby high levels of antisocial behavior are a deterrent to marriage rather than the reverse. Both of these alternative processes are consistent with the possibility that some men have a genetically based proclivity to become married, known as an active genotype–environment correlation. Using four complementary methods, we tested the hypothesis that marriage limits men's antisocial behavior. These approaches have different strengths and weaknesses and collectively help to rule out alternative explanations, including active genotype–environment correlations, for a causal association between marriage and men's antisocial behavior. Data were drawn from the in-home interview sample of the National Longitudinal Study of Adolescent Health, a large, longitudinal survey study of a nationally representative sample of adolescents in the United States. Lagged negative binomial and logistic regression and propensity score matching models (n = 2,250), fixed-effects models of within-individual change (n = 3,061), and random-effects models of sibling differences (n = 618) all showed that married men engaged in significantly less antisocial behavior than unmarried men. Our findings replicate results from other quasiexperimental studies of marriage and men's antisocial behavior and extend the results to a nationally representative sample of young adults in the United States.

The momentum of genomic science will carry it far into the future and into the heart of research on typical and atypical behavioral development. The purpose of this paper is to focus on a few implications and applications of these advances for understanding behavioral development. Quantitative genetics is genomic and will chart the course for molecular genomic research now that these two worlds of genetics are merging in the search for many genes of small effect. Although current attempts to identify specific genes have had limited success, known as the missing heritability problem, whole-genome sequencing will improve this situation by identifying all DNA sequence variations, including rare variants. Because the heritability of complex traits is caused by many DNA variants of small effect in the population, polygenic scores that are composites of hundreds or thousands of DNA variants will be used by developmentalists to predict children's genetic risk and resilience. The most far-reaching advance will be the widespread availability of whole-genome sequence for children, which means that developmentalists would no longer need to obtain DNA or to genotype children in order to use genomic information in research or in the clinic.

This study examined dimensions of callous behaviors in early childhood and the role of these behaviors in the development of conduct problems, as well as responsiveness to a family-centered preventative intervention. Caregiver reports of callous behaviors were examined using exploratory and confirmatory factor analysis. Problem behavior was examined using within- and cross-informant reports of these behaviors. Parenting was measured using observational methods within the context of a randomized control trial of the Family Check-Up with a sample of 731 ethnically diverse boys and girls (followed from ages 2 to 4) at high risk for later conduct problems. Results demonstrated that a measure of deceitful–callous (DC) behaviors had acceptable factor loadings and internal consistency at ages 3 and 4. DC behaviors at age 3 predicted problem behavior concurrently and longitudinally within and across informant. However, DC behaviors did not reduce the effectiveness of the family preventative intervention. These findings have implications for our understanding of behaviors that may precede later callous–unemotional traits and for our understanding of the development and prevention of early starting conduct problems.

Although circumscribed interests are pathognomonic with autism, much about these interests remains unknown. Using the Interests Scale (IS), this study compares interests between 76 neurotypical (NT) individuals and 109 individuals with high-functioning autism spectrum disorder (HF-ASD) matched groupwise on age, IQ, and gender ratio. Participants and their parents/caregivers completed diagnostic measures (the Autism Diagnostic Interview—Revised and the Autism Diagnostic Observation Schedule; HF-ASD only), cognitive tests (Wechsler IQ Scales), and questionnaires (the Repetitive Behavior Scale—Revised, the Behavior Rating Inventory of Executive Function, and the Social Responsiveness Scale), in addition to the IS. Consistent with previous research, HF-ASD and NT individuals did not differ in number of interest areas, but the types of interests and intensity of those interests differed considerably. Using only the IS intensity score, 81% of individuals were correctly classified (NT or HF-ASD) in a logistic regression analysis. Among individuals with HF-ASD, Interests Scale scores were significantly related to Autism Diagnostic Observation Schedule, Behavior Rating Inventory of Executive Function, Repetitive Behavior Scale—Revised, and Social Responsiveness Scale scores, but they were not related to Autism Diagnostic Interview—Revised scores, IQ, gender, age, or psychotropic medication use. The type and intensity, but not the number, of interests distinguish high-functioning individuals with ASD from NT individuals.

Fragile X syndrome (FXS) has a characteristic cognitive “signature” that by late childhood includes core weaknesses in attention and working memory (WM), but their earlier developmental trajectories remain uncharted. Using a combined cross-sectional and prospective longitudinal design, we tested whether early profiles of attention and WM impairment in FXS indicate developmental freeze or developmental change. In Study 1, 26 young boys with FXS and 55 typically developing (TD) boys completed two experimental paradigms designed to assess cognitive aspects of attention and WM, in addition to behavioral indices of inattention and hyperactivity. Study 2 mapped longitudinal changes in 21 children with FXS and 21 TD children. In Study 1, significant weaknesses emerged for boys with FXS, with no substantial improvement over chronological age. Mapping performance against mental age level revealed delay, but it also yielded a similar attention and WM profile to TD boys. In Study 2, longitudinal improvements for boys with FXS paralleled those in TD children. In conclusion, cognitive attention and WM, although delayed in FXS, reveal developmental change, rather than “arrest.” Our findings underscore the need for going beyond cross-sectional group comparisons and gross behavioral indices to map cognitive changes longitudinally in developmental disorders.

In the past decade, there have been exciting advances in the field of behavioral epigenetics that have provided new insights into a biological basis of neural and behavioral effects of gene–environment interactions. It is now understood that changes in the activity of genes established through epigenetic alterations occur as a consequence of exposure to environmental adversity, social stress, and traumatic experiences. DNA methylation in particular has thus emerged as a leading candidate biological pathway linking gene–environment interactions to long-term and even multigenerational trajectories in behavioral development, including the vulnerability and resilience to psychopathology. This paper discusses what we have learned from research using animal models and from studies in which the translation of these findings has been made to humans. Studies concerning the significance of DNA methylation alterations in outcomes associated with stress exposure later in life and dysfunction in the form of neuropsychiatric disorders are highlighted, and several avenues of future research are suggested that promise to advance our understanding of epigenetics both as a mechanism by which the environment can contribute to the development of psychiatric disorders and as an avenue for more effective intervention and treatment strategies.

The additive and interactive relations of parenting styles (authoritative and authoritarian parenting) and child temperament (anger/frustration, sadness, and effortful control) to children's internalizing problems were examined in a 3.8-year longitudinal study of 425 Chinese children (aged 6–9 years) from Beijing. At Wave 1, parents self-reported on their parenting styles, and parents and teachers rated child temperament. At Wave 2, parents, teachers, and children rated children's internalizing problems. Structural equation modeling indicated that the main effect of authoritative parenting and the interactions of Authoritarian Parenting × Effortful Control and Authoritative Parenting × Anger/Frustration (parents' reports only) prospectively and uniquely predicted internalizing problems. The above results did not vary by child sex and remained significant after controlling for co-occurring externalizing problems. These findings suggest that (a) children with low effortful control may be particularly susceptible to the adverse effect of authoritarian parenting and (b) the benefit of authoritative parenting may be especially important for children with high anger/frustration.

Early disruptive behaviors, such as aggressive and hyperactive behaviors, known to be influenced by genetic factors, have been found to predict early school peer relation difficulties, such as peer rejection and victimization. However, there is no consensus regarding the developmental processes underlying this predictive association. Genetically informative designs, such as twin studies, are well suited for investigating the underlying genetic and environmental etiology of this association. The main goal of the present study was to examine the possible establishment of an emerging gene–environment correlation linking disruptive behaviors to peer relationship difficulties during the first years of school. Participants were drawn from an ongoing longitudinal study of twins who were assessed with respect to their social behaviors and their peer relation difficulties in kindergarten and in Grade 1 through peer nominations measures and teacher ratings. As predicted, disruptive behaviors were concurrently and predictively associated with peer relation difficulties. Multivariate analyses of these associations indicate that they were mainly accounted for by genetic factors. These results emphasize the need to adopt an early and persistent prevention framework targeting both the child and the peer context to alleviate the establishment of a negative coercive process and its consequences.

Is it always or necessarily the case that common and important parenting practices are better, insofar as they occur more often, or worse, because they occur less often? Perhaps, less is more, or some is more. To address this question, we studied mothers' microcoded contingent responsiveness to their infants (M = 5.4 months, SD = 0.2) in relation to independent global judgments of the same mothers' parenting sensitivity. In a community sample of 335 European American dyads, videorecorded infant and maternal behaviors were timed microanalytically throughout an extended home observation; separately and independently, global maternal sensitivity was rated macroanalytically. Sequential analysis and spline regression showed that, as maternal contingent responsiveness increased, judged maternal sensitivity increased to significance on the contingency continuum, after which mothers who were even more contingent were judged less sensitive. Just significant levels of maternal responsiveness are deemed optimally sensitive. Implications of these findings for typical and atypical parenting, child development, and intervention science are discussed.

Developmental psychopathology researchers and practitioners commonly conduct behavioral assessments using multiple informants' reports (e.g., parents, teachers, practitioners, children, and laboratory observers). These assessments often yield inconsistent conclusions about important questions in developmental psychopathology research, depending on the informant (e.g., psychiatric diagnoses and risk factors of disorder). Researchers have theorized why informant discrepancies exist and advanced methodological models of informant discrepancies. However, over 50 years of empirical data has uncovered little knowledge about these discrepancies beyond that they exist, complicate interpretations of research findings and assessment outcomes in practice, and correlate with some characteristics of the informants providing reports (e.g., demographics and mood levels). Further, recent studies often yield take-home messages about the importance of taking a multi-informant approach to clinical and developmental assessments. Researchers draw these conclusions from their work, despite multi-informant approaches to assessment long being a part of best practices in clinical and developmental assessments. Consequently, developmental psychopathology researchers and practitioners are in dire need of a focused set of research priorities with the key goal of rapidly advancing knowledge about informant discrepancies. In this paper, I discuss these research priorities, review work indicating the feasibility of conducting research addressing these priorities, and specify what researchers and practitioners would gain from studies advancing knowledge about informant discrepancies in developmental psychopathology research.

This study investigated the prospective pathways of children's exposure to interparental violence (EIPV) in early and middle childhood and externalizing behavior in middle childhood and adolescence as developmental predictors of dating violence perpetration and victimization at ages 23 and 26 years. Participants (N = 168) were drawn from a longitudinal study of low-income families. Path analyses examined whether timing or continuity of EIPV predicted dating violence and whether timing or continuity of externalizing behavior mediated these pathways. Results indicated that EIPV in early childhood directly predicted perpetration and victimization at age 23. There were significant indirect effects from EIPV to dating violence through externalizing behavior in adolescence and life stress at age 23. Independent of EIPV, externalizing behavior in middle childhood also predicted dating violence through externalizing behavior in adolescence and life stress at age 23, but this pathway stemmed from maltreatment. These results highlight that the timing of EIPV and both the timing and the continuity of externalizing behavior are critical risks for the intergenerational transmission of dating violence. The findings support a developmental perspective that negative early experiences and children's externalizing behavior are powerful influences for dating violence in early adulthood.

The development of socioemotional functioning is a complex process that occurs over a protracted time period and requires coordinating affective, cognitive, and social faculties. At many points in development, the trajectory of socioemotional development can be deleteriously altered due to a combination of environmental insults and individual vulnerabilities. The result can be psychopathology. However, researchers are just beginning to understand the neural and genetic mechanisms involved in the development of healthy and disordered socioemotional functioning. We propose a translational developmental neuroscience framework to understand the transactional process that results in socioemotional functioning in both healthy and disordered populations. We then apply this framework to healthy socioemotional development, pediatric anxiety, pediatric depression, and autism spectrum disorder, selectively reviewing current literature in light of the framework. Finally, we examine ways that the framework can help to frame future directions of research on socioemotional development and translational implications for intervention.

This longitudinal study examined the joint role of pubertal timing and temperament variables (emotional reactivity and self-regulation) in predicting adolescents' internalizing symptoms. The multiethnic sample included 1,025 adolescent girls and boys followed from age 11 to age 15 (M age = 11.03 years at Time 1). In structural equation models, age 11 measures of pubertal timing, emotional reactivity, and self-regulation and their interactions were used to predict adolescents' internalizing behavior concurrently and at age 15. Results indicated that, among girls, early pubertal timing, higher emotional reactivity, and lower self-regulation predicted increased internalizing behavior. In addition, self-regulation moderated the effect of pubertal timing such that effects of earlier timing on subsequent internalizing were seen primarily among girls with relatively poor self-regulation. Among boys, higher levels of emotional reactivity and lower self-regulation predicted increased internalizing, but there were no effects of pubertal timing. After controlling for Time 1 internalizing symptoms, only self-regulation predicted change in internalizing symptoms. Discussion focuses on the possible interplay of temperament and pubertal development in predicting internalizing problems during adolescence.

Depression is known to be associated with a wide array of environmental factors. Such associations are due at least in part to genetic influences on both. This issue has been little explored with preadolescent children. Measures of family chaos and parenting style at age 9 and child depressive symptoms at age 12 were completed by 3,258 twin pairs from the Twins Early Development Study and their parents. Quantitative genetic modeling was used to explore common and unique genetic and environmental influences on both family environment and later depressive symptoms. Depressive symptoms at age 12 were significantly heritable. Moderate genetic effects influenced parenting style and family chaos at the age of 9, indicating gene–environment correlation. There were significant genetic correlations between family environment and depressive symptoms. There was some evidence of a Gene × Environment interaction, with stronger genetic effects on depressive symptoms for children with more suboptimal family environment. There was an Environment × Environment interaction, with effects of nonshared environment on depressive symptoms stronger for twins with more adverse parenting experiences. There is some evidence for gene–environment correlation between aspects of family environment in middle childhood and subsequent depressive symptoms. This suggests that one of the mechanisms by which genes lead to depressive symptoms may be by themselves influencing depressogenic environments.