The study examined whether reciprocal friendship quantity or quality can mitigate genetic vulnerability for depression symptoms in children. The sample comprised 168 monozygotic twin pairs and 126 same-sex dizygotic twin pairs assessed in Grade 4 (mean age = 10.04 years). Friendship participation was measured via reciprocal nominations of close friendships within the classroom. Friendship quality was measured through self-reports. Depression symptoms were measured through teacher and peer reports. Genetic vulnerability for depression symptoms was unrelated to friendship participation or the number of reciprocal friends, but it was negatively related to positive friendship quality. In line with gene–environment interaction, genetic risk effects on depression symptoms were mitigated in girls who had at least one close reciprocal friend. In boys, only moderate main effects of genetic vulnerability and friendship participation were found but no interaction between them. However, among boys with at least one reciprocal friend, a greater number of friends was related to fewer depression symptoms whereas no cumulative effect of friendship was found for girls. Finally, positive friendship quality was related to fewer depression symptoms in girls and boys even when controlling for genetic risk. The findings emphasize the importance of teaching social interactional skills that promote high-quality friendship relations to help prevent the development of depression symptoms in children.

Evidence suggests that the 7-repeat variant of a 48 base pair variable number tandem repeat polymorphism in the dopamine receptor D4 (DRD4) gene may be associated with the development of attention problems. A parallel literature suggests that genes linked to dopaminergic functioning may be associated with differential sensitivity to context, such that the direction of the genetic effect is hypothesized to vary across environmental experience. Guided by these literatures, we used data from the NICHD Study of Early Child Care and Youth Development to consider (a) whether individual differences in children's inattention problems across middle childhood are predicted by gene–environment interactions between the DRD4 gene 7-repeat polymorphism and children's experiences of maternal sensitivity across infancy and early childhood and (b) the degree to which such interactions are consistent with the differential-sensitivity model. Largely consistent with the hypothesized model, gene–environment interactions indicated that, in the context of insensitive early maternal care, the DRD4 7-repeat polymorphism was associated with higher levels of inattention. Although somewhat less consistently, there was also evidence that, in the context of highly sensitive care, the 7-repeat polymorphism was associated with lower levels of inattention. Overall, the magnitude of the absolute genetic effect increased over time, as children's inattention trajectories diverged.

This cross-sectional study seeks to (a) describe developmental correlates of sensory hyporesponsiveness to social and nonsocial stimuli, (b) determine whether hyporesponsiveness is generalized across contexts in children with autism relative to controls, and (c) test the associations between hyporesponsiveness and social communication outcomes. Three groups of children ages 11–105 months (N = 178; autism = 63, developmental delay = 47, typical development = 68) are given developmental and sensory measures including a behavioral orienting task (the Sensory Processing Assessment). Lab measures are significantly correlated with parental reports of sensory hyporesponsiveness. Censored regression models show that hyporesponsiveness decreased across groups with increasing mental age (MA). Group differences are significant but depend upon two-way interactions with MA and context (social and nonsocial). At a very young MA (e.g., 6 months), the autism group demonstrates more hyporesponsiveness to social and nonsocial stimuli (with larger effects for social) than developmental delay and typically developing groups, but at an older MA (e.g., 60 months) there are no significant differences. Hyporesponsiveness to social and nonsocial stimuli predicts lower levels of joint attention and language in children with autism. Generalized processes in attention disengagement and behavioral orienting may have relevance for identifying early risk factors of autism and for facilitating learning across contexts to support the development of joint attention and language.

The present study examined the specificity of autobiographical memory in adolescents and adults with versus without child sexual abuse (CSA) histories. Eighty-five participants, approximately half of whom per age group had experienced CSA, were tested on the Autobiographical Memory Interview. Individual difference measures, including those for trauma-related psychopathology, were also administered. Findings revealed developmental differences in the relation between autobiographical memory specificity and CSA. Even with depression statistically controlled, reduced memory specificity in CSA victims relative to controls was observed among adolescents but not among adults. A higher number of posttraumatic stress disorder criteria met predicted more specific childhood memories in participants who reported CSA as their most traumatic life event. These findings contribute to the scientific understanding of childhood trauma and autobiographical memory functioning and underscore the importance of considering the role of age and degree of traumatization within the study of autobiographical memory.

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.

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.

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.

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.

The development of emotional regulation capacities in children at high versus low risk for externalizing disorder was examined in a longitudinal study investigating: (a) whether disturbances in emotion regulation precede and predict the emergence of externalizing symptoms and (b) whether sensitive maternal behavior is a significant influence on the development of child emotion regulation. Families experiencing high (n = 58) and low (n = 63) levels of psychosocial adversity were recruited to the study during pregnancy. Direct observational assessments of child emotion regulation capacities and maternal sensitivity were completed in early infancy, at 12 and 18 months, and at 5 years. Key findings were as follows. First, high-risk children showed poorer emotion regulation capacities than their low-risk counterparts at every stage of assessment. Second, from 12 months onward, emotion regulation capacities showed a degree of stability and were associated with behavioral problems, both concurrently and prospectively. Third, maternal sensitivity was related to child emotion regulation capacities throughout development, with poorer emotion regulation in the high-risk group being associated with lower maternal sensitivity. The results are consistent with a causal role for problems in the regulation of negative emotions in the etiology of externalizing psychopathology and highlight insensitive parenting as a potentially key developmental influence.

Poor self-regulation has been implicated as a significant risk factor for the development of multiple forms of psychopathology. This research examined the proposition that self-regulation deficits differentially predict aggressive behavior and depressive symptoms, depending on children's social approach versus avoidance motivation. A prospective, multiple-informant approach was used to test this hypothesis in 419 children (M age = 8.92, SD = 0.36). Parents rated children's inhibitory control. Children completed measures of social approach–avoidance motivation and depressive symptoms. Teachers rated children's aggressive behavior. As anticipated, poor inhibitory control predicted aggressive behavior in boys with high but not low approach motivation and low but not high avoidance motivation, whereas poor inhibitory control predicted depressive symptoms in girls with high but not low avoidance motivation. This research supports several complementary theoretical models of psychopathology and provides insight into the differential contributions of poor self-regulation to maladaptive developmental outcomes. The findings suggest the need for targeted intervention programs that consider heterogeneity among children with self-regulatory deficits.

We investigated the roles of sex and respiratory sinus arrhythmia (RSA), an index of autonomic parasympathetic nervous system activity, as predictors of codeveloping externalizing and internalizing symptoms in middle childhood. We expected that sex, baseline RSA (RSA-B), and RSA reactivity (RSA-R) to two types of tasks would interact to differentiate co-occurring trajectories of symptoms. We tested these hypotheses by combining longitudinal data from two independent samples (n = 390; 210 girls, 180 boys) with repeated measures at ages 8, 9, 10, and 11. RSA-R was measured in response to a socially stressful and frustrating stressor. Indicators of growth in externalizing and internalizing symptoms were derived from multiple domain growth models and used in person-centered growth mixture analyses. Three groups of externalizing and internalizing trajectories were found. Profile membership was predicted by several two-way interactions among sex, RSA-B, or RSA-R but was not predicted by three-way interactions. Children with low RSA-B and strong RSA withdrawal, girls with low RSA-B, and girls with strong RSA withdrawal were more likely to be on a developmental trajectory of low externalizing symptoms and moderately elevated internalizing symptoms. Membership in the high externalizing and high internalizing trajectory was predicted by weak RSA withdrawal for boys and strong RSA withdrawal for girls. The type of stressor task also played a role in predicting probability of profile membership. Results are discussed in the context of developmental psychobiology and implications for the codevelopment of psychopathology symptoms in childhood.

Emotional distress experienced by mothers increases young children's risk of externalizing problems through suboptimal parenting and child self-regulation. An integrative structural equation model tested hypotheses that mothers’ parenting (i.e., low levels of inductive discipline and maternal warmth) would mediate adverse effects of early maternal distress on child effortful control, which in turn would mediate effects of maternal parenting on child externalizing behavior. This longitudinal study spanning ages 3, 6, and 10 included 241 children, mothers, and a subset of teachers. The hypothesized model was partially supported. Elevated maternal distress was associated with less inductive discipline and maternal warmth, which in turn were associated with less effortful control at age 3 but not at age 6. Inductive discipline and maternal warmth mediated adverse effects of maternal distress on children's effortful control. Less effortful control at ages 3 and 6 predicted smaller relative decreases in externalizing behavior at 6 and 10, respectively. Effortful control mediated effects of inductive discipline, but not maternal warmth, on externalizing behavior. Findings suggest elevated maternal distress increases children's risk of externalizing problems by compromising early parenting and child self-regulation.

This longitudinal study examined personal-accentuation and contextual-amplification models of pubertal timing. In these models, individual and contextual risk factors during childhood and adolescence can magnify the effects of early or late puberty on depression symptoms that occur years later. The moderating role of prepubertal individual factors (emotional problems in late childhood) and interpersonal factors (deviant peer affiliation, early dating, perceived peer popularity, and perceived parental rejection during adolescence) were tested. A representative sample of 1,431 Canadian adolescents between 10–11 and 16–17 years of age was followed biannually. In line with the personal-accentuation model, early puberty has been shown to be a predictor for depression in both girls and boys who presented emotional problems in childhood. This effect was also noted for late maturing boys. Consistent with the contextual-amplification model, early puberty predicted later depression in youth who perceived greater parental rejection. Interpersonal experiences such as early dating in girls and deviant peer affiliation in boys predicted depression in early maturers as well. For girls, early dating was also found to be amplified by childhood emotional problems. In line with biopsychosocial models, results indicate that the effect of pubertal timing on depressive symptoms must be conceptualized through complex interactions between characteristics of adolescents' interpersonal relationships and prepubertal vulnerabilities.

Different patterns of emotional reactivity characterize proactive and reactive functions of aggressive behavior, and theory also suggests a link of both types with narcissism. How people with narcissistic traits respond emotionally to competitive scenarios could influence their aggressiveness. Participants were 85 adolescent boys from a detention center. Several indices of emotional functioning were assessed, including attentional bias to negative emotional stimuli and psychophysiological responding. In addition, we included self-report and laboratory measures of aggression and measures of psychopathy-linked narcissism, callous–unemotional traits, and impulsivity. Psychopathy-linked narcissism was uniquely related to unprovoked aggression (i.e., proactive aggression) and to heightened attention to pictures depicting others’ distress. Compared with those scoring low on narcissism, those high on narcissism, who were the least physiologically reactive group, evinced greater proactive aggression, whereas those showing a pattern of coactivation (i.e., sympathetic and parasympathetic autonomic reactivity) evinced greater reactive aggression. Results are consistent with descriptions of narcissistic individuals as being hypervigilant to negative cues and exhibiting poor emotion regulation. These characteristics may lead to aggressive and violent behavior aimed at maintaining dominance over others.

Little is known about how genetic and environmental factors contribute to the association between parental negativity and behavior problems from early childhood to adolescence. The current study fitted a cross-lagged model in a sample consisting of 4,075 twin pairs to explore (a) the role of genetic and environmental factors in the relationship between parental negativity and behavior problems from age 4 to age 12, (b) whether parent-driven and child-driven processes independently explain the association, and (c) whether there are sex differences in this relationship. Both phenotypes showed substantial genetic influence at both ages. The concurrent overlap between them was mainly accounted for by genetic factors. Causal pathways representing stability of the phenotypes and parent-driven and child-driven effects significantly and independently account for the association. Significant but slight differences were found between males and females for parent-driven effects. These results were highly similar when general cognitive ability was added as a covariate. In summary, the longitudinal association between parental negativity and behavior problems seems to be bidirectional and mainly accounted for by genetic factors. Furthermore, child-driven effects were mainly genetically mediated, and parent-driven effects were a function of both genetic and shared-environmental factors.

School mobility has been shown to increase the risk of poor achievement, behavior problems, grade retention, and high school dropout. Using data over 25 years from the Chicago Longitudinal Study, we investigated the unique risk of school moves on a variety of young adult outcomes including educational attainment, occupational prestige, depression symptoms, and criminal arrests. We also investigated how the timing of school mobility, whether earlier or later in the academic career, may differentially predict these outcomes over and above associated risks. Results indicate that students who experience more school changes between kindergarten and 12th grade are less likely to complete high school on time, complete fewer years of school, attain lower levels of occupational prestige, experience more symptoms of depression, and are more likely to be arrested as adults. Furthermore, the number of school moves predicted outcomes above and beyond associated risks such as residential mobility and family poverty. When timing of school mobility was examined, results indicated more negative outcomes associated with moves later in the grade school career, particularly between 4th and 8th grades.

An important function of the brain is to scan incoming sensory information for the presence of relevant signals and act on this information. For humans, the most salient signals are often social in nature, such as the identity and the emotional expression of the faces we encounter in our everyday lives. It can be argued that our survival as a species depends in large measure on these skills.

This study examines historical variation in individual trajectories of heavy drinking and marijuana use from age 18 to 22. Unlike most studies that have examined cohort differences in drug use, it focuses on differences in both level of use and rates of change (growth). Nearly 39,000 youths from the high school classes of 1976–2004 were surveyed at biennial intervals between the ages of 18 and 22 as part of the national Monitoring the Future study. Between 1976 and 2004, adolescent heavy drinking decreased substantially. However, because the age 18–22 heavy drinking growth rate increased threefold for males and sixfold for females during this period, heavy drinking among 21- to 22-year-olds remained largely stable. The growth rate for marijuana use was more stable across cohorts, and historical declines in use were sizable across the entire 18–22 age band. Generally, historical variation in use was unrelated to college status and living arrangements as well as to historical changes in the distribution of young adult social roles. Findings suggest that historical fluctuations in use were less the result of proximal young adult factors and more the result of historical variation in distal adolescent factors, the effect of which diminished with age, especially for heavy drinking.

We investigated differences in multiple-object tracking among individuals with Down syndrome (DS) as compared to typically developing children matched on a visual–spatial mental age of approximately 5.5 years. In order to ensure that these effects did not originate in differences in encoding or reporting the positions of targets in distracters after a delay, immediate and delayed report were measured for static items. Although their immediate and delayed report for multiple static items was comparable to that of the typically developing children, the participants with DS performed as if they were only capable of tracking a single item at a time regardless of the number of targets that needed to be tracked. This finding is surprising because the operations used in multiple-object tracking are thought to be necessary for visuospatial tasks, which are an area of relative strength among persons with DS. These results call into question the idea that abilities or deficits in multiple-object tracking predict visuospatial performance, and highlight ways that atypical development can inform our understanding of typical development.

Genetic factors can play a key role in the multiple level of analyses approach to understanding the development of child psychopathology. The present study examined gene–environment correlations and Gene × Environment interactions for polymorphisms of three target genes, the serotonin transporter gene, the D4 dopamine receptor gene, and the monoamine oxidase A gene in relation to symptoms of anxiety, depression, and oppositional behavior. Saliva samples were collected from 175 non-Hispanic White, 4-year-old children. Psychosocial risk factors included socioeconomic status, life stress, caretaker depression, parental support, hostility, and scaffolding skills. In comparison with the short forms (s/s, s/l) of the serotonin transporter linked polymorphic repeat, the long form (l/l) was associated with greater increases in symptoms of oppositional defiant disorder in interaction with family stress and with greater increases in symptoms of child depression and anxiety in interaction with caretaker depression, family conflict, and socioeconomic status. In boys, low-activity monoamine oxidase A gene was associated with increases in child anxiety and depression in interaction with caretaker depression, hostility, family conflict, and family stress. The results highlight the important of gene–environment interplay in the development of symptoms of child psychopathology in young children.