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.

Drawing on a two-wave, multimethod, multi-informant design, this study provides the first test of a process model of spillover specifying why and how disruptions in the coparenting relationship influence the parent–adolescent attachment relationship. One hundred ninety-four families with an adolescent aged 12–14 (M age = 12.4) were followed for 1 year. Mothers and adolescents participated in two experimental tasks designed to elicit behavioral expressions of parent and adolescent functioning within the attachment relationship. Using a novel observational approach, maternal safe haven, secure base, and harshness (i.e., hostility and control) were compared as potential unique mediators of the association between conflict in the coparenting relationship and adolescent problems. Path models indicated that, although coparenting conflicts were broadly associated with maternal parenting difficulties, only secure base explained the link to adolescent adjustment. Adding further specificity to the process model, maternal secure base support was uniquely associated with adolescent adjustment through deficits in adolescents' secure exploration. Results support the hypothesis that coparenting disagreements undermine adolescent adjustment in multiple domains specifically by disrupting mothers' ability to provide a caregiving environment that supports adolescent exploration during a developmental period in which developing autonomy is a crucial stage-salient task.

Consistent evidence shows both genetic and stress-related risks on child and adolescent anxiety, yet few studies have considered the degree to which genetic effects are moderated by stress (gene–environment interaction). We used longitudinal data from both a child and adolescent sample of twins to examine three novel issues on the presence of gene–environment interaction on anxiety symptoms. First, we assessed moderation of genetic risks on anxiety symptoms by negative life events in each age group. Second, by distinguishing between “stable” and “age-specific” genetic factors, we explored the continuity of gene–environment interaction across time and/or its emergence at specific ages. Third, we compared the presence of gene–environment interaction across different symptom types (general, panic, social, and separation). Genetic effects on separation anxiety symptoms in childhood (mean age = 8 years, 6 months) and panic anxiety symptoms in adolescence (mean age = 15 years) increased across independent negative life events. Shared environmental effects on separation anxiety symptoms and nonshared environmental effects on general anxiety symptoms in adolescence were also moderated by negative life events. We interpret these preliminary findings tentatively in the context of gene–environment interaction on anxiety in general, and on early separation and later panic anxiety in particular.

The papers in this special issue attest to the theoretical and empirical advances that have been made in understanding the epidemiology, subtypes, etiology, neuropsychology, psychobiology, course, consequences, prevention, and treatment of conduct disorder (CD) (see also Kazdin, 1987; Loeber, 1990; Loeber & Stouthamer-Loeber, 1986; Moffitt, 1990; Patterson, 1982; Robins, 1991; White, Moffitt, Earls, Robins, & Silva, 1990). A number of theoretical conceptualizations have been forwarded in an attempt to comprehend this complex form of disorder in children. Such divergence in thinking indicates that the topic of CD has evolved into an active and significant domain of inquiry. To date, however, there has been no unifying theoretical framework for bringing conceptual clarity to the diverse perspectives represented in the study of conduct disorder. Although existing work within particular disciplines and subdisciplines has provided substantial contributions to our understanding of CD, these accounts typically have not considered the broader matrix of complex and evolving biological, cognitive, socioemotional, representational, and social-cognitive capacities of the developing child. As a consequence, disparate theoretical formulations are often too narrow in focus to address the range of processes and mechanisms that will be necessary to explain adequately how and why manifestations of CD emerge, change overtime and are influenced by children's developmental levels.

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.

The impact of socioeconomic status (SES) and genetic polymorphisms on individual differences for externalized behaviors have often been investigated separately in studies of children and adults. In a general population sample of 607 Italian preadolescents, we examined the independent and joint effects of SES and the dopamine receptor D4 (DRD4) and serotonin transporter linked promoter region (5-HTTLPR) polymorphisms upon rule-breaking and aggressive behaviors measured with the Child Behavior CheckList/6–18. We found evidence, which was based on both one locus and two-loci genotype analyses, that low SES and DRD4 long and 5-HTTLPR long alleles, both alone and in interaction, are associated with higher aggressive behavior scores. The effects were similar but more modest and limited to one locus genotype analyses for rule-breaking behavior. Consistent with studies that showed the effects of societal moderators on the heritability of externalized behaviors across different segments of the population, we suggest that diminished social constraints associated with low parental SES may act as enhancers of the genetic influence of specific DRD4 and 5-HTTLPR alleles over aggressive behaviors in preadolescence.

The present study examined the effect of various dimensions of child maltreatment (i.e., developmental timing of maltreatment, number of maltreatment subtypes, and chronicity of maltreatment) on methylation of the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), and investigated the associations between NR3C1 methylation and child outcomes. Participants included 534 children who attended a research summer camp program for school-aged maltreated (53.4%) and nonmaltreated (46.6%) children from low socioeconomic backgrounds. Results show that children with early onset maltreatment evidence significant hypermethylation compared to nonmaltreated children. Moreover, more maltreatment subtypes experienced and more chronic maltreatment are both related to greater NR3C1 hypermethylation. Findings also indicate that hypermethylation of NR3C1 is linked with a number of negative child outcomes including greater emotional lability–negativity, higher levels of ego undercontrol, more externalizing behavior, and greater depressive symptoms. Together, results highlight the role of methylation of NR3C1 in the effects of child maltreatment on the development of emotion dysregulation and psychopathology.

The role of environmental adversity in the development of high callous–unemotional (CU) traits in children is controversial. Evidence speaks to the traits being largely independent of adversity; however, recent data shows that those with high CU traits and high adversity and/or high anxiety might differ in important ways from those with no such history. We tested this using emotion recognition (ER) skills. We tested whether maltreatment history and anxiety levels moderated the relationship between level of CU traits and ER skills in N = 364 children with behavioral problems who were 3 to 16 years old. As hypothesised, in the full sample, the relationship between CU traits and ER differed according to maltreatment history, such that CU traits were associated with poorer recognition for those with zero or negligible history of maltreatment. This moderation of the CU-ER relationship by maltreatment was inconsistent across subgroups, however, and for the cohort utilizing youth self-report of maltreatment, high CU traits were associated with poor ER in those with lower anxiety levels. Maltreatment history and/or anxiety levels can identify different emotional impairments associated with high CU traits, and the impairments might be characteristic of “primary” high CU traits defined as occurring independently of maltreatment and/or high anxiety.

Childhood maltreatment is associated with lasting changes in neuroendocrine regulation, alterations in brain structure and function, and symptoms of “limbic irritability.” Limbic irritability symptoms include somatic, sensory, and behavioral phenomena and may stem from increased excitatory neurotransmission following maltreatment. We tested the hypotheses that child maltreatment is indirectly associated with depressive and dissociative symptomatology via indicators of limbic irritability and that variation within the FK506 binding protein 5 gene (FKBP5), a gene involved in glucorticoid receptor functioning, moderates these effects. The sample consisted of high-risk, low-income women (N = 236) living in an inner-city environment. Child maltreatment, limbic irritability, and symptoms of depression and dissociation were measured cross-sectionally using self-report assessments. Haplotype analyses were conducted across four FKBP5 single nucleotide polymorphisms: rs3800373, rs9296158, rs1360870, and rs9470080. Path analysis using bootstrapping procedures was performed to test hypotheses regarding indirect and conditional indirect effects. We found significant indirect effects of maltreatment on depression (β = 0.088, p < .01) and dissociation (β = 0.105, p < .01) via limbic irritability. In addition, variation within FKBP5 moderated these significant indirect effects. For individuals with one to two copies of the CATT haplotype, the indirect effects of maltreatment on depression (β = 0.137, p < .01) and dissociation (β = 0.132, p < .01) via limbic irritability were significant, whereas the indirect paths were not significant for individuals with no copies of this haplotype (depression: β = 0.037, p > .05; dissociation: β = 0.002, p > .05). These results add to the growing evidence that child maltreatment may lead to symptoms of internalizing psychopathology through its impact on the limbic system. In addition, this study revealed a potential role of FKBP5 gene variants in contributing to risk for limbic system dysfunction.

Forty adults with serious psychopathological disorders were administered the Adult Attachment Interview (AAI). Attachment strategies were assessed using Kobak's (1989) Q-sort method, which yields scores along the two dimensions of security/anxiety and repression/preoccupation. Expressed emotion was rated for a close family member based on the Five-Minute Speech Sample (FMSS). In addition, premorbid competence was assessed, and subjects completed a psychiatric symptom inventory. Subjects who used more extreme secondary attachment strategies (whether preoccupied or repressing) were more likely to have family members who were overinvolving. Symptom inventories revealed greater symptom reporting by individuals who relied more on preoccupied than on repressing strategies and by individuals who were in high expressed emotion families. Higher levels of premorbid competence were associated with more secure attachment strategies. These findings are consistent with a transactional model of relationships whereby the attachment strategies of these adults affect the involvement of their family members, which in turn further perpetuate behaviors associated with their attachment strategies.

Expressed emotion was examined in families of toddlers (N = 101) whose mothers had experienced major depressive disorder occurring since the child's birth, and contrasted with expressed emotion in demographically comparable families (N = 54) with no history of parental mental disorder to elucidate family systems processes as contributors to child functioning. Both mothers and fathers provided Five-Minute Speech Samples on their child, their spouse, and themselves, and completed measures of marital adjustment, trait affect, relationship quality with their own parents in childhood, and child behavior problems. Maternal-expressed emotion criticism regarding child, self, and spouse was higher in the families with depressed mothers; paternal criticism regarding self and spouse also was higher in the depressed families. Mothers and fathers in the depressed group also differed on relational/affective features, exhibiting lower marital satisfaction, higher trait negative affect, and more negative childhood relationship representations, relative to the nondepressed group, and mothers reported more child behavior problems. Mediational models were evaluated separately for the different targets of maternal and paternal criticism and child behavior problems, and findings supported both individual parent and spouse contributions as mediators of the relation between depression group status and expressed criticism and child behavior problems. The findings are discussed in terms of the multiple levels of family system influence on negativity in the emotional environment of toddlers of depressed mothers, developmental risk, and the need for family-level interventions.Completion of this work was supported by grant funding from the National Institute of Mental Health (R01MH45027) and the Spunk Fund, Inc. We thank Traci McCabe for her diligent coding of the Five Minute Speech Samples.

In a sample of 18-, 30-, and 42-month-olds, the relations among parenting, effortful control (EC), and maladjustment were examined. Parenting was assessed with mothers' reports and observations; EC was measured with mothers' and caregivers' reports, as well as a behavioral task; and externalizing and internalizing symptoms were assessed with parents' and caregivers' reports. Although 18-month unsupportive (vs. supportive) parenting negatively predicted EC at 30 months, when the stability of these variables was taken into account, there was no evidence of additional potentially causal relations between these two constructs. Although EC was negatively related to both internalizing and externalizing problems within all three ages as well as across 1 year, EC did not predict maladjustment once the stability of the constructs and within time covariation between the constructs were taken into account. In addition, externalizing problems at 30 months negatively predicted EC at 42 months, and internalizing problems at 30 months positively predicted EC at 42 months, but only when the effects of externalizing on EC were controlled. The findings are discussed in terms of the reasons for the lack of causal relations over time.

Early life stress (ELS) is a significant risk factor for the emergence of internalizing problems in adolescence. Beginning in adolescence, females are twice as likely as males to experience internalizing disorders. The present study was designed to examine sex differences in the association between ELS and internalizing problems in early pubertal adolescents, and whether and how corticolimbic function and connectivity may underlie these associations. Fifty-nine early pubertal males and 78 early pubertal females, ages 9–13 years (all Tanner Stage 3 or below) underwent functional magnetic resonance imaging as they performed an emotion label task that robustly interrogates corticolimbic function. Participants were also interviewed about their experience of ELS. Females exhibited a positive association between ELS and internalizing problems, whereas males exhibited no such association. Whole-brain and amygdala region of interest analyses indicated that whereas females exhibited a positive association between ELS and the ventrolateral prefrontal cortex during implicit emotion regulation, males showed no such association. Activation in these regions was positively associated with internalizing problems in females but not males; however, activation in these regions did not mediate the association between ELS and internalizing problems. Finally, both boys and girls exhibited an association between ELS and increased negative connectivity between the right ventrolateral prefrontal cortex and bilateral amygdala. Using a carefully characterized sample of early pubertal adolescents, the current study highlights important sex differences in the development of corticolimbic circuitry during a critical period of brain development. These sex differences may play a significant role in subsequent risk for internalizing problems.

The relation among family relationships was explored for (a) couple pairings and (b) parent-child dyads. In S3 maltreating and adequate families, mothers' and male partners' quality of attachment (drawn from interviews) was compared with each other and with child quality of attachment (drawn from the Strange Situation). The notion of internal representational models, drawn from attachment theory, provided the basis for seeking continuity, that is, matches and meshes between partners and coherence from parent to child. Both concordance and discordance were found; in particular, a hypothesis of meshed adult relationships and parent-child transformations was supported. The conditions leading to meshed partnerships and transformed parent-to-child patterns require further study. In addition, the results suggest the need for greater incorporation of regulation of affect in assessment procedures, greater theory development, and precision in validation and application of assessment procedures. Finally, this study highlights the advantages of using atypical samples to explore aspects of normative development that are obscured in normative samples.

The present research examined how family psychosocial risk may be associated with emotional availability (EA) across age and time in two longitudinal, intergenerational studies with high-risk, disadvantaged mother–child dyads. Study 1 examined dyads during preschool and middle childhood. Study 2 examined a different sample of dyads, tested intensively at five time points (6, 12, and 18 months; preschool; and school age). Across studies, maternal childhood histories of aggression and social withdrawal predicted negative EA (higher levels of maternal hostility) during mother–child interactions at preschool age. In Study 1, mothers with higher levels of social withdrawal during childhood had preschoolers who were less appropriately responsive to and involving of their mothers during interactions. In Study 2, higher levels of observed appropriate maternal structuring predicted child responsiveness while observed maternal sensitivity (and structuring) predicted observed child involvement. More maternal social support and better home environment combined with lower stress predicted better mother–child relationship quality. Findings contribute to the burgeoning literature on EA by focusing on a high-risk community sample across time and generations. Results are interpreted in light of the developmental psychopathology framework, and have implications for a broader understanding of how EA is related to parental history and personal characteristics, as well as ongoing family and environmental context.

According to data from the 1997 NICHD Study of Child Care, center-based child care can have deleterious effects on children's social–emotional development. We hypothesized that training child care professionals to develop positive relationships with children in their care would improve the quality of center-based child care. Thirty-three professional caregiver–child pairs participated in the intervention group and 24 professional caregiver–child pairs were assigned to a care as usual comparison group. The intervention consisted of an informational and a practice component with an emotional availability (EA) coach. The infants and toddlers (ages 11 to 23 months) in the classrooms were enrolled in the project only if they spent at least 20 hr per week in center-based care. The measures included were (a) the EA Scales, (b) the Attachment Q-Sort, and (c) the Classroom Interaction Scale. The intervention group professional caregiver–child relationships showed improvements on the EA Scales, Attachment Q-Sort, and the Classroom Interaction Scale from pre- to posttest, compared to the comparison group, who showed some decrements over a comparable period of time.

Executive tasks typically contain a prepotent lure. In addition, they require individuals either to (a) follow arbitrary procedures or (b) update their model of the physical world. Recent research suggests that children with autism may be challenged only by executive tasks of the former kind (containing arbitrary rules). We asked whether this continues to be true when there is no prepotent lure, comparing performance on (a) a task with arbitrariness but without prepotency with (b) a task with both features and (c) a task with neither. The participants with autism performed at a lower level than comparison groups on the first and second task but not on the third task. This outcome is consistent with the view that autism is associated with difficulties in following arbitrary procedures per se. We try to locate difficulties with acting on the basis arbitrary rules in relation to more mainstream ideas about autistic executive dysfunction.

Based on an emerging neuroscience model of addiction, this study examines how an imbalance between two neurobehavioral systems (reward motivation and executive control) can distinguish between early adolescent progressive drug use and mere experimentation with drugs. Data from four annual assessments of a community cohort (N = 382) of 11- to 13-year-olds were analyzed to model heterogeneity in patterns of early drug use. Baseline assessments of working memory (an indicator of the functional integrity of the executive control system) and three dimensions of impulsivity (characterizing the balance between reward seeking and executive control systems) were used to predict heterogeneous latent classes of drug use trajectories from early to midadolescence. Findings revealed that an imbalance resulting from weak executive control and heightened reward seeking was predictive of early progression in drug use, while heightened reward seeking balanced by a strong control system was predictive of occasional experimentation only. Implications of these results are discussed in terms of preventive interventions that can target underlying weaknesses in executive control during younger years, and potentially enable at-risk adolescents to exercise greater self-restraint in the context of rewarding drug-related cues.

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.

Data from a community-based sample of 1,126 10th- and 11th-grade adolescents were analyzed using a model-based cluster analysis approach to empirically identify heterogeneous adolescent subpopulations from the person-oriented and pattern-oriented perspectives. The model-based cluster analysis is a new clustering procedure to investigate population heterogeneity utilizing finite mixture multivariate normal densities and accordingly to classify subpopulations using more rigorous statistical procedures for the comparison of alternative models. Four cluster groups were identified and labeled multiproblem high-risk, smoking high-risk, normative, and low-risk groups. The multiproblem high risk exhibited a constellation of high levels of problem behaviors, including delinquent and sexual behaviors, multiple illicit substance use, and depressive symptoms at age 16. They had risky temperamental attributes and lower academic functioning and educational expectations at age 15.5 and, subsequently, at age 24 completed fewer years of education, and reported lower levels of physical health and higher levels of continued involvement in substance use and abuse. The smoking high-risk group was also found to be at risk for poorer functioning in young adulthood, compared to the low-risk group. The normative and the low risk groups were, by and large, similar in their adolescent and young adult functioning. The continuity and comorbidity path from middle adolescence to young adulthood may be aided and abetted by chronic as well as episodic substance use by adolescents.