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.

We observed gendered coping strategies and conflict resolution outcomes used by adolescents and parents during a conflict discussion task to evaluate associations with current and later adolescent psychopathology. We studied 137 middle- to upper-middle-class, predominantly Caucasian families of adolescents (aged 11–16 years, 65 males) who represented a range of psychological functioning, including normative, subclinical, and clinical levels of problems. Adolescent coping strategies played key roles both in the extent to which parent–adolescent dyads resolved conflict and in the trajectory of psychopathology symptom severity over a 2-year period. Gender-prototypic adaptive coping strategies were observed in parents but not youth, (i.e., more problem solving by fathers than mothers and more regulated emotion-focused coping by mothers than fathers). Youth–mother dyads more often achieved full resolution of conflict than youth–father dyads. There were generally not bidirectional effects among youth and parents’ coping across the discussion except boys’ initial use of angry/hostile coping predicted fathers’ angry/hostile coping. The child was more influential than the parent on conflict resolution. This extended to exacerbation/alleviation of psychopathology over 2 years: higher conflict resolution mediated the association of adolescents’ use of problem-focused coping with decreases in symptom severity over time. Lower conflict resolution mediated the association of adolescents’ use of angry/hostile emotion coping with increases in symptom severity over time. Implications of findings are considered within a broadened context of the nature of coping and conflict resolution in youth–parent interactions, as well as on how these processes impact youth well-being and dysfunction over time.

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.

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.

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.

Improving parenting, child attachment, and externalizing behaviors: Meta-analysis of the first 25 randomized controlled trials on the effects of Video-feedback Intervention to promote Positive Parenting and Sensitive Discipline (VIPP-SD). VIPP-SD combines support of parental sensitive responsiveness with coaching parents in sensitive limit setting. Here, we present meta-analyses of 25 RCTs conducted with more than 2,000 parents and caregivers. Parents or children had various risks. We examined its effectiveness in promoting parental cognitions and behavior regarding sensitive parenting and limit setting, in promoting secure child–parent attachment, and reducing externalizing child behavior. Web of Science, MEDLINE, PubMed, and recent reviews were searched for relevant trials (until May 10, 2021). Multilevel meta-analysis with META, METAFOR, and DMETAR in R took account of the 3-level structure of the datasets (studies, participants, measures). The meta-analyses showed substantial combined effect sizes for parenting behavior (r = .18) and attitudes (r = .16), and for child attachment security (r = .23), but not for child externalizing behavior (r = .07). In the subset of studies examining effects on both parenting and attachment, the association between effect sizes for parenting and for attachment amounted to r = .48. We consider the way in which VIPP-SD uses video-feedback an active intervention component. Whether VIPP-SD indeed stimulates secure attachment through enhanced positive parenting remains an outstanding question for further experimental study and individual participant data meta-analysis.

A significant discrepancy between intelligence and daily adaptive functioning, or adaptive disability (AD), has been previously found to be a associated with significant psychological morbidity in preschool children with disruptive behavior (DB). The utility of AD as a predictor of later developmental risks was examined in a 3-year longitudinal study of normal ( N= 43) and DB preschool children. The DB children were grouped into those with AD (DB+AD; N = 28) and those without AD (DB-only; N = 98). All children were followed with annual evaluations to the end of second grade. Both DB groups demonstrated substantial and pervasive psychological and educational morbidity at 3-year follow-up. In comparison to DB-only children, DB+AD children had more symptoms of attention-deficit hyperactivity disorder (ADHD) and conduct disorder (CD), more severe and pervasive behavior problems at home, more parent-rated externalizing and internalizing, and lower academic competence and more behavioral problems at school. Parents of DB+AD children also reported greater parenting stress than did parents in the other groups. A significant contribution of AD to adverse outcomes in the DB group remained on some measures even after controlling for initial severity of DB. AD also contributed significantly to CD symptoms at follow-up after controlling for initial DB severity and initial CD symptoms. The results corroborate and extend earlier findings of the utility of AD as a risk indicator above severity of DB alone. They also imply that AD in the context of normal intellectual development may arise from both the deficient self-regulation associated with ADHD and from disrupted parenting, with exposure to kindergarten moderating these adverse effects.

This study was focused on contextual variations in the parenting dimensions salient for preadolescent adjustment. The sample consisted of 614 sixth graders from two communities, one low and the other high income. Parenting dimensions included those known to be significant in each socioeconomic context: isolation from parents (emotional and physical), and parents' emphasis on achievements (overall expectations and emphasis on integrity over success). Adjustment outcomes included subjective well-being as well as school competence. Contradicting stereotypes, results showed that on average, very affluent children can perceive their parents as emotionally and physically unavailable to the same degree that youth in serious poverty do. The ramifications for adjustment also seem to be largely similar: Closeness to parents was beneficial for all, just as criticism was deleterious. Even after considering the quality of parent–child relationships, parents' physical absence (e.g., at dinner) connoted vulnerability for distress and for poor school performance in both groups. The connotations of a few parenting dimensions varied by context and gender; these variations are discussed as are overall implications for future research and practice.Preparation of the manuscript was funded in part by grants from the National Institutes of Health (RO1-DA10726, RO1-DA11498, R01-DA14385), the William T. Grant Foundation, and the Spencer Foundation.

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.

Extremes in fearful temperament have long been associated with later psychopathology and risk pathways. Whereas fearful children are inhibited and anxious and avoid novel events, fearless individuals are disinhibited and more likely to engage in aggressive behavior. However, very few studies have examined fear in infants from a multimethod and prospective longitudinal perspective. This study had the following objectives: to examine behavioral, maternal reported, and physiological indices of fearful temperament in infancy, together with their relations and stability over time; and to establish whether early indices of fear predict fear later in toddlerhood. We also examined the association between behavioral and physiological measures of fear and guilt and whether fear in infancy predicts guilt in toddlers. Finally, we investigated infant risk factors for later psychopathology. We recorded skin conductance level (SCL) and heart rate (HR) and observed children's responses during a Laboratory Temperament Assessment Battery fear paradigm across the first 3 years of life and during a guilt induction procedure at age 3 (N = 70). The results indicate that different measures of infant fear were associated across time. Observed fearlessness in infancy predicted observed fearlessness and low levels of SCL arousal to fear and guilt in toddlers. Low levels of HR and SCL to fear in infancy predicted low levels of physiological arousal to the same situation and to guilt 2 years later. Fear and guilt were significantly associated across measures. Finally, toddlers with clinically significant internalizing problems at age 3 were already notably more fearful in Year 1 as reflected by their significantly higher HR levels. The results indicated that assessments of children in infancy are predictive of how these children react 2 years later and therefore lend support to the idea that the emotional thermostat is set in the first 3 years of life. They also showed, for the first time, that infant fear is a predictor of guilt, which is an emotion that develops later. The implications of these findings for our understanding of developmental psychopathology are discussed.

We examine the hypothesis that children's exposure to ethnic–political conflict and violence over the course of a year stimulates their increased aggression toward their own in-group peers in subsequent years. In addition, we examine what social cognitive and emotional processes mediate these effects and how these effects are moderated by gender, age, and ethnic group. To accomplish these aims, we collected three waves of data from 901 Israeli and 600 Palestinian youths (three age cohorts: 8, 11, and 14 years old) and their parents at 1-year intervals. Exposure to ethnic–political violence was correlated with aggression at in-group peers among all age cohorts. Using a cross-lagged structural equation model from Year 1 to Year 3, we found that the relation between exposure and aggression is more plausibly due to exposure to ethnic–political violence stimulating later aggression at peers than vice versa, and this effect was not moderated significantly by gender, age cohort, or ethnic group. Using three-wave structural equation models, we then showed that this effect was significantly mediated by changes in normative beliefs about aggression, aggressive script rehearsal, and emotional distress produced by the exposure. Again the best fitting model did not allow for moderation by gender, age cohort, or ethnic group. The findings are consistent with recent theorizing that exposure to violence leads to changes both in emotional processes promoting aggression and in the acquisition through observational learning of social cognitions promoting aggression.

Autism is a developmental disorder with variable severity, occurring at all levels of cognitive ability and having a number of slightly different clinical presentations. It is associated with neuropsychological deficits that occur in other conditions also, but its pattern may be specific to autism. Genetic and environmental early insults to brain development are etiological determinants of the disorder. Brain circuitries important for social, communicative, and integrational purposes have been suggested to be dysfunctional in autism. There could be at least two different pathways to autism, one connected with primary temporofrontal dysfunction (and late prenatal–early postnatal origins) and another linked to primary brain-stem dysfunction (and early prenatal origins). Further study of neurodevelopmental and neuropsychological processes in autism will help elucidate not only the pathological mechanisms involved in the specific syndromes but also the underpinnings of normal brain development.

The hypothesis that prenatal masculinization of the brain increases risk of tic disorders in postnatal life was tested by measuring gender and gender role behavior in 89 children and adults with a clinical diagnosis of Tourette syndrome or obsessive compulsive disorder and 67 healthy, unaffected children and adults. Consistent with this hypothesis, a tic disorder in females was associated with more gender dysphoria, increased masculine play preferences, and a more typically “masculine” pattern of performance on two sex-typed spatial tasks. Males with tic disorders reported increased masculine play preferences, and the strength of these preferences was positively associated with the severity of tic symptoms. In addition, unlike their female counterparts, males with tic disorders showed a relative impairment in mental rotation ability. These behavioral profiles are consistent with those of children who have verifiable elevations in prenatal androgen levels. These findings therefore support the hypothesis that an altered androgen-dependent process of sexual differentiation during prenatal life may contribute to the development of tic-related disorders.This work was supported by National Institutes of Health Grants MH01232 (B. P.) and MH59139 (B. P.) and the Suzanne Crosby Murphy endowment in Pediatric Neuropsychiatry, College of Physicians and Surgeons, Columbia University. The authors thank Amy Basile and Shibani Mukerji for their valuable assistance with behavioral testing.

The recurrent affective disorders are discussed from the perspective of accumulating inherited and experiential effects on gene expression. Stress and episodes of affective illness are viewed as leaving biochemical and microstructural residues in the central nervous system (CNS) in relation to their patterning, severity, and recurrence. Comorbid factors such as substance abuse and developmental disturbances may also interact with these illness-related variables. In addition to the primary pathological processes, secondary adaptive changes can also be induced, which, in concert with pharmacological interventions, may be sufficient to counter episode occurrences and illness progression. We postulate that the balance of primary pathological and secondary adaptive changes at multiple levels of CNS regulation accounts for recurrence and cyclicity in the affective disorders. The importance of early, effective, long-term interventions in the recurrent affective disorders and the therapeutic potential of several new treatment modalities including repeated transcranial magnetic stimulation (rTMS) are discussed.

In the present investigation, we examined the developmental viability of the externalizing behavior construct spanning the period from 8 to 24 months of age. A sample of 274 psychologically aggressive couples was recruited from hospital maternity wards and followed from childbirth through 24 months of age. Mothers and fathers completed questionnaire measures of infant physical aggression, defiance, activity level, and distress to limitations at 8, 15, and 24 months. The developmental viability of externalizing behavior at each age studied was suggested by several results. Physical aggression, defiance, activity level, and distress to limitations reflected the operation of a single underlying externalizing behavior factor. In some cases, these individual facets of externalizing behavior became more strongly associated with one another over time. The externalizing construct exhibited remarkable longitudinal stability, with the stability of physical aggression and defiance increasing with age. The externalizing behavior construct was concurrently and prospectively associated with several factors in its nomological network (e.g., interparental conflict and poor parental bond with the infant). Our findings suggest that externalizing behaviors coalesce into a psychologically meaningful construct by 8 months of infant life. Researchers who seek to chart the emergence of the externalizing behavior construct may now need to look to earlier months.

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.

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.

Children who are victims of interpersonal violence have a markedly elevated risk of engaging in aggressive behavior and perpetrating violence in adolescence and adulthood. Although alterations in social information processing have long been understood as a core mechanism underlying the link between violence exposure and externalizing behavior, scant research has examined more basic social cognition abilities that might underlie this association. To that end, this study examined the associations of interpersonal violence exposure with cognitive and affective theory of mind (ToM), core social-cognitive processes that underlie many aspects of social information processing. In addition, we evaluated whether difficulties with ToM were associated with externalizing psychopathology. Data were collected in a community-based sample of 246 children and adolescents aged 8–16 who had a high concentration of exposure to interpersonal violence. Violence exposure was associated with lower accuracy during cognitive and affective ToM, and the associations persisted after adjusting for co-occurring forms of adversity characterized by deprivation, including poverty and emotional neglect. Poor ToM performance, in turn, was associated with externalizing behaviors. These findings shed light on novel pathways that increase risk for aggression in children who have experienced violence.