Adopting a developmental epidemiology perspective, the current study examines sources of risk heterogeneity for internalizing symptomatology among children of alcoholic parents (COAs). Parent-based factors, including comorbid diagnoses and the number of alcoholic parents in the family, as well as child-based factors, namely child gender, formed the indicators of heterogeneity. Following a novel approach to cross-study methods, we present a three-stage analysis involving measurement development using item response theory, examination of study effects on latent trajectories over time using latent curve modeling, and prediction of these latent trajectories testing our theoretically derived hypotheses in two longitudinal investigations across both mother- and self-reported symptomatology. Specifically, we replicated previous findings that parent alcoholism has a unique effect on child internalizing symptoms, above and beyond those of both parent depression and antisocial personality disorder. However, we also found important subgroup differences, explaining heterogeneity within COAs' risk profile in terms of the number of alcoholic parents in the family, comorbid diagnoses for the alcoholic parent and, for self-reported symptoms, child gender. Such factors serve to refine the definition of risk among COAs, suggesting a more severely impaired target group for preventive interventions, identifying the significance of familial alcoholism in individual differences underlying internalizing symptoms over time, and further specifying the distal risk matrix for an internalizing pathway to alcohol involvement.

Empathic concern for others is an essential motive for challenges of self-regulation at all developmental stages. A child who never develops the capacity for empathic concern may become an ineffective parent, such that developmental psychopathology propagates across generations. We draw on evidence and theory by Panksepp and associates that indicates that infant–mother bonding is mediated by opiate mechanisms. We review the neural systems of pain perception and find these are closely aligned with those for attentional and cognitive self-regulation. Analysis of the limbic and neocortical representations for interpersonal reasoning suggests there are important contributions from visceral, affective, and somatic and cognitive levels. We draw on modern learning theory to propose a critical role for frustration training in development to allow the child to achieve the capacity for tolerating psychological pain that allows effective empathic concern in later relationships.

Borderline personality disorder (BPD) is characterized by a broad pattern of impulsivity and suicidality. BPD usually begins in adolescence; the full clinical picture of the disorder is associated with developmental increases in impulsivity. However, BPD also has childhood precursors. The developmental pathways are similar to those found in other impulsive spectrum disorders, but children who later develop BPD probably have both externalizing and internalizing symptoms. Research in this area has made use of retrospective data from adults, prospective data from community studies, follow-up studies from children at risk, as well as research on “borderline pathology of childhood” (a condition with symptoms similar to adult BPD). Existing evidence suggests that both temperamental and environmental risk factors play a role in the development of the behavioral patterns associated with the disorder. These pathways also help account for the life course and outcome of BPD in adulthood.This paper benefited from suggestions made by Jenny Macfie.

There is growing recognition that traditional strategies, such as pullout special education programs and on-site casework and guidance, are no longer sufficient to address the staggering needs of a growing number of troubled children entering U.S. schools. This paper introduces a school-based prevention and intervention method for young adolescents called Responsive Advocacy for Life and Learning in Youth (RALLY). Prevention practitioners, a new role developed by the program, work in classrooms and after-school settings to provide nonstigmatizing support to students. Using a three-tiered prevention model, practitioners integrate a mental health and educational focus to foster students' academic, social, and emotional success. The intervention involves all children of an age cohort in middle schools. The practitioners are developmental specialists who create relationships with youth, teachers, and families in high-risk environments and serve triage functions to existing community and health care institutions. The RALLY intervention builds on normative developmental and developmental psychopathology theory, especially a risk and resilience framework. The paper describes the principles behind the practice and how the work in this field has created innovations in theory and a new impetus for research.

Internal representations of self and primary attachment figures may be one mechanism by which maltreatment affects children's interpersonal behavior and relationships with others. Research on the continuity and influence of maltreated children's attachment representations, however, has not included youngsters removed from abusive or neglectful home environments. This paper examines the influence of maltreated children's maternal and self-representations on subsequent relationships with foster mothers and behavioral adjustment in foster care. Participants included 32 children, ages 9–13 years, who entered foster placement for the first time after a sustained relationship with a maltreating biological mother. Upon initially entering foster care, children's maternal and self-representations were significantly related to each other and to severity of maltreatment history but not to other factors believed to influence the quality of parent–child relationship (e.g., maternal mental health, partner stability). In addition, these representations significantly predicted children's subsequent views of their relationships with foster mothers. Finally, children's behavior in their foster homes was associated with maltreatment severity, internal representations assessed at entry into foster care, and to concurrent perceptions of their new foster mothers. These findings advance our understanding of foster placement's role in maltreated children's development and provide preliminary insight into the processes associated with the formation of potentially compensatory relationships.

Prior research has found inconsistent evidence regarding the association among childhood adversity, inflammation, and internalizing symptoms, perhaps because previous studies have yet to adequately integrate important factors such as the timing of the adversity, genetic variation, and other relevant processes such as neuroendocrine regulation. The aims of the present study were threefold: (a) to determine whether the effect of the timing of child maltreatment on C-reactive protein (CRP), an inflammatory marker, varies by CRP gene variation; (b) to explore whether links between salivary CRP and childhood internalizing symptoms depend on the presence and timing of maltreatment experiences; and (c) to investigate the role of CRP in the relations between child neuroendocrine regulation and internalizing symptoms and examine whether these associations are moderated by the presence and timing of child maltreatment. Participants included a sample of 267 maltreated and 222 nonmaltreated children (M age = 9.72, SD = 0.99; 52.4% male; 66% African American) who attended a summer day camp research program designed for school-aged low-income children. Department of Human Services records were examined to determine the onset and recency of maltreatment for children in the maltreated group. The results indicated that among children with recent onset maltreatment, those with at least one A allele from CRP single nucleotide polymorphism rs1417938 evidenced significantly higher CRP levels compared to recently maltreated children carrying the TT genotype. Moreover, higher levels of CRP were associated with higher levels of internalizing symptoms only for recently maltreated children. Finally, we did not find support for salivary CRP as a mechanism in the relation between neuroendocrine regulation and childhood internalizing symptoms. Our findings highlight the importance of the timing of child maltreatment and have important implications for characterizing variability in inflammation and internalizing symptoms among youth.

Poor effortful control is a key temperamental factor underlying behavioral problems. The bidirectional association of child effortful control with both positive parenting and negative discipline was examined from ages approximately 3 to 13–14 years, involving five time points, and using data from parents and children in the Oregon Youth Study—Three Generational Study (N = 318 children from 150 families). Based on a dynamic developmental systems approach, it was hypothesized that there would be concurrent associations between parenting and child effortful control and bidirectional effects across time from each aspect of parenting to effortful control and from effortful control to each aspect of parenting. It was also hypothesized that associations would be more robust in early childhood, from ages 3 to 7 years, and would diminish as indicated by significantly weaker effects at the older ages, 11–12 to 13–14 years. Longitudinal feedback or mediated effects were also tested. The findings supported (a) stability in each construct over multiple developmental periods; (b) concurrent associations, which were significantly weaker at the older ages; (c) bidirectional effects, consistent with the interpretation that at younger ages children's effortful control influenced parenting, whereas at older child ages, parenting influenced effortful control; and (d) a transactional effect, such that maternal parenting in late childhood was a mechanism explaining children's development of effortful control from middle childhood to early adolescence.

Despite widespread recognition that the physiological systems underlying stress reactivity are well coordinated at a neurobiological level, surprisingly little empirical attention has been given to delineating precisely how the systems actually interact with one another when confronted with stress. We examined cross-system response proclivities in anticipation of and following standardized laboratory challenges in 664 4- to 14-year-olds from four independent studies. In each study, measures of stress reactivity within both the locus coeruleus-norepinephrine system (i.e., the sympathetic and parasympathetic branches of the autonomic nervous system) and the corticotrophin releasing hormone system (i.e., the hypothalamic–pituitary–adrenal axis) were collected. Latent profile analyses revealed six distinctive patterns that recurred across the samples: moderate reactivity (average cross-system activation; 52%–80% of children across samples), parasympathetic-specific reactivity (2%–36%), anticipatory arousal (4%–9%), multisystem reactivity (7%–14%), hypothalamic–pituitary–adrenal axis specific reactivity (6%–7%), and underarousal (0%–2%). Groups meaningfully differed in socioeconomic status, family adversity, and age. Results highlight the sample-level reliability of children's neuroendocrine responses to stress and suggest important cross-system regularities that are linked to development and prior experiences and may have implications for subsequent physical and mental morbidity.

This paper proposes a model for developmental psychopathology that is informed by recent research suggestive of a single model of mental health disorder (the p factor) and seeks to integrate the role of the wider social and cultural environment into our model, which has previously been more narrowly focused on the role of the immediate caregiving context. Informed by recently emerging thinking on the social and culturally driven nature of human cognitive development, the ways in which humans are primed to learn and communicate culture, and a mentalizing perspective on the highly intersubjective nature of our capacity for affect regulation and social functioning, we set out a cultural-developmental approach to psychopathology.

This study examined developmentally salient risk and protective factors of adolescent substance use assessed during early childhood and early adolescence using a sample of 310 low-income boys. Child problem behavior and proximal family risk and protective factors (i.e., parenting and maternal depression) during early childhood, as well as child and family factors and peer deviant behavior during adolescence, were explored as potential precursors to later substance use during adolescence using structural equation modeling. Results revealed that early childhood risk and protective factors (i.e., child externalizing problems, mothers' depressive symptomatology, and nurturant parenting) were indirectly related to substance use at the age of 17 via risk and protective factors during early and middle adolescence (i.e., parental knowledge and externalizing problems). The implications of these findings for early prevention and intervention are discussed.

We tested for gender moderation within a multidomain model of antisocial behavior (ASB) among community youth, drawn from the Project on Human Development in Chicago Neighborhoods study. Youths (N = 1,639) were 9 to 12 years old at baseline and were followed for two additional waves, spaced approximately 2.5 years apart. We hypothesized that harsh and physically coercive parenting, a familial level risk factor, would impact individual level risk factors for ASB, such as childhood temperament ratings of emotionality and inhibitory control, and preadolescent externalizing and internalizing symptoms, as well as involvement with antisocial peers. We further hypothesized that this process and its impact on ASB would be moderated by gender. We used both multiple indicator multiple causes and multiple group analyses to test for gender moderation and a structural equation modeling multiple mediation framework to evaluate the strength of indirect effects. We tested the role of family, individual, and peer level influences on ASB, after accounting for the role of known contextual factors, including poverty, race, and neighborhood. Our overall model fit the data well for males and females, indicating harsh parenting, disinhibition, emotionality, and peers exert a strong influence on risk for ASB. Gender moderated the pathway from harsh parenting to externalizing behavior, such that this was a significant pathway for girls, but not boys. We discussed the importance of these findings with regard to intervention planning for youth at risk for ASB and future gender-informed models of ASB.

Rates of self-inflicted injury among adolescents have risen in recent years, yet much remains to be learned about the pathophysiology of such conduct. Self-injuring adolescents report high levels of both impulsivity and depression behaviorally. Aberrant neural responding to incentives, particularly in striatal and prefrontal regions, is observed among both impulsive and depressed adolescents, and may mark common vulnerability to symptoms of anhedonia, irritability, and low positive affectivity. To date, however, no studies have examined associations between central nervous system reward responding and self-injury. In the current study, self-injuring (n = 19) and control (n = 19) adolescent females, ages 13–19 years, participated in a monetary incentive delay task in which rewards were obtained on some trials and losses were incurred on others. Consistent with previous findings from impulsive and depressed samples, self-injuring adolescents exhibited less activation in both striatal and orbitofrontal cortex regions during anticipation of reward than did controls. Self-injuring adolescents also exhibited reduced bilateral amygdala activation during reward anticipation. Although few studies to date have examined amygdala activity during reward tasks, such findings are common among adults with mood disorders and borderline personality disorder. Implications for neural models of impulsivity, depression, heterotypic comorbidity, and development of both self-injury and borderline personality traits are discussed.

Relationships with parents and peers are crucial for children's socialization, but how parent–child and peer relationships mutually affect each other is not well understood. Guided by spillover theory, we zoomed in on the bidirectional interplay between parental rejection and warmth on the one hand and peer victimization on the other, and examined whether children's maladjustment symptoms mediated hypothesized cross-domain spillover effects. Data stem from five waves of the longitudinal KiVa study among 9,770 children (50% boys; mean age = 9.16, standard deviation = 1.29). Results from random intercept cross-lagged panel models showed that higher parental rejection and lower parental warmth predicted increases in peer victimization and vice versa across waves, thus supporting the bidirectional model. Moreover, spillover from parent–child rejection and warmth to peer victimization was partially driven by children's depressive symptoms and bullying perpetration. Vice versa, spillover from peer victimization to parent–child rejection and warmth was partially driven by children's social anxiety, depressive symptoms, conduct problems, and bullying perpetration. Thus, children might get caught in persistent problems in two important social domains, and these two domains influence each other through children's maladjustment. Family and school interventions should be integrated to prevent a downwards spiral.

Allostatic load is the “wear and tear” of the body resulting from the repeated activation of compensatory physiological mechanisms in response to chronic stress. Allostatic load can significantly affect the aging process and result in reduced longevity, accelerated aging, and impaired health. Although low socioeconomic status is associated with high allostatic load during aging, the effects of status-related psychosocial stress on allostatic load are often confounded by lifestyle variables. Chronic psychosocial stress associated with low dominance rank in nonhuman primates represents an excellent animal model with which to investigate allostatic load and aging in humans. Research conducted with free-ranging rhesus monkeys suggests that female reproduction can also be a source of stress and allostatic load. Female reproduction is associated with increased risk of mortality and hyperactivation of the hypothalamic–pituitary–adrenal axis. Reproduction is especially stressful and costly for aging females of low rank. Although many indicators of body condition and neuroendocrine and immune function are influenced by aging, there are marked and stable individual differences among aging females in body condition, plasma cortisol responses to stress, and cytokine responses to stress. These differences are consistent with the hypothesis that there are strong differences in chronic stress among individuals, and that allostatic load resulting from chronic stress affects health during aging. Comparisons between captive and free-ranging rhesus monkey populations may allow us to understand how differences in environmental stress and allostatic load affect rates of aging, and how these in turn translate into differences in longevity and health.

Gene–environment correlation (rGE) exists both within and between families. Between families, accumulating rGE has been used to explain dramatic changes in phenotypic means over time. The Dickens and Flynn model of increases in cognitive ability over generational time, for example, suggests that small changes in phenotype can lead to subsequent reallocation of environmental resources. This process sets up a reciprocal feedback loop between phenotype and environment, producing accumulating rGE that can cause large changes in the mean of ability, even though ability remains highly heritable in cross-sectional data. We report simulations suggesting that similar processes may operate within twin and sibling pairs. Especially in dizygotic twins and siblings, small differences in phenotype can become associated with reallocations of environmental resources within families. We show that phenotype–environment effects can account for age-related increases in rGE, rapid differentiation of siblings raised together, and widely reported increases in the heritability of behavior during childhood and adolescence.

Childhood maltreatment, including abuse and neglect, may have sustained effects on the integrity and functioning of the brain, alter neurophysiological responsivity later in life, and predispose individuals toward psychiatric conditions involving socioaffective disturbances. This meta-analysis aims to quantify associations between self-reported childhood maltreatment and brain function in response to socioaffective cues in adults. Seventeen functional magnetic resonance imaging studies reporting on data from 848 individuals examined with the Childhood Trauma Questionnaire were included in a meta-analysis of whole-brain findings, or a review of region of interest findings. The spatial consistency of peak activations associated with maltreatment exposure was tested using activation likelihood estimation, using a threshold of p < .05 corrected for multiple comparisons. Adults exposed to childhood maltreatment showed significantly increased activation in the left superior frontal gyrus and left middle temporal gyrus, and decreased activation in the left superior parietal lobule and the left hippocampus. Although hyperresponsivity to socioaffective cues in the amygdala and ventral anterior cingulate cortex in correlation with maltreatment severity is a replicated finding in region of interest studies, null results are reported as well. The findings suggest that childhood maltreatment has sustained effects on brain function into adulthood, and highlight potential mechanisms for conveying vulnerability to development of psychopathology.

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.

This study examined exposure to peer delinquency as a mediator between pubertal timing and self-reported delinquency longitudinally and whether this mediational model was moderated by either gender or maltreatment experience. Data were obtained from Time 1, 2, and 3 of a longitudinal study of maltreatment and development. At Time 1 the sample comprised 454 children aged 9–13 years. Analyses via structural equation modeling supported full mediation. Gender did not moderate this mediational relationship, but maltreatment experience did. The results show that early maturing males and females are both at risk for being exposed to peers that may draw them into delinquent behavior. In addition, the mechanism linking early pubertal timing to delinquency differs depending on maltreatment experience.

This study examined the longitudinal implications of adolescents' exposure to interparental conflict for their developmental success. In the proposed developmental cascade model, adolescents' perceptions of parental conflict as threatening is a risk factor for diminished self-efficacy, which would account for diminished adjustment. This study presents longitudinal data for 768 sixth-grade students and their families over four time points, ending in eighth grade. Analyses were conducted in three steps. First, replication of longitudinal support for threat as a mediator of the link between interparental conflict and emotional distress was found; however, findings did not support threat as a mediator of behavior problems or subjective well-being. Second, threat was found to mediate the longitudinal association between interparental conflict and self-efficacy. Third, a developmental cascade model supported a risk process in which interparental conflict was related to adolescents' threat appraisals, which undermined self-efficacy beliefs, and was then linked with emotional distress, behavior problems, and subjective well-being.

This study examined whether peer rejection and affiliation with deviant friends throughout childhood could mediate the link between early disruptiveness and two aspects of delinquent behaviors (i.e., violence and substance use) in a sample of 375 children. Furthermore, we tested whether the two putative mediators operated in a sequential manner or in a parallel manner. Participants' disruptiveness, peer rejection, and friends' deviancy were assessed throughout childhood (ages 7 to 13). Delinquency-related outcomes were assessed at ages 14 and 15 years. Results indicate that the sequential mediational model was supported when delinquency-related violence was the outcome, but not when substance use was the outcome. The discussion stresses the differential role of peer rejection and affiliation with deviant friends in regard to the two outcomes considered in this study and in regard to the time frame when they were measured.This research was made possible by a grant from the Social Sciences and Humanities Research Council of Canada. We thank the authorities and directors of schools in the Val d'Or School Board as well as the teachers and children for their first-rate collaboration.