We present a developmental cascade model of the longitudinal relationships between internalizing symptoms, externalizing problems, and academic performance in middle childhood, utilizing a large sample (N = 1,771) from the United Kingdom in a 3-year, cross-lag design. Three hypotheses were tested: adjustment erosion, academic incompetence, and (cumulative) shared risk. In addition, we sought to examine whether developmental cascade pathways varied across gender, while also statistically exploring indirect, mediation pathways. Structural equation models that accounted for within-time covariance, data nesting, and temporal stability provided evidence of gender-specific effects as follows: externalizing-attainment adjustment erosion pathways were found only in boys, while attainment-internalizing/externalizing academic incompetence pathways were found only in girls. Analysis of mediation pathways provided further support for these gender-specific longitudinal profiles. Protective longitudinal internalizing-externalizing and externalizing-internalizing pathways were found for both boys and girls. Finally, while it improved model fit for both genders, the influence of cumulative shared risk on the aforementioned pathways was relatively meager, substantively affecting only one (externalizing-attainment adjustment erosion pathway in boys). The implications of these findings are discussed, and study limitations noted.

Two experiments were conducted to evaluate symbolic-deficit and memory-deficit hypotheses to account for the cognitive problems seen in children with autism. Experiment 1 tested imitation, in immediate and deferred conditions, of familiar actions with different sets of objects representing the developmental progression from functional to symbolic play. The results showed that the autism group and both their receptive language and nonverbal IQ-matched controls imitated familiar actions with realistic objects (evidence for functional play) and placeholder objects (evidence for symbolic play) after delays ranging from 24 hr to 3 weeks. Experiment 2 tested familiar three-step event sequences in which a placeholder object was substituted for the second step in half the events. The results showed that the autism group remembered as many of the actions with the placeholder objects as their language-matched controls and as many correctly ordered sequences, a finding that supports a symbolic-delay (rather than deficit) hypothesis. These results were obtained in highly structured test situations and sharply contrast with the impairments seen in children with autism who are observed in naturalistic settings. Two interpretations of these findings are offered. First, structured test settings minimize distractions that typically occur in naturalistic settings that may interfere or disrupt symbolic play in children with autism. Second, the results are consistent with an executive function deficit in that the autistic group demonstrated more knowledge in the test settings than they demonstrate spontaneously in naturalistic ones.

The independent contributions of preschool children's noncompliance and overactivity/inattention and measures of family stress to the prediction of negative maternal control were examined in two cohorts of children. In Cohort 1, children's noncompliant and hyperactive behavior each predicted more negative maternal control, whereas in Cohort 2, the interaction between noncompliance and overactivity was predictive of particularly high levels of negative control. In Cohort 2, stressful life events, maternal depression, and marital distress were also associated with negative maternal control. Stressful life events interacted with noncompliance indicating that the combination of a difficult child and a high level of family stress exacerbated the tendency of mothers of preschool children to exert negative control to gain compliance. Results indicate that factors external to the mother-child relationship exert an independent influence on maternal behavior.

Deviance proneness models propose a multilevel interplay in which transactions among genetic, individual, and family risk factors place children at increased risk for substance use. We examined bidirectional transactions between impulsivity and family conflict from middle childhood to adolescence and their contributions to substance use in adolescence and emerging adulthood (n = 380). Moreover, we examined children's, mothers’, and fathers’ polygenic risk scores for behavioral undercontrol, and mothers’ and fathers’ interparental conflict and substance disorder diagnoses as predictors of these transactions. The results support a developmental cascade model in which children's polygenic risk scores predicted greater impulsivity in middle childhood. Impulsivity in middle childhood predicted greater family conflict in late childhood, which in turn predicted greater impulsivity in late adolescence. Adolescent impulsivity subsequently predicted greater substance use in emerging adulthood. Results are discussed with respect to evocative genotype–environment correlations within developmental cascades and applications to prevention efforts.

Interparental conflict is a known risk factor for child adjustment problems; yet few studies have examined its long-term effects. This study tests the following hypotheses: Interparental conflict has both longitudinal and concurrent influences on the functioning of young adult children, and the relationship between young adults and their parents mediates these influences. We assessed a community sample (N = 243) of families when the target child was in early to middle adolescence. We then reassessed them 6 years later during young adulthood. The links of interparental conflict measured at the two time points to young adults' general psychopathology and antisocial behavior were examined using multiple regression analyses. The quality of the relationship between young adults and each parent was added to each equation as a potential mediating variable. Results showed that concurrent, but not earlier, interparental conflict predicted males' antisocial behavior. No support was found for the mediational model, but support was found for an alternate model positing direct effects for interparental conflict and the parent-young adult relationship on young adult functioning. For females and males, problematic relationships with mothers and fathers predicted greater general psychopathology, while problems in paternal relationships predicted higher levels of antisocial behavior only for females.

Bipolar affective disorder is a recurrent, disabling, and potentially lethal illness that typically begins early in life. Although the disorder is defined by the manic and hypomanic episodes, for most people the depression episodes are the more virulent aspect of the illness. Specifically, the depressive episodes are more numerous, last longer, and are more difficult to treat than the manias, and depression is the principal cause of the illness's increased mortality due to suicide. For people with early-onset depression, predictors of subsequent bipolarity include a family history, psychotic features, and reverse neurovegetative features. Initial episodes of depression are commonly misdiagnosed, which often delays initiation of appropriate therapy and increases the likelihood of treatment with antidepressants alone. Unfortunately, the correct diagnosis is often not made until there has been a treatment–emergent affective switch. There are no treatments specifically approved for bipolar disorder in youth and, among antidepressants, only fluoxetine has received approved. When bipolarity is suspected, treatment with mood stabilizers, both conventional (i.e., lithium, valproate, and carbamazapine) and more recently classified (lamotrigine) and atypical antipsychotics should be prioritized. When antidepressants are indicated in combination with mood stabilizers, first choice options include bupropion and the selective serotonin reuptake inhibitors. Studies of adults indicate that several forms of focused psychotherapy may improve longer term outcomes.

Data gathered over the course of a 25-year longitudinal study of 1,055 young people was used to examine gender differences in the onset of early parenthood and the developmental processes that place males and females at risk of becoming a young parent. Results revealed clear gender differences in the timing of early parenthood, with females being twice as likely as males to become a parent between the ages of 16 and 25 years. In contrast, the risk factors and life course processes that placed males and females at risk of an early transition to parenthood were very similar. Two exceptions were a gender-specific effect for maternal age and exposure to parental change, suggesting that having been raised by a younger mother and having experienced parental changes in your family of origin increased risks of early parenthood for females but not males. These findings contribute to our understanding of the effects of gender on life course development.This research was funded by grants from the Health Research Council of New Zealand, the National Child Health Research Foundation, the Canterbury Medical Research Foundation and the New Zealand Lottery Grants Board.

Researchers are becoming increasingly interested in linking specific forms of early life stress (ELS) to specific neurobiological markers, including alterations in the morphology of stress-sensitive brain regions. We used a person-centered, multi-informant approach to investigate the associations of specific constellations of ELS with hippocampal and amygdala volume in a community sample of 211 9- to 13-year-old early adolescents. Further, we compared this approach to a cumulative risk model of ELS, in which ELS was quantified by the total number of stressors reported. Using latent class analysis, we identified three classes of ELS (labeled typical/low, family instability, and direct victimization) that were distinguished by experiences of family instability and victimization. Adolescents in the direct victimization class had significantly smaller hippocampal volume than did adolescents in the typical/low class; ELS classes were not significantly associated with amygdala volume. The cumulative risk model of ELS had a poorer fit than did the person-centered model; moreover, cumulative ELS was not significantly associated with hippocampal or amygdala volume. Our results underscore the utility of taking a person-centered approach to identify alterations in stress-sensitive brain regions based on constellations of ELS, and suggest victimization is specifically associated with hippocampal hypotrophy observed in early adolescence.

There is increasing evidence for multiple pathways in the development of callous-unemotional (CU) features, including primary and secondary profiles. Understanding affect regulation strategies among variants may provide further insight to the development and treatment of CU features. This study evaluated whether profiles of CU features could be identified within a clinical sample of youth using measures of affect dysregulation, affect suppression, anxiety, and maltreatment. We also examined whether these profiles were consistent across gender. Participants (N = 418; 56.7% female) ranged in age from 12 to 19 years (M = 15.04, SD = 1.85) and were drawn from a clinical sample. Latent profile analysis (LPA) was conducted using five indicators, including affect regulation, suppression, anxiety, CU features, and maltreatment. The best fitting model, a four-profile solution, included a low (low CU/dysregulation), anxious (low CU/high dysregulation), primary CU (high CU/low dysregulation), and secondary CU profile (high CU/dysregulation/maltreatment). LPAs found the same four-profile model when conducted separately for males and females. This is the first study to examine gender and include affect regulation strategies in the examination of primary and secondary profiles of CU.

The quality of the environment experienced by an individual across his or her lifespan can result in a unique developmental trajectory with consequences for adult phenotype and reproductive success. However, it is also evident that these experiences can impact the development of offspring with continued effect on subsequent generations. Epigenetic mechanisms have been proposed as a mediator of both these within- and across-generation effects, and there is increasing evidence to support the role of environmentally induced changes in DNA methylation, posttranslational histone modifications, and noncoding RNAs in predicting these outcomes. Advances in our understanding of these molecular modifications contribute to increasingly nuanced perspectives on plasticity and transmission of phenotypes across generations. A challenge that emerges from this research is in how we integrate these “new” perspectives with traditional views of development, reproduction, and inheritance. This paper will highlight evidence suggestive of an epigenetic impact of the environment on mothers, fathers, and their offspring, and illustrate the importance of considering the dynamic nature of reproduction and development and inclusive views of inheritance within the evolving field of behavioral and environmental epigenetics.

The developmental approach toward mental retardation historically has examined whether retarded individuals behave as do nonretarded individuals. An alternative approach involves using data from handicapped populations as “experiments of nature” to provide information about typical developmental processes. Three examples of this use of mental retardation findings include examinations of sequences, rates, and cross-domain relations. Certain instances of universal sequences appear to have been replicated by findings from children with mental retardation, but in other cases mentally retarded children help illustrate the extremes to which certain individual styles of development can be taken. Changing rates of development in different types of retarded children sometimes appear due to changes in the developmental tasks facing the child, sometimes to changes in neurobiologic factors related to chronological age. Cross-domain findings from children of diverse etiologies suggest the necessity of certain, specific connections among seemingly disparate behaviors in development. The article concludes with a discussion of mental retardation research as an experiment of nature that serves to replicate and amplify existing findings as well as to spur new extensions of developmental theory.

Emotion dysregulation characterizes many forms of psychopathology. Patterns of dysregulation occur as a function of a developmental process in which normative and adaptive emotion regulation skills fail to become part of the child's behavioral repertoire due to biological, psychological, and contextual processes and experiences. Here we highlight the processes involved in the dysregulation of temperamental anger and frustration that become core features of externalizing problems and place children at risk for more serious forms of psychopathology. We imbed these processes in a larger self-regulatory framework, and we discuss how they influence mental as well as physical health, using data from our 20-year longitudinal study following a large cohort of children into young adulthood. Recommendations are made for future research involving the integration of biological systems with mental and physical health outcomes.

The current study sought to advance our understanding of transactional processes among maternal depression, neighborhood deprivation, and child conduct problems (CP) using two samples of low-income families assessed repeatedly from early childhood to early adolescence. After accounting for initial levels of negative parenting, independent and reciprocal effects between maternal depressive symptoms and child CP were evident across both samples, beginning in early childhood and continuing through middle childhood and adolescence. In addition, neighborhood effects were consistently found in both samples after children reached age 5, with earlier neighborhood effects on child CP and maternal depression found in the one exclusively urban sample of families with male children. The results confirm prior research on the independent contribution of maternal depression and child CP to the maintenance of both problem behaviors. The findings also have implications for designing preventative and clinical interventions to address child CP for families living in high-risk neighborhoods.

The national priority to advance early detection and intervention for children with autism spectrum disorder (ASD) has not reduced the late age of ASD diagnosis in the US over several consecutive Centers for Disease Control and Prevention (CDC) surveillance cohorts, with traditionally under-served populations accessing diagnosis later still. In this review, we explore a potential perceptual barrier to this enterprise which views ASD in terms that are contradicted by current science, and which may have its origins in the current definition of the condition and in its historical associations. To address this perceptual barrier, we propose a re-definition of ASD in early brain development terms, with a view to revisit the world of opportunities afforded by current science to optimize children's outcomes despite the risks that they are born with. This view is presented here to counter outdated notions that potentially devastating disability is determined the moment a child is born, and that these burdens are inevitable, with opportunities for improvement being constrained to only alleviation of symptoms or limited improvements in adaptive skills. The impetus for this piece is the concern that such views of complex neurodevelopmental conditions, such as ASD, can become self-fulfilling science and policy, in ways that are diametrically opposed to what we currently know, and are learning every day, of how genetic risk becomes, or not, instantiated as lifetime disabilities.

This study examined the transactional interplay among dimensions of destructive interparental conflict (i.e., hostility and dysphoria), children's emotional insecurity, and their psychological problems from middle childhood and adolescence. Participants were 232 families, with the first of five measurement occasions occurring when children were in first grade (M age = 7 years). Cross-lagged, autoregressive models were conducted with a multiple-method, multiple-informant measurement approach to identify developmental cascades of interparental and child cascades. Results indicated that emotional insecurity was a particularly powerful mediator of prospective associations between interparental conflict (i.e., dysphoria and hostility) and child adjustment during adolescence rather than childhood. In reflecting bidirectionality in relationships between interparental and child functioning, children's psychological problems predicted increases in interparental dysphoria during childhood and adolescence. Although emotional insecurity was not identified as a proximal predictor of interparental difficulties, an indirect cascade was identified whereby insecurity in early adolescence was associated with increases in teen psychological problems, which in turn predicted greater interparental dysphoria over time. Results are interpreted in the context of how they advance transactional formulation of emotional security theory and its resulting translational implications for clinical initiatives.

There is a relative consensus about the detrimental impact of childhood maltreatment on later mental health problems and behavioral difficulties. Prior research suggests that neurophysiological stress mechanisms may partly mediate this association. However, inconsistent findings regarding hypothalamic-pituitary-adrenal axis and sympathetic responses to stress complicate this investigation. Furthermore, the concordance in these two stress systems is not well understood. We tested whether the severity of maltreatment affected the association between maltreatment and cortisol and heart rate (HR) stress responses and the symmetry of these responses. Participants were 155 males (56 maltreated and 99 controls) aged 18 to 35 years. Cortisol and HR were measured in response to the Trier Social Stress Test. Childhood maltreatment, sociodemographic factors, and health-related factors were measured using self-reported questionnaires. Maltreated participants had higher cortisol responses to stress in comparison to controls. However, a shift from moderate to lower to higher cortisol responses was noted as the severity of the experiences increased. Participants exposed to more experiences of maltreatment also showed a greater symmetry between cortisol and HR stress responses. Our findings provide further support for persistent dysregulation of the HPA axis following childhood maltreatment, of which the expression and symmetry with the sympathetic system may change according to the severity of experiences.

The present study incorporates a person-based approach to identify spillover and compartmentalization patterns of interpartner conflict and maternal parenting practices in an ethnically diverse sample of 192 2-year-old children and their mothers who had experienced higher levels of socioeconomic risk. In addition, we tested whether sociocontextual variables were differentially predictive of theses profiles and examined how interpartner-parenting profiles were associated with children's physiological and psychological adjustment over time. As expected, latent class analyses extracted three primary profiles of functioning: adequate functioning, spillover, and compartmentalizing families. Furthermore, interpartner-parenting profiles were differentially associated with both sociocontextual predictors and children's adjustment trajectories. The findings highlight the developmental utility of incorporating person-based approaches to models of interpartner conflict and maternal parenting practices.

Using a family systems perspective, we examined the trajectories of father-child and mother-child closeness and conflict across Grades 1, 3, 4, 5, and 6, and their associations with child depressive symptoms across middle childhood among 685 families in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Study of Early Child Care and Youth Development (SECCYD). Father-child and mother-child relationship conflict increased, whereas relationship closeness decreased from Grades 1 to 6. Girls with more slowly increasing father-child conflict, and more slowly decreasing father-child closeness, were at lower risk for depressive symptoms. Boys with more slowly increasing mother-child conflict were at lower risk for depressive symptoms. These findings highlight the important roles of both father-child and mother-child relationships in children's emotional adjustment during middle childhood.

Maternal depression negatively impacts children's development, yet few studies have focused on fathering and the family process in cases of maternal depression. A community cohort of married/cohabitating women was recruited on the second postbirth day (N = 1,983) and maternal depression repeatedly assessed across the first year and again at 6 years to form two cohorts: mothers chronically depressed from birth to 6 (N = 46) and nondepressed controls (N = 103). At 6 years, mother–child, father–child, and family interactions were observed. In families of depressed mothers, both mother and father exhibited lower sensitivity and higher intrusiveness, and children displayed lower social engagement during interactions with mother and father. Fathering moderated the effects of maternal depression on the family process. When fathers showed low sensitivity, high intrusiveness, and provided little opportunities for child social engagement, the family process was less cohesive, implying a decrease in the family's harmonious, warm, and collaborative style. However, in cases of high father sensitivity, low intrusiveness, and increased child engagement, the family process was unaffected by maternal depression. Findings describe both comparability and compensatory mechanisms in the effects of fathering on family life when maternal care is deficient, highlight the buffering role of fathers, and underscore the importance of father-focused interventions when mothers are depressed.

Child maltreatment is associated with disruptions in physiological arousal, emotion regulation, and defensive responses to cues of threat and distress, as well as increased risk for callous unemotional (CU) traits and externalizing behavior. Developmental models of CU traits have focused on biological and genetic risk factors that contribute to hypoarousal and antisocial behavior, but have focused less on environmental influences (Blair, 2004; Daversa, 2010; Hare, Frazell, & Cox, 1978; Krueger, 2000; Shirtcliff et al., 2009; Viding, Fontaine, & McCrory, 2012). The aim of the present investigation was to measure the independent and combined effects of child maltreatment and high CU traits on emotion-modulated startle response in children. Participants consisted of 132 low-income maltreated (n = 60) and nonmaltreated (n = 72) children between 8 and 12 years old who attended a summer camp program. Acoustic startle response (ASR) was elicited in response to a 110-dB 50-ms probe while children viewed a slideshow of pleasant, neutral, and unpleasant IAPS images. Maltreatment status was assessed through examination of Department of Human Services records. CU traits were measured using counselor reports from the Inventory of Callous and Unemotional Traits (Frick, 2004), and conduct problems were measured using counselor and child self-report. We found no significant differences in emotion-modulated startle in the overall sample. However, significant differences in ASR by maltreatment status, maltreatment subtype, and level of CU traits were apparent. Results indicated differential physiological responses for maltreated and nonmaltreated children based on CU traits, including a pathway of hypoarousal for nonmaltreated/high CU children that differed markedly from a more normative physiological trajectory for maltreated/high CU children. Further, we found heightened ASR for emotionally and physically neglected children with high CU and elevated antisocial behavior in these children. Results provide further support for differential trajectories by which experience and biology may influence the development of antisocial behavior in youth and highlight potential avenues for intervention.