One goal of developmental psychopathology is to understand the origins and course of mental disorders. I argue that pursuit of this goal requires a valid conceptual understanding of disorder and that this understanding can be provided by the “harmful dysfunction” analysis of the concept of disorder. The harmful dysfunction analysis holds that a disorder is a condition that is both harmful according to social values and caused by an internal dysfunction, that is, by a failure of an internal mechanism to perform a function for which it was naturally selected. This analysis explains why many of the distinctive features of developmental psychopathology are appropriate to the study of disorder. It is argued that the harmful dysfunction analysis is a necessary supplement to other proposed criteria for disorder, such as developmental deviation or predictive validity.

Social withdrawal and social anxiety are believed to have a bidirectional influence on one another, but it is unknown if their relationship is bidirectional, especially within person, and if peer experiences influence this relationship. We investigated temporal sequencing and the strength of effects between social withdrawal and social anxiety, and the roles of peer victimization and acceptance in the pathways. Participants were 2,772 adolescents from the population-based and clinically referred cohorts of the Tracking Adolescents' Individual Lives Survey. Self- and parent-reported withdrawal, and self-reported social anxiety, peer victimization, and perceived peer acceptance were assessed at 11, 13, and 16 years. Random-intercept cross-lagged panel models were used to investigate within-person associations between these variables. There was no feedback loop between withdrawal and social anxiety. Social withdrawal did not predict social anxiety at any age. Social anxiety at 11 years predicted increased self-reported withdrawal at 13 years. Negative peer experiences predicted increased self- and parent-reported withdrawal at 13 years and increased parent-reported withdrawal at 16 years. In turn, self-reported withdrawal at 13 years predicted negative peer experiences at 16 years. In conclusion, adolescents became more withdrawn when they became more socially anxious or experienced greater peer problems, and increasing withdrawal predicted greater victimization and lower acceptance.

The present study tested several predictions related to the theory that girls with conduct disorder (CD) follow a single delayed onset pathway. The following hypotheses were tested among a high-risk, stratified random sample of youth who used public services during a 6-month period: boys will be more likely to have childhood onset CD (COCD) than girls; girls with COCD will be less common than girls with adolescent onset CD (AOCD); COCD girls, AOCD girls, and COCD boys will be similar in terms of risk profiles and AOCD boys will have a less severe risk profile than COCD girls; and risk factors that differentiate between COCD and AOCD among males will not differentiate between COCD and AOCD among females. Among those youth who met the criteria for CD, males were significantly more likely to have COCD than females. However, close to half of females with CD met the criteria for the COCD subtype. Of the seven risk factors that were examined, girls with COCD scored higher than COCD boys on three factors and higher than AOCD girls on four factors; however, only one significant difference was found between AOCD girls and COCD boys. Finally, risk factors appeared to differentiate between COCD and AOCD groups in a similar way among males and females. These findings suggest that COCD is not rare among females in public service sectors, COCD girls can be distinguished from AOCD girls in terms of risk factors, and risk factors for COCD among males are also relevant to females.The Patterns of Youth Mental Health Care in Public Service Systems Study is supported by National Institute of Mental Health (NIMH) Grant U01 MH55282. Preparation of this article was supported by Research Scientist Development Awards K01MH01767 and K01MH01924. The authors are most grateful for the comments and suggestions on this manuscript that were provided by Dr. Persephanie Silverthorn and Dr. Theodore Beauchaine.

This article serves to outline a research paradigm to investigate main effects and interactions of genes, environment, and development on behavior and psychiatric illness. We provide a historical context for candidate gene studies and genome-wide association studies, including benefits, limitations, and expected payoffs. Using substance use and abuse as our driving example, we then turn to the importance of etiological psychological theory in guiding genetic, environmental, and developmental research, as well as the utility of refined phenotypic measures, such as endophenotypes, in the pursuit of etiological understanding and focused tests of genetic and environmental associations. Phenotypic measurement has received considerable attention in the history of psychology and is informed by psychometrics, whereas the environment remains relatively poorly measured and is often confounded with genetic effects (i.e., gene–environment correlation). Genetically informed designs, which are no longer limited to twin and adoption studies thanks to ever-cheaper genotyping, are required to understand environmental influences. Finally, we outline the vast amount of individual difference in structural genomic variation, most of which remains to be leveraged in genetic association tests. Although the genetic data can be massive and burdensome (tens of millions of variants per person), we argue that improved understanding of genomic structure and function will provide investigators with new tools to test specific a priori hypotheses derived from etiological psychological theory, much like current candidate gene research but with less confusion and more payoff than candidate gene research has to date.

Dispositional trait frameworks offer great potential to elucidate the nature and development of psychopathology, including the construct of relational aggression. The present study sought to explore the dispositional context of relational aggression across three dispositional frameworks: temperament, personality, and personality pathology. Participants comprised a large community sample of youth, aged 6 to 18 years (N = 1,188; 51.2% female). Ratings of children's relational aggression, temperament, personality, and personality pathology traits were obtained through parent report (86.3% mothers). Results showed convergence and divergence across these three dispositional frameworks. Like other antisocial behavior subtypes, relational aggression generally showed connections with traits reflecting negative emotionality and poor self-regulation. Relational aggression showed stronger connections with temperament traits than with personality traits, suggesting that temperament frameworks may capture more relationally aggressive content. Findings at the lower order trait level help differentiate relational aggression from other externalizing problems by providing a more nuanced perspective (e.g., both sociability and shyness positively predicted relational aggression). In addition, there was little evidence of moderation of these associations by gender, age, or age2, and findings remained robust even after controlling for physical aggression. Results are discussed in the broader context of conceptualizing relational aggression in an overarching personality-psychopathology framework.

We conducted signal detection analyses to test for curvilinear, U-shaped relations between early experiences of adversity and heightened physiological responses to challenge, as proposed by biological sensitivity to context theory. Based on analysis of an ethnically diverse sample of 338 kindergarten children (4–6 years old) and their families, we identified levels and types of adversity that, singly and interactively, predicted high (top 25%) and low (bottom 25%) rates of stress reactivity. The results offered support for the hypothesized U-shaped curve and conceptually replicated and extended the work of Ellis, Essex, and Boyce (2005). Across both sympathetic and adrenocortical systems, a disproportionate number of children growing up under conditions characterized by either low or high adversity (as indexed by restrictive parenting, family stress, and family economic condition) displayed heightened stress reactivity, compared with peers growing up under conditions of moderate adversity. Finally, as hypothesized by the adaptive calibration model, a disproportionate number of children who experienced exceptionally stressful family conditions displayed blunted cortisol reactivity to stress.

Two sets of evidence reviewed herein, one indicating that prenatal stress is associated with elevated behavioral and physiological dysregulation and the other that such phenotypic functioning is itself associated with heightened susceptibility to positive and negative environmental influences postnatally, raises the intriguing hypothesis first advanced by Pluess and Belsky (2011) that prenatal stress fosters, promotes, or “programs” postnatal developmental plasticity. Here we review further evidence consistent with this proposition, including new experimental research systematically manipulating both prenatal stress and postnatal rearing. Collectively this work would seem to explain why prenatal stress has so consistently been linked to problematic development: stresses encountered prenatally are likely to continue postnatally, thereby adversely affecting the development of children programmed (by prenatal stress) to be especially susceptible to environmental effects. Less investigated are the potential benefits prenatal stress may promote, due to increased plasticity, when the postnatal environment proves to be favorable. Future directions of research pertaining to potential mechanisms instantiating postnatal plasticity and moderators of such prenatal-programming effects are outlined.

This study examined the prospective relations of adolescents' perceptions of discrimination and their genetic status with increases in conduct problems. Participants were 461 African American youths residing in rural Georgia (Wave 1 mean age = 15.5 years) who provided three waves of data and a saliva sample from which a polymorphism in the SCL6A4 (serotonin transporter [5-HTT]) gene polymorphism known as the 5-HTT linked promoter region (5-HTTLPR) was genotyped. Data analyses using growth curve modeling indicated that perceived discrimination was significantly related to the slope of conduct problems. As hypothesized, interactions between perceived discrimination and genetic status emerged for male but not female youths. Compared with those carrying two copies of the long allele variant of 5-HTTLPR, male youths carrying one or two copies of its short allele variant evinced higher rates of conduct problems over time when they perceived high levels of racial discrimination. These findings are consistent with resilience and differential susceptibility propositions stating that genes can both foster sensitivity to adverse events and confer protection from those events.

Findings of the few psychotherapy outcome studies with depressed children and adolescents raise questions about whether or not treatments are sufficiently sensitive to developmental factors. Here we review the outcome data, then survey potentially relevant research on the cognitions, competencies, and coping behavior of depressed youngsters. Much of the work in each domain is both procedurally and theoretically adevelopmental, and the psychotherapy research does not appear to be well informed by research in the other domains. To help remedy this situation, for each domain we suggest key developmental questions that need to be answered, and we discuss implications for psychotherapy. We also propose a three-way partnership involving basic developmental research linked with research on relations between depression and various cognitive and behavioral processes, with both lines of inquiry informing the development and refinement of interventions.

When children are exposed to serious life adversities, Ed Zigler believed that developmental scientists must expediently strive to illuminate the most critical directions for beneficial interventions. In this paper, we present a new study on risk and resilience on adolescents during COVID-19, bookended – in introductory and concluding discussions – by descriptions of programmatic work anchored in lessons learned from Zigler. The new study was conducted during the first two months of the pandemic, using a mixed-methods approach with a sample of over 2,000 students across five high schools. Overall, rates of clinically significant symptoms were generally lower as compared to norms documented in 2019. Multivariate regressions showed that the most robust, unique associations with teens’ distress were with feelings of stress around parents and support received from them. Open ended responses to three questions highlighted concerns about schoolwork and college, but equally, emphasized worries about families’ well-being, and positive outreach from school adults. The findings have recurred across subsequent school assessments, and strongly resonate with contemporary perspectives on resilience in science and policy. If serious distress is to be averted among youth under high stress, interventions must attend not just to the children's mental health but that of salient caregiving adults at home and school. The article concludes with some specific recommendations for community-based initiatives to address mental health through continued uncertainties of the pandemic.

We evaluate the usefulness of 11 key epigenetic concepts from the behavior genetic research paradigm for advancing the field of developmental psychopathology. Key assumptions, empirical examples, and caveats in interpreting results are presented. We emphasize the usefulness of incorporating both dimensional (e.g., temperament trait) and categorical (e.g., diagnosis) variables, environmental measures, direct behavioral assessments, and multiple, theoretically relevant occasions of study into classic twin and family studies. We highlight contemporary techniques for identifying specific chromosomal regions associated with behavioral patterns, and the importance of considering nonmendelizing genetic influences when discerning the panorama of genetic influences on behavior.

Cognitive impulsivity may increase children's risk of developing delinquent behavior. However, the influence of cognitive impulsivity may depend on social environmental risk factors. This study examined the moderating effect of late childhood parenting behaviors and peer relations on the influence of children's cognitive impulsivity on delinquency development across adolescence and early adulthood, while taking possible interactions with intelligence also into account. Delinquent behavior of 412 boys from the Pittsburgh Youth Study was measured annually from ages 13 to 29 years with official arrest records. Cognitive impulsivity (neurocognitive test scores) and intelligence were assessed at age 12–13. Parenting behaviors (persistence of discipline, positive reinforcement, and parental knowledge), peer delinquency, and peer conventional activities were assessed between ages 10 and 13 years. Results showed that, while controlling for intelligence, the influence of youths' cognitive impulsivity on delinquency depended on their parents' behaviors. An interaction was found among cognitive impulsivity, intelligence, and peer delinquency, but instead of cognitive impulsivity, the effect of intelligence on delinquency was particularly moderated. Overall, findings suggest that when there was moderation, high cognitive impulsivity and low intelligence were associated with an increased probability for engaging in delinquency predominantly among boys in a good social environment, but not in a poor social environment.

The association between young adolescents' psychological profiles and their subsequent adjustment was examined in a sample of 606 adolescents (ages 12–13) drawn from the mother–child data set of the National Longitudinal Survey of Youth. Cluster analysis was used to identify distinct groups of youth based on self-regulation, proneness to risk, self-worth, and perceived academic competence. Five replicable clusters were identified corresponding to optimal, average, behavioral risk, low self-regulation, and emotional risk groups. These clusters were associated with distinct patterns of adjustment 4 years later. At ages 16–17, youth in the optimal group tended to report better academic performance, less problem behavior, and less depression than youth in the three risk groups; however, their functioning did not differ significantly from youth in the average group. The three risk groups differed in self-reported depression symptoms and academic performance but not in levels of problem behavior. Differences among the five groups persisted when demographic and contextual variables were controlled. These results support the existence of different groups of youth who follow distinct developmental trajectories and may experience different patterns of adjustment.This research was funded by a grant to M. Raffaelli and L. Crockett from the National Institute of Mental Health (R01-MH62977). We thank Rebecca Colman, Yuh-Ling Shen, Sam Hardy, Rebecca Goodvin, Myesha Albert, Andy Peytchev, Jenenne Geske, Jennifer Bowers, Devan Starks, and Brett Avila for their contributions to the project. We also thank Cal Garbin for his statistical advice and several anonymous reviewers for their suggestions.

The ability to use language to identify causes for emotion and to describe the subjective experience of various emotions was examined in 28 male and female children and adolescents with autism compared to 28 normally developing and mentally handicapped subjects of equivalent chronological age and mean length of utterance. Mentally handicapped and lower functioning autistic subjects were also similar in verbal IQ. Individuals with autism did not grossly differ from other participants in their descriptions of emotion but were less likely to relate emotions to either reaching a goal or social interaction and more likely to attribute positive emotions to concrete events (e.g., going on a trip). Results are discussed in terms of current cognitive and affective theories of autism.

Negative experiences with a caregiver during infancy can result in long-term changes in brain function and behavior, but underlying mechanisms are not well understood. It is our central hypothesis that brain and behavior changes are conferred by early childhood adversity through epigenetic changes involving DNA methylation. Using a rodent model of early-life caregiver maltreatment (involving exposure to an adverse caregiving environment for postnatal days 1–7), we have previously demonstrated abnormal methylation of DNA associated with the brain-derived neurotrophic factor (Bdnf) gene in the medial prefrontal cortex (mPFC) of adult rats. The aim of the current study was to characterize Bdnf DNA methylation in specific cell populations within the mPFC. In the prefrontal cortex, there is approximately twice as many neurons as glia, and studies have recently shown differential and distinctive DNA methylation patterns in neurons versus nonneurons. Here, we extracted nuclei from the mPFC of adult animals that had experienced maltreatment and used fluorescence-activated cell sorting to isolate cell types before performing bisulfite sequencing to estimate methylation of cytosine–guanine sites. Our data indicate that early-life stress induced methylation of DNA associated with Bdnf IV in a cell-type and sex-specific manner. Specifically, females that experienced early-life maltreatment exhibited greater neuronal cytosine–guanine methylation compared to controls, while no changes were detected in Bdnf methylation in males regardless of cell type. These changes localize the specificity of our previous findings to mPFC neurons and highlight the capacity of maltreatment to cause methylation changes that are likely to have functional consequences for neuronal function.

The current study examines the relation between distress tolerance, perceived stress, and internalizing symptoms across adolescence. Participants included 331 youth, ages 10 to 14 at the first wave of the study, assessed annually over 5 years. A latent growth curve approach was used to test three research questions, including whether perceived stress would increase across adolescence, whether distress tolerance (as measured by a behavioral task) would predict changes in perceived stress, and whether changes in perceived stress would mediate the relation between distress tolerance and internalizing symptoms. Results suggest that, consistent with previous findings, rates of perceived stress do increase across adolescence. Further, findings indicate that distress intolerance at baseline predicted increases in perceived stress, which in turn drove increases in internalizing symptoms. These findings point to the critical role of distress tolerance in bringing about changes in depression and anxiety symptoms and suggest support for utilizing a negative reinforcement framework to understand the emergence of internalizing symptomology.

Attachment theory and research have traditionally been subspecialties in infant social development. Recent work has extended the relevance of attachment theory and assessments well into childhood and has established firm ties to work with adults. Many of the same variables associated with the development of disruptive behavior problems also influence the development of attachment. In addition, recent data point to consistent relations between attachment status and disruptive behavior problems. This paper reviews attachment theory, summarizes mechanisms through which attachment might be related to disruptive behavior problems, and discusses the relevance of attachment theory to prevention and therapy. We emphasize the diversity of possible relations between attachment and disruptive behavior problems and the fact that incorporating attachment theory into research on disruptive behavior problems does not mean interpreting every disruptive behavior as attachment related or every attachment-related disruption as serving the same function.

Educational attainment and occupational status are key markers of success in adulthood. We expand upon previous research that focused primarily on the contributions of academic competence and family socioeconomic status (SES) by investigating the role of mental health in predicting adult SES. In a longitudinal study spanning 30 years, we used structural equation modeling to examine how parental mental health in early childhood and family SES, offspring academic competence, and offspring mental health in adolescence relate to occupational and educational attainment at age 30. Results were that adolescent academic competence predicted adult educational attainment, and that educational attainment then predicted occupational attainment. The pathways between academic competence and occupational attainment, family SES and educational attainment, and family SES and occupational attainment were not significant. In contrast, adolescent mental health not only predicted educational attainment, but was also directly related to adult occupational attainment. Finally, early maternal mental health was associated with offspring's adult socioeconomic attainment through its relations with adolescent academic competence and mental health. These results highlight the importance of mental health to adult socioeconomic attainment.

This study examined peer predictors of variation and growth in depressed mood among high-risk adolescents, using child and parent reports of monthly symptoms. One hundred seventy-six parents and their 10- to 14-year-old children separately took part in a series of up to nine monthly interviews. Multilevel growth models examined both time-varying peer predictors of parent and child reports of the child's depressive symptoms, controlling for age, gender, and treatment status. Deviant peer affiliation significantly predicted elevated depressive symptoms in the monthly child-report of depressed mood, especially for younger adolescents. Children's level of delinquency was significantly related to parent-reported depressive symptoms, and to child-reported symptoms in older adolescents only. As expected, depressed mood was higher for girls and more prevalent among older adolescents. The results suggest that peer processes may be linked in time to the development of depression, especially among high-risk adolescents.This project was supported by grants to the second author (T.J.D.) from the National Institute on Drug Abuse (DA 07031) and the National Institute of Mental Health (Development and Psychopathology Research Training Grant MH 20012), both at the National Institutes of Health. Thanks to Ann Simas for editing this manuscript.

Although the relation between child maltreatment and psychiatric impairment is well documented and preliminary evidence has linked child maltreatment with aberrant cortical connectivity of the left hemisphere, no investigations have attempted to examine these relations in the same study. Here, we examined the links among early adversity, brain connectivity, and functional outcomes. We collected resting regional EEG intra- and interhemispheric α-band (7.5–12.5 Hz) coherence and measures of general psychiatric impairment from a cohort of 38 adolescent females exposed to child maltreatment (M age = 14.47) and 24 adolescent females not exposed to child maltreatment (M age = 14.00). Maltreated youths exhibited more left hemisphere EEG coherence than the control youths, suggesting a suboptimal organization of cortical networks. Maltreated participants also showed reduced frontal (anterior) interhemispheric coherence. These differences in brain circuitry remained statistically significant even after controlling for group differences in pubertal status and socioeconomic status. Measures of functional brain connectivity were associated with several subtypes of abuse and neglect. It was important that atypical left hemisphere EEG coherence mediated the effects of child maltreatment on levels of psychiatric impairment. The findings are discussed in the context of models linking early adversity to brain function and psychopathology.