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.

The dopamine active transporter 1 (DAT1) gene is implicated in psychopathology risk. Although the processes by which this gene exerts its effects on risk are poorly understood, a small body of research suggests that the DAT1 gene influences early emerging negative emotionality, a marker of children's psychopathology risk. As child negative emotionality evokes negative parenting practices, the DAT1 gene may also play a role in gene–environment correlations. To test this model, children (N = 365) were genotyped for the DAT1 gene and participated in standardized parent–child interaction tasks with their primary caregiver. The DAT1 gene 9-repeat variant was associated with child negative affect expressed toward the parent during parent–child interactions, and parents of children with a 9-repeat allele exhibited more hostility and lower guidance/engagement than parents of children without a 9-repeat allele. These gene–environment associations were partially mediated by child negative affect toward the parent. The findings implicate a specific polymorphism in eliciting negative parenting, suggesting that evocative associations play a role in elevating children's risk for emotional trajectories toward psychopathology risk.

In this paper, I propose a roadmap for the integration of culture in developmental psychopathology. This integration is pressing because culture continues to be somewhat disconnected from theory, research, training, and interventions in developmental psychopathology, thus limiting our understanding of the epigenesis of mental health. I argue that in order to successfully integrate culture into developmental psychopathology, it is crucial to (a) study cultural development, (b) consider both individual-level and social-level cultural processes, (c) examine the interplay between culture and biology, and (d) promote improved and direct cultural assessment. I provide evidence in support of each of these guidelines, present alternative conceptual frameworks, and suggest new lines of research. Hopefully, that these directions will contribute to the emerging field of cultural development and psychopathology, which focuses on the elucidation of the cultural processes that initiate, maintain, or derail trajectories of normal and abnormal behavior.

Researchers studying longitudinal relationships among multiple problem behaviors sometimes characterize autoregressive relationships across constructs as indicating “protective” or “launch” factors or as “developmental snares.” These terms are used to indicate that initial or intermediary states of one problem behavior subsequently inhibit or promote some other problem behavior. Such models are contrasted with models of “general deviance” over time in which all problem behaviors are viewed as indicators of a common linear trajectory. When fit of the “general deviance” model is poor and fit of one or more autoregressive models is good, this is taken as support for the inhibitory or enhancing effect of one construct on another. In this paper, we argue that researchers consider competing models of growth before comparing deviance and time-bound models. Specifically, we propose use of the free curve slope intercept (FCSI) growth model (Meredith & Tisak, 1990) as a general model to typify change in a construct over time. The FCSI model includes, as nested special cases, several statistical models often used for prospective data, such as linear slope intercept models, repeated measures multivariate analysis of variance, various one-factor models, and hierarchical linear models. When considering models involving multiple constructs, we argue the construct of “general deviance” can be expressed as a single-trait multimethod model, permitting a characterization of the deviance construct over time without requiring restrictive assumptions about the form of growth over time. As an example, prospective assessments of problem behaviors from the Dunedin Multidisciplinary Health and Development Study (Silva & Stanton, 1996) are considered and contrasted with earlier analyses of Hussong, Curran, Moffitt, and Caspi (2008), which supported launch and snare hypotheses. For antisocial behavior, the FCSI model fit better than other models, including the linear chronometric growth curve model used by Hussong et al. For models including multiple constructs, a general deviance model involving a single trait and multimethod factors (or a corresponding hierarchical factor model) fit the data better than either the “snares” alternatives or the general deviance model previously considered by Hussong et al. Taken together, the analyses support the view that linkages and turning points cannot be contrasted with general deviance models absent additional experimental intervention or control.

This study evaluated whether exposure to maternal pre- or postnatal depression or anxiety symptoms predicted psychopathology in adolescent offspring. Growth mixture modeling was used to identify trajectories of pre- and postnatal depression and anxiety symptoms in 577 women of low socioeconomic status selected from a prenatal clinic. Logistic regression models indicated that maternal pre- and postnatal depression trajectory exposure was not associated with offspring major depression, anxiety, or conduct disorder, but exposure to the high depression trajectory was associated with lower anxiety symptoms in males. Exposure to medium and high pre- and postnatal anxiety was associated with the risk of conduct disorder among offspring. Male offspring exposed to medium and high pre- and postnatal anxiety had higher odds of conduct disorder than did males with low exposure levels. Females exposed to medium or high pre- and postnatal anxiety were less likely to meet conduct disorder criteria than were females with lower exposure. To the best of our knowledge, this is the first study to examine the effect of pre- and postnatal anxiety trajectories on the risk of conduct disorder in offspring. These results suggest new directions for investigating the etiology of conduct disorder with a novel target for intervention.

A randomized clinical trial was conducted to evaluate the efficacy of interpersonal psychotherapy (IPT) for ethnically and racially diverse, economically disadvantaged women with major depressive disorder. Non-treatment-seeking urban women (N = 128; M age = 25.40, SD = 4.98) with infants were recruited from the community. Participants were at or below the poverty level: 59.4% were Black and 21.1% were Hispanic. Women were screened for depressive symptoms using the Center for Epidemiologic Studies Depression Scale; the Diagnostic Interview Schedule was used to confirm major depressive disorder diagnosis. Participants were randomized to individual IPT or enhanced community standard. Depressive symptoms were assessed before, after, and 8 months posttreatment with the Beck Depression Inventory—II and the Revised Hamilton Rating Scale for Depression. The Social Support Behaviors Scale, the Social Adjustment Scale—Self-Report, and the Perceived Stress Scale were administered to examine mediators of outcome at follow-up. Treatment effects were evaluated with a growth mixture model for randomized trials using complier-average causal effect estimation. Depressive symptoms trajectories from baseline through postintervention to follow-up showed significant decreases among the IPT group compared to the enhanced community standard group. Changes on the Perceived Stress Scale and the Social Support Behaviors Scale mediated sustained treatment outcome.

Research on ethnic-minority youths' mental health has rarely examined developmental trajectories for the same ethnic group in contexts where they are a minority versus where they are the majority or mechanisms accounting for differences in trajectories across such contexts. This study examines Puerto Rican youth residing in two contexts, one in which they are in their home culture of Puerto Rico and one in which they are a minority group, in New York. We explore the relationship among social context, minority status, risk, resilience, and trajectories of internalizing symptoms after adjusting for factors related to migration. We found that youths' reports of internalizing symptoms declined over time. Youths in New York had higher levels of internalizing symptoms than did youths in Puerto Rico, but they had similar trajectories. Differences in internalizing symptoms across the two social contexts were accounted for by experiences of discrimination and exposure to violence. Parental monitoring was associated with fewer internalizing symptoms across the two sites, although this effect diminished over time. Contrary to what was expected, family religiosity was associated with higher levels of internalizing symptoms. This association was stronger in New York than in the Puerto Rico site.

Although considerable research has examined the relations between parental behavior and a range of child developmental outcomes, much of this work has been conducted at a very broad level of behavioral analysis. A developmental psychopathology framework and recent research conducted within this framework point to the need for models of parenting and child psychopathology that offer greater specificity regarding processes that may be implicated in the effects of these relationships. In addition, recent animal work and some human work has focused more on the proximal biological and social mechanisms through which parenting affects child outcomes. Our conceptualization of parenting effects acknowledges that family and child factors are embedded in a dynamic biological and social context that is key to understanding developmental trajectories of child adjustment. In this paper, we review two areas of research that are illuminating the biological processes underlying links between parenting and child psychopathology: molecular genetics and psychophysiology. We adopt a biopsychosocial perspective on developmental psychopathology that implies that a set of hierarchically organized, but reciprocally interacting, processes, from the genetic to the environmental, provide the essential elements of both normative and nonnormative development (Gottlieb, 2007). New directions stimulated by this general approach are discussed, with an emphasis on the contextual and developmental issues and applications implied by such a perspective.

Gene–environment correlations (rGE) have been demonstrated in behavioral genetic studies, but rGE have proven elusive in molecular genetic research. Significant gene–environment correlations may be difficult to detect because potential moderators could reduce correlations between measured genetic variants and the environment. Molecular genetic studies investigating moderated rGE are lacking. This study examined associations between child catechol-O-methyltransferase genotype and aspects of positive parenting (responsiveness and warmth), and whether these associations were moderated by parental personality traits (neuroticism and extraversion) among a general community sample of third, sixth, and ninth graders (N = 263) and their parents. Results showed that parent personality traits moderated the rGE association between youths' genotype and coded observations of positive parenting. Parents with low levels of neuroticism and high levels of extraversion exhibited greater sensitive responsiveness and warmth, respectively, to youth with the valine/valine genotype. Moreover, youth with this genotype exhibited lower levels of observed anger. There was no association between the catechol-O-methyltransferase genotype and parenting behaviors for parents high on neuroticism and low on extraversion. Findings highlight the importance of considering moderating variables that may influence child genetic effects on the rearing environment. Implications for developmental models of maladaptive and adaptive child outcomes, and interventions for psychopathology, are discussed within a developmental psychopathology framework.

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.

There is growing evidence that many offspring of parents with bipolar disorder (BD) will develop moderate to severe forms of psychopathology during childhood and adolescence, including thought problems. The purpose of this study was to evaluate the developmental progression of thought problems within the context of a family risk study. Repeated assessments of thought problems, spanning approximately 15 years, were conducted in offspring (N = 192 from 98 families) of parents diagnosed with BD (O-BD), unipolar depression (O-UNI), or no significant psychiatric or medical problems (O-WELL). Survival analysis showed that the O-BD group had the greatest estimated probability of developing thought problems over time, followed by O-UNI, and then O-WELL and O-BD exhibiting higher levels of persistence than O-WELL. Parent-reported thought problems in childhood and adolescence predicted a range of problems in young adulthood. Disturbances in reality testing and other atypical behaviors are likely to disrupt progression through important developmental periods and to associate with poor outcomes. These findings are likely relevant to preventing the occurrence or progression of problems in offspring of bipolar parents. The study of thought problems across development represents an important area of continued research in children at risk for development of affective disorders.

Attachment theory has been generating creative and impactful research for almost half a century. In this article we focus on the documented antecedents and consequences of individual differences in infant attachment patterns, suggesting topics for further theoretical clarification, research, clinical interventions, and policy applications. We pay particular attention to the concept of cognitive “working models” and to neural and physiological mechanisms through which early attachment experiences contribute to later functioning. We consider adult caregiving behavior that predicts infant attachment patterns, and the still-mysterious “transmission gap” between parental Adult Attachment Interview classifications and infant Strange Situation classifications. We also review connections between attachment and (a) child psychopathology; (b) neurobiology; (c) health and immune function; (d) empathy, compassion, and altruism; (e) school readiness; and (f) culture. We conclude with clinical–translational and public policy applications of attachment research that could reduce the occurrence and maintenance of insecure attachment during infancy and beyond. Our goal is to inspire researchers to continue advancing the field by finding new ways to tackle long-standing questions and by generating and testing novel hypotheses.

Restricted and repetitive behaviors (RRBs) are hallmark symptoms of autism spectrum disorders (ASDs); however, it has proven difficult to understand the mechanisms underlying these behaviors. One hypothesis suggests that RRBs are the result of a core deficit in attention. Alternatively, abnormalities of the motor system may constitute the central mechanism underlying RRBs, given motor deficits observed in ASDs. In this experiment, we investigated the etiology of RRBs and the relationship between attention and motor deficits. Movement impairments (a) may be indirectly related to attention deficits, (b) may result from a shared compromised process, or (c) may be independent. Twenty-two adolescents with ASD and 20 typically developing participants performed a spatial attention task. Movement impairments were assessed with a rhythmic tapping task. Attentional orienting and motor control were found to be related and supported the hypothesis that these impairments in ASD arise from a shared process. In contrast, measures of attention switching and motor control were found to be independent. Stereotyped behaviors, as assessed by parental ratings, were related more to the degree of motor impairment than to deficits of attention. These results suggest that both attentional orienting deficits and stereotyped RRBs are related to a compromised motor system.

This review discusses neurobiological studies of oppositional defiant disorder and conduct disorder within the conceptual framework of three interrelated mental domains: punishment processing, reward processing, and cognitive control. First, impaired fear conditioning, reduced cortisol reactivity to stress, amygdala hyporeactivity to negative stimuli, and altered serotonin and noradrenaline neurotransmission suggest low punishment sensitivity, which may compromise the ability of children and adolescents to make associations between inappropriate behaviors and forthcoming punishments. Second, sympathetic nervous system hyporeactivity to incentives, low basal heart rate associated with sensation seeking, orbitofrontal cortex hyporeactiviy to reward, and altered dopamine functioning suggest a hyposensitivity to reward. The associated unpleasant emotional state may make children and adolescents prone to sensation-seeking behavior such as rule breaking, delinquency, and substance abuse. Third, impairments in executive functions, especially when motivational factors are involved, as well as structural deficits and impaired functioning of the paralimbic system encompassing the orbitofrontal and cingulate cortex, suggest impaired cognitive control over emotional behavior. In the discussion we argue that more insight into the neurobiology of oppositional defiance disorder and conduct disorder may be obtained by studying these disorders separately and by paying attention to the heterogeneity of symptoms within each disorder.

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.

A fundamental question in the discipline of developmental psychopathology is whether early interpersonal experiences influence maladaptation in enduring or transient ways. We address this issue by applying a structural modeling approach developed by us to examine data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development on maternal sensitivity in the first 3 years of life and its association with symptoms of psychopathology through age 15. Results suggest that there may be enduring effects of early caregiving experiences on symptomatology as rated by teachers, although such effects were not found for maternal report. Additional analyses indicated that enduring associations found via teacher report could not be fully accounted for by continuity in caregiving experiences or by early contextual adversity.

In the psychological tradition, desistance from antisocial behavior is viewed as the product of psychosocial maturation, including increases in the ability to control impulses, consider the implications of one's actions on others, delay gratification in the service of longer term goals, and resist the influences of peers. The present study investigates how individual variability in the development of psychosocial maturity is associated with desistance from antisocial behavior in a sample of 1,088 serious juvenile offenders followed from adolescence to early adulthood (ages 14–25). We find that psychosocial maturity continues to develop to the midtwenties and that different developmental patterns of maturation are found among those who desist and those who persist in antisocial behavior. Compared to individuals who desisted from antisocial behavior, youths who persisted exhibited diminished development of psychosocial maturity. Moreover, earlier desistance compared to later desistance is linked to greater psychosocial maturity, suggesting that there is an association between desistance from antisocial behavior and normative increases in psychosocial maturity.

The purpose of the present study is to identify child and adult correlates that differentiate (a) individuals with persistent alcohol dependence from individuals with developmentally limited alcohol dependence and (b) individuals with adult-onset alcohol dependence from individuals who never diagnose. There are 1,037 members of the Dunedin Longitudinal Study, which is a birth cohort followed prospectively from birth until age 32. Past-year DSM-IV alcohol dependence diagnoses are ascertained with structured diagnostic interviews at ages 18, 21, 26, and 32. Individuals are classified as developmentally limited, persistent, or adult-onset subtypes based on their time-ordered pattern of diagnoses. The persistent subtype generally exhibits the worst scores on all correlates, including family psychiatric history, adolescent and adult externalizing and internalizing problems, adolescent and adult substance use, adult quality of life, and coping strategies. The prospective predictors that distinguished them from the developmentally limited subtype involved family liability, adolescent negative affectivity, daily alcohol use, and frequent marijuana use. Furthermore, young people who develop the persistent subtype of alcohol dependence are distinguished from the developmentally limited subtype by an inability to reduce drinking and by continued use despite problems by age 18. The adult-onset group members are virtually indistinguishable from ordinary cohort members as children or adolescents; however, in adulthood, adult-onset cases are distinguished by problems with depression, substance use, stress, and strategies for coping with stress. Information about age of onset and developmental course is fundamental for identifying subtypes of alcohol dependence. Subtype-specific etiologies point to targeted prevention and intervention efforts based on the characteristics of each subtype.

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.

Although children's security in the context of the interparental relationship has been identified as a key explanatory mechanism in pathways between family discord and child psychopathology, little is known about the inner workings of emotional security as a goal system. Thus, the objective of this paper is to describe how our reformulation of emotional security theory within an ethological and evolutionary framework may advance the characterization of the architecture and operation of emotional security and, in the process, cultivate sustainable growing points in developmental psychopathology. The first section of the paper describes how children's security in the interparental relationship is organized around a distinctive behavioral system designed to defend against interpersonal threat. Building on this evolutionary foundation for emotional security, the paper offers an innovative taxonomy for identifying qualitatively different ways children try to preserve their security and its innovative implications for more precisely informing understanding of the mechanisms in pathways between family and developmental precursors and children's trajectories of mental health. In the final section, the paper highlights the potential of the reformulation of emotional security theory to stimulate new generations of research on understanding how children defend against social threats in ecologies beyond the interparental dyad, including both familial and extrafamilial settings.