Behavioral genetic studies indicate that nongenetic factors play a role in the development of bipolar and major depressive disorders. The trait of neuroticism is common among individuals with major affective disorders. We hypothesized that high neuroticism among parents affects the family environment and parenting practices and thereby increases the risk of psychosocial problems among offspring. This hypothesis is tested in a sample of participants at high and low risk for major affective disorders, which contained parents with bipolar disorder (55), major depression (21), or no mental disorder (148) and their 146 children between 4 and 14 years of age. Parents with high neuroticism scores were characterized by low psychosocial functioning, poor parenting, more dependent stressful life events, and the use of more emotion-focused and less task-oriented coping skills. High neuroticism in parents was associated with internalizing and externalizing problems among the children, as assessed by parent and teacher ratings on the Child Behavior Checklist and clinician ratings. The results suggest that high neuroticism in parents with major affective disorders is associated with inadequate parenting practices and the creation of a stressful family environment, which are subsequently related to psychosocial problems among the offspring.This work was supported by a grant to the Research Team for the Study of the Development of Affective Disorders (Drs. S. Hodgins, A. Schwartzman, L. Serbin, O. Bernazzani, C. Laroche, W. R. Beardslee, G. A. Carlson, and R. Rende) from the Fonds de la Recherche en Santé du Québec and by grants from the combined program of the Conseil Québecois de la Recherche Sociale and Fonds de la Recherche en Santé du Québec (1994–1998) as awarded to S. Hodgins. M. A. Ellenbogen is supported by a postdoctoral fellowship from the Canadian Institutes of Health Research. The authors would like to thank members of the Research Team for the Study of the Development of Affective Disorders and anonymous reviewers for their helpful comments on these findings.

Many delinquent youth stop offending sometime in late adolescence or early adulthood. However, little is known about individual differences in desistance and which factors promote or inhibit desistance. In the current study, young males in the oldest sample of the Pittsburgh Youth Study were followed from ages 13 to 25. About one-third became persistent serious delinquents between ages 13 and 19. Out of that group, almost 40% desisted in serious offending between ages 20 and 25. Significantly more of the desisters, compared to the persisters in serious delinquency, had been employed or in school. Bivariate analyses demonstrated many predictors of desistance of serious delinquency in early adulthood in the domains of individual, family, and peer factors measured from early adolescence onward. Multiple regression analyses showed that the following promotive factors were associated with desistance: low physical punishment by parents in early adolescence and being employed or in school in early adulthood. The following risk factors were inversely associated with desistance during early adulthood: serious delinquency during late adolescence, hard drug use, gang membership, and positive perception of problem behavior in early adulthood. The article discusses the implications of promotive and risk factors for preventive interventions.This article was prepared under Grant 96-MU-FX-0012 from the Office of Juvenile Justice and Delinquency Prevention and Grant 050778 from the National Institute of Mental Health. The points of view in this document are those of the authors and do not necessarily represent the official position or policies of the US Department of Justice. We acknowledge Rebecca Stallings for assistance in preparing the data files. Our coauthor, Evelyn Wei, has unfortunately died in a car accident.

This article argues for the importance of focusing explicitly on the construct of boundary disturbances in families to understand the development of depressive, anxious, and attention-deficit/hyperactivity disorder (ADHD) symptoms in middle childhood. Grounded in family systems theory, this study examined traditional parent–child antecedents of childhood depression and anxiety (hostile, controlling, and disengaged interactions) in the context of the entire family as well as enmeshed patterns, whereby one parent drew in the child by turning to the child for caregiving or intimacy and excluded the spouse, and balanced patterns, whereby all family members expressed vulnerabilities and asserted their needs or desires. Mostly White, middle-class mothers, fathers, and children were observed at home interacting on a series of everyday tasks when the children were 24 months old, and mothers and teachers rated children's symptoms of anxiety, depression, somatic problems, and ADHD at age 7. Regression analyses revealed that, after controlling for maternal depression and the effects of other family patterns, enmeshed family patterns forecast children's depressive symptoms; controlling and disengaged interactions predicted anxious and depressive symptoms; and hostility forecast ADHD and somatic complaints. Intriguing gender differences emerged. As predicted, whereas boys who experienced enmeshed family patterns more often developed symptoms of ADHD, girls who experienced enmeshed family interactions later showed symptoms of depression.This research was supported by Grant SBR-9212990 from the National Science Foundation and Grant 3332 from the Hogg Foundation for Mental Health. The authors thank the families who participated in this study, as well as Lisa Steffeck who assisted with coding the data.

Using a short-term longitudinal design, internalizing and externalizing emotions were examined as risk factors for being victimized by peers in early childhood. Regulation, aggression, and withdrawal were also tested as mediators. We found that anger, mediated by aggression and regulation, positively predicted being victimized, although the way in which anger related to victimization risk varied for boys and girls and across time. These findings were robust, particularly for girls, attesting to the importance of externalizing variables as risk factors for young children's victimization. Support for internalizing variables as risk factors for being victimized was weak. The implications of the findings for developmental models connecting symptomatology and victimization are discussed.The authors thank all of the students, children, parents, and teachers who participated in this research. Richard A. Fabes and Nancy Eisenberg were funded in part by grants from the National Institute of Mental Health (R01 HH55052 and R01 MH60838) and a Research Scientist Award to Nancy Eisenberg (K05 M801321). Laura D. Hanish was funded by an Arizona State University Faculty Grant-in-Aid. An earlier draft of this paper was presented at the 108th Annual Convention of the American Psychological Association, August 2000, Washington, DC.

To examine the effects of early emotional neglect on children's affective development, we assessed children who had experienced institutionalized care prior to adoption into family environments. One task required children to identify photographs of facial expressions of emotion. A second task required children to match facial expressions to an emotional situation. Internationally adopted, postinstitutionalized children had difficulty identifying facial expressions of emotion. In addition, postinstitutionalized children had significant difficulty matching appropriate facial expressions to happy, sad, and fearful scenarios. However, postinstitutionalized children performed as well as comparison children when asked to identify and match angry facial expressions. These results are discussed in terms of the importance of emotional input early in life on later developmental organization.The authors thank Paul Ekman and Linda Camras for making their facial expression stimuli available to us. Dirk Wilker, Ziggy Bialzik, and Craig Rypstat provided invaluable assistance with computer programming and the computerized implementation of the tasks reported in this article. We also appreciate the assistance of Gabrielle Sowle, Marna Brown, Justin Martin, Susan Perlman, Kristi Johnson, Anne Kolan, Erin Eatough, and Sarah Pluck in the collection of these data. Linda Camras provided very helpful comments on an earlier version of this manuscript. These experiments would not be possible without the participation of many children and their families, for whose collaboration we are extremely appreciative. A preliminary version of these data were presented at the 2003 Biennial Meeting of the Society for Research in Child Development. This research was supported by grants from the National Institute of Mental Health to Seth Pollak (MH 68858 and MH 61285). Alison Wismer Fries was also supported by a National Institutes of Health Training Program in Emotion Research (MH 18931).

Theoretical models and empirical studies suggest that there are a number of distinct pathways of aggressive behavior development in childhood that place youth at risk for antisocial outcomes in adolescence and young adulthood. The prediction of later antisocial behavior based on these early pathways, although substantial, is not perfect. The goal of the present study was to identify factors that explain why some boys on a high-risk developmental trajectory in middle childhood do not experience an untoward outcome, and, conversely, why some boys progressing on a low-risk trajectory do become involved in later antisocial behavior. To that end, we explored a set of theoretically derived predictors measured at entrance to elementary and middle school and examined their utility in explaining discordant cases. First-grade reading achievement, race, and poverty status proved to be significant early predictors of discordance, whereas the significant middle-school predictors were parent monitoring, deviant peer affiliation, and neighborhood level of deviant behavior.This research was supported by grants from the National Institutes of Mental Health (RO1 MH42968 to Sheppard G. Kellam, PI, and T-32 MH18834 to Nick Ialongo, PI) and the Centers for Disease Control and Prevention (R49/CCR318627-03). We thank the Baltimore City Public Schools for their continuing collaborative efforts and the parents, children, teachers, principals, and school psychologists and social workers who participated.

Although neurocognitive impairments in theory of mind and in executive functions have both been hypothesized to play a causal role in autism, there has been little research investigating the explanatory power of these impairments with regard to autistic symptomatology. The present study examined the degree to which individual differences in theory of mind and executive functions could explain variations in the severity of autism symptoms. Participants included 31 verbal, school-aged children with autism who were administered a battery of tests assessing the understanding of mental states (knowledge and false belief) and executive control skills (working memory, combined working memory and inhibitory control, and planning) and who were behaviorally evaluated for autism severity in the three core symptom domains. Whereas theory of mind and executive control abilities explained the significant variance beyond that accounted for by language level in communication symptoms, neither explained the significant variance in reciprocal social interaction or repetitive behaviors symptoms. These findings are discussed in terms of a proposed distinction between higher level, cognitive–linguistic aspects of theory of mind and related executive control skills, and more fundamental social–perceptual processes involved in the apprehension of mental state information conveyed through eyes, faces, and voices, which may be more closely linked to autistic deficits in social reciprocity.This research was supported by grants from the National Institute on Child Health and Human Development (RO3 HD37898) to Robert Joseph and from the National Institute on Deafness and Other Communication Disorders (PO1 DC03610) to Helen Tager–Flusberg. In addition, this study was conducted as part of the NICHD/NIDCD Collaborative Programs of Excellence in Autism. We thank the following individuals for their assistance in collecting and preparing the data reported in this article: Susan Bacalman, Laura Becker, June Chu, Susan Folstein, Anne Gavin, Margaret Kjelgaard, Lauren McGrath, Echo Meyer, and Shelly Steele. We are especially grateful to the children and families who generously participated in this study.

This article examines the relationship between coparenting and family-level processes during preschool and peer relationship outcomes in middle childhood, and the hypothesis that children's ability to regulate emotion (as indexed by basal vagal tone and the ability to suppress vagal tone) may moderate this relationship. We predicted that high vagal tone and a greater ability to suppress vagal tone would buffer children from the effects of negative coparenting and family processes. Results indicated that hostile–withdrawn coparenting predicted higher levels of conflicted play and lower levels of positive peer conversation. Vagal suppression also moderated the relationship between hostile–withdrawn coparenting and peer conflict. For children who were unable to suppress vagal tone, hostile–withdrawn coparenting was associated with higher levels of peer conflict, while for children who were able to suppress vagal tone there was no relationship hostile–withdrawn coparenting and peer conflict. The relationship between hostile–withdrawn coparenting and positive peer conversation was also moderated by children's ability to suppress vagal tone. For children who were unable to suppress vagal tone, there was no relationship between hostile–withdrawn coparenting and positive peer conversation, while for those who were able to suppress vagal tone, hostile–withdrawn coparenting was associated with less positive peer conversation. Cohesive family-level processes also predicted positive conversation in play at age 9 after controlling for positive conversation at age 5; however, this relationship was not moderated by vagal suppression. Basal vagal tone also did not function as a moderator of relations between hostile–withdrawn coparenting and peer play. Results are discussed in terms of the effects of negative coparenting on children with different patterns of modulating physiological arousal.This research was supported by a research grant from the National Institute of Mental Health to the second author (1 R01 49141). The authors thank the families involved for their participation.

We examined the relations between emotionality, emotion processing, and aggression in 182 first- and second-grade children. Consistent with Tomkins' and Izard's theoretical predictions, emotionality correlated with emotion processing. In particular, the happiness component of emotionality correlated with emotion attribution accuracy and empathy, the anger component correlated with anger attribution bias and empathy, and the fear component correlated with fear attribution bias. Multiple emotion processing deficits—including emotion attribution accuracy, anger attribution bias, and self-report of empathy—placed children at risk for heightened levels of teacher-reported aggression. Mediational analyses revealed that an emotion processing risk index fit a model of significant partial mediation between happiness and aggression but not between anger and aggression. The results suggest the multifaceted manner in which children's emotion experiences may influence the development of aggressive tendencies.The authors thank the teachers, staff, parents, and students of the Smyrna, DE, school district for their enthusiastic participation in this project and the dedicated work of Fran Haskins and our many research assistants at the University of Delaware.

Genetic and environmental influences on symptoms of adult antisocial behavior (AAB) and alcohol dependence at ages 17, 20, and 24 were examined cross-sectionally and longitudinally in 188 monozygotic and 101 dizygotic male twin pairs. A moderate genetic influence on both AAB and alcohol dependence was found at each age, with a substantial proportion of this influence common to the two disorders, suggesting they share susceptibility genes. Biometrical models showed that continuity effects accounted for most of the stable variance in symptoms of both AAB and alcohol dependence, indicating that genetic and environmental effects associated with each of these disorders were similar at each age. Significant cross-lag effects (effects of alcohol dependence contributing to variance in AAB and vice versa) were observed at ages 20 and 24 for both disorders. The largest and theoretically most interesting of these effects indicated that one sixth of the genetic influence on AAB at age 20 was due to genetic effects associated with alcohol dependence at age 17. Thus, alcohol dependence symptoms at age 17 in particular had an effect on antisocial behavior symptoms at age 20, suggesting that alcohol involvement in adolescence may ensnare otherwise desisting youth in persistent antisocial behavior.The present study was supported in part by grants from the National Institute of Drug Abuse (DA 05147) and the National Institute on Alcohol Abuse and Alcoholism (AA09367). We are grateful to a number of individuals for their assistance in coding and entering data that were not previously available. Our special thanks are due to Irene Elkins, Linda Springer, Kari Melchert, and Kristen Abernethy for their gracious and timely help.

Power dynamics in the marital dyad and systemic elements of whole-family functioning (cohesion, subsystem boundary formations) were examined in relation to each other and also in relation to child adjustment in a multiethnic sample of families. Support was found for a mediational model, such that family functioning was found to mediate the relationship between marital power dynamics and children's internalizing and externalizing behavior. Some support also was found for ethnicity as a moderator of the association between systemic family processes and children's adjustment. Disturbances in family cohesion and subsystem boundaries were more strongly related to internalizing symptomatology for children in European American families compared to children in Hispanic American families.This research was funded by National Institute of Mental Health Grant R03 MH54631. We thank Jean–Philippe Laurenceau for his feedback on drafts of this manuscript and for statistical consultation. We also are very grateful to the participating families for the generous donation of their time and effort.

We investigated the expression and understanding of jealousy in 16 high-functioning children with autism and 17 typically developing children matched for IQ, chronological age, gender, and maternal education. We examined the expression of jealousy via children's behaviors, verbalizations, and affects demonstrated during two jealousy-provoking triadic scenarios (drawing and playing) enacted among the child in the experimental group (autism or typical), that child's main caregiver (mostly mothers), and a familiar peer or sibling. The two scenarios corresponded with the two types of jealousy described in past studies: social-comparison jealousy (drawing scenario) and social-relational jealousy (playing scenario). To tap children's understanding, we asked them to identify jealousy from a picture, to provide examples of times they felt jealous, and to offer suggestions for coping with jealousy. The main results revealed that children with autism expressed jealousy in situations similar to their typical age mates but manifested it in different behaviors. Moreover, children with autism revealed a less coherent understanding of the feeling. We discuss the meaning of the gap between demonstrating and understanding jealousy in light of the two central theoretical views conceptualizing the core emotional deficit in children with autism.The Internal Grants Program of Bar-Ilan University supported this research. The author extends special thanks to the children and families who were willing to take part in this study and expresses her appreciation to Dee B. Ankonina for her editorial contribution and to Dov Har-Even for his statistical assistance. The author would also like to thank Galit Halevy–Tendler for her inspiring remarks, Cory Shulman for her help in data collection, and the four anonymous reviewers for their thought-provoking comments.

Patterns of lower autonomic nervous system (ANS) and hypothalamic–pituitary–adrenal (HPA) axis activity have been found in children with oppositional defiant disorder (ODD). The aim of the present study was to investigate whether children with attention-deficit/hyperactivity disorder (ADHD) differ from ODD children with (OD/AD) or without comorbid ADHD in ANS and HPA axis activity under baseline and stressful conditions. The effects of stress on cortisol, heart rate (HR), and skin conductance level (SCL) were studied in 95 children (26 normal control [NC] children and 69 child psychiatric patients referred for externalizing behavior problems [15 ODD, 31 OD/AD, and 23 ADHD]). No baseline differences were found in cortisol between the four groups. However, the ODD and OD/AD groups showed a significantly weaker cortisol response to stress compared to the ADHD and NC groups; the ADHD group had a similar cortisol response as the NC group. Within the ODD group this pattern of low cortisol responsivity was most clearly present in the more severely affected inpatients. With respect to HR, the ODD group had a significantly lower HR during baseline and stressful conditions. The higher HR levels in the OD/AD and ADHD groups were likely to be caused by methylphenidate. The externalizing groups had significantly lower SCL levels, and no differences were found between these groups. It was concluded that differences in cortisol responsivity during stress exposure are important in distinguishing within a group of children with externalizing behavior between those with ODD and ADHD.

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.

The prevalence, recurrence, and incidence of depression in adolescence and young adulthood are substantial for both males and females. In this study, we examined social setting variables that influence depression in males and females from adolescence to young adulthood. Rather than focusing on single ecological factors, we examined multiple settings including families, peers, and neighborhoods using longitudinal data from 372 families living in a large eastern urban area. We found that variables related to depression differed for males and females depending on the developmental period being examined. Family and peer variables in adolescence were significantly related to change in depression during the transition to adulthood for males, whereas family and neighborhood variables were marginally significant for females. Family and neighborhood variables in adulthood were significantly related to change in depression for females, and peer variables were significant for both males and females. Overall, contextual variables in adolescence had a more significant impact on change in depression for males, whereas contemporary variables in young adulthood had a more significant impact on change in depression for females.The authors acknowledge the assistance of Frank Furstenberg for the collection of this data with funds from the John D. and Catherine T. MacArthur Foundation's Network on Successful Adolescence in High Risk Environments. The authors also acknowledge partial support for the writing of this article from a National Institute of Mental Health Behavioral Science Research Center Grant awarded to the second author.

Parent–child conflict and perceived attachments to parents were examined as predictors, mediators, and moderators in the marital conflict–child adjustment connection in a sample of older children and young adolescents. After controlling for marital conflict, parent–child conflict predicted additional unique variance mainly for children's externalizing problems, and attachments to parents accounted for unique variance in children's externalizing and internalizing problems. Moderation effects illustrated that a higher level of parent–child conflict was a vulnerability factor, whereas a secure attachment was a protective factor, for behavior problems associated with marital conflict. Mediation effects were also evident and supported the proposition that parent–child conflict and attachment to parents mostly are partial mediators of effects in the marital conflict–child outcomes link. The findings illustrate the aggregation, potentiation, and amelioration of risk for adjustment problems associated with marital conflict, and highlight the importance of assessing multiple systems within the family.This research was supported by NIAAA Grant R29 AA10591. We would like to thank the research participants for their time and effort, and Stephanie Whitson and Karen Martin for their assistance with data collection.

This study draws on the family systems concepts of triangulation and wholism to investigate how interparental conflict may affect adolescents' psychological adjustment. An ethnically and socioeconomically diverse sample (N = 388) of 14- to 18-year-olds completed measures of interparental conflict, family relationships, internalizing problems, and externalizing problems. We found that triangulation into parental disagreements mediated the association between parental conflict and both internalizing and externalizing problems. Adolescents exposed to more frequent, intense, and poorly resolved conflict were more likely to feel triangulated, but this association was moderated by the nature of the alliances they had with their parents. Specifically, at low levels of interparental conflict, adolescents who had substantially stronger alliances with one parent than the other reported greater triangulation than those with more balanced alliances. At high levels of conflict, these groups reported similar degrees of triangulation. We also found that supportive parent–child relationships reduced adolescents' appraisals of threat and self-blame for interparental conflict, while more empathic relationships with siblings increased these appraisals. Finally, close relationships with fathers acted as a protective factor that reduced symptoms of maladjustment.

The present study takes a developmental approach to subgrouping and examines the trajectories of substance use from early adolescence through young adulthood among a community sample of 481 individuals. The patterns of use were examined, subgroups were identified separately for men and women and for alcohol and marijuana, and psychosocial predictors and psychopathology outcomes that differentiated the groups were identified. The results revealed three substantially overlapping subgroups for both alcohol and marijuana: early onset, late onset, and nonuser. Although the general patterns of which dependent variables were related to group were similar for alcohol and marijuana, a closer examination revealed important subgroup differences. For alcohol use, the early-onset group was more dysfunctional in terms of predictors and outcomes whereas the late-onset and nonuser groups were better adjusted. In contrast, for marijuana, the early- and late-onset groups were both more dysfunctional than the nonuser group. In a final analysis, we examined the predictive utility of our developmental approach to subgrouping compared to a traditional, static approach.This research was supported by NIH National Research Service Award DA07304 from NIDA, Grant DA05312-10 from NIDA, NIH General Clinical Research Center Grant M01 RR026202, and a University of Kentucky Research Challenge Trust Fund Fellowship awarded to Kate Flory.

The transition to young adulthood is both a time when risky health behaviors such as substance misuse peak and a time of opportunity for growth and development through the acquisition of adult roles. In this transition, coping styles include responses to the stressors and opportunities associated with the emergence of adulthood. The extent to which such coping styles are skillfully employed in part determines adjustment into adulthood. The current study used a high-risk, longitudinal design to examine the development of coping styles over adolescence, continuity in these coping styles from adolescence to adulthood, the impact of coping on adult stress and substance misuse, the ability of coping to buffer effects of stress on substance use, and differences in coping between at-risk youth (i.e., children of alcoholics [COAs]) and their peers. A sample of 340 adolescents completed four assessments over ages 11–23. We used latent trajectory models to examine interindividual and intraindividual change in coping over time. Evidence for both change and continuity in the development of coping from adolescence to adulthood was found, although adolescent coping had limited impact on stress and substance use in adulthood. Support was also found for complex stress-buffering and stress-exacerbating effects of coping on the relations between major life events and adult drug use and between stress associated with the new roles of adulthood and heavy alcohol use. Implications of these findings for development and adjustment in the transition to adulthood are discussed.

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.