The current study filled significant gaps in our knowledge of developmental psychopathology by examining the influence of multilevel risk factors and developmental assets on longitudinal trajectories of internalizing symptoms and self-esteem in an exceptionally culturally diverse sample of rural adolescents. Integrating ecological and social capital theories, we explored if positive microsystem transactions are associated with self-esteem while negative microsystem transactions increase the chances of internalizing problems. Data came from the Rural Adaptation Project, a 5-year longitudinal panel study of more than 4,000 middle school students from 28 public schools in two rural, disadvantaged counties in North Carolina. Three-level hierarchical linear modeling models were estimated to predict internalizing symptoms (e.g., depression, anxiety) and self-esteem. Relative to other students, risk for internalizing problems and low self-esteem was elevated for aggressive adolescents, students who were hassled or bullied at school, and those who were rejected by peers or in conflict with their parents. Internalizing problems were also more common among adolescents from socioeconomically disadvantaged families and neighborhoods, among those in schools with more suspensions, in students who reported being pressured by peers, and in youth who required more teacher support. It is likely that these experiences left adolescents disengaged from developing social capital from ecological microsystems (e.g., family, school, peers). On the positive side, support from parents and friends and optimism about the future were key assets associated with lower internalizing symptoms and higher self-esteem. Self-esteem was also positively related to religious orientation, school satisfaction, and future optimism. These variables show active engagement with ecological microsystems. The implications and limitations were discussed.

Recent work on the molecular genetics of complex traits in typical and atypical human development has focused primarilyon associations of single genes with behavior. Disparate literature suggests that the presence of one or two copies of the short allele of the serotonin transporter (5-HTT) gene and the long allele (7-repeat allele) version of the dopamine receptor D4 (DRD4) gene predicts internalizing- and externalizing-related behaviors, respectively. Apparently for the first time in the extant literature, we report a gene–gene statistical interaction on behavior problems in a group of typically developing children at age 7. DNA was extracted from buccal cells collected from 108 children and genotyped for short and long alleles of the 5-HTT gene and the short (2–5 repeats) versus long (6–8 repeats) allele of the DRD4 gene. Mothers completed the Child Behavior Checklist. As predicted, children with one or two copies of the short allele of the 5-HTT gene and the long allele version of the DRD4 gene exhibited significantly more internalizing and externalizing behaviors at age 7 than children with other combinations of the 5-HTT and DRD4 short and long genotypes. As well, children with the 5-HTT long and DRD4 long genotypes had the lowest reported scores on internalizing and externalizing behaviors at age 7, suggesting that the presence of the 5-HTT long genotype may serve as a protective factor against these behaviors in children with the long DRD4 genotype. Implications of these findings for understanding cumulative biological risk and protective factors in childhood behavior problems and psychopathology are discussed.

Whereas child personality, IQ, and family factors have been identified as enabling a resilient response to psychosocial adversity, more direct biological resilience factors have been less well delineated. This is particularly so for child attention-deficit/hyperactivity disorder (ADHD), which has received less attention from a resilience perspective than have associated externalizing disorders. Children from two independent samples were classified as resilient if they avoided developing ADHD, oppositional defiant disorder (ODD), or conduct disorder (CD) in the face of family adversity. Two protective factors were examined for their potential relevance to prefrontal brain development: neuropsychological response inhibition, as assessed by the Stop task, and a composite catecholamine genotype risk score. Resilient children were characterized in both samples by more effective response inhibition, although the effect in the second sample was very small. Genotype was measured in Sample 1, and a composite high risk genotype index was developed by summing presence of risk across markers on three genes expressed in prefrontal cortex: dopamine transporter, dopamine D4 receptor, and noradrenergic alpha-2 receptor. Genotype was a reliable resilience indicator against development of ADHD and CD, but not ODD, in the face of psychosocial adversity. Results illustrate potential neurobiological protective factors related to development of prefrontal cortex that may enable children to avoid developing ADHD and CD in the presence of psychosocial adversity.

Several research teams have previously traced patterns of emerging conduct problems (CP) from early or middle childhood. The current study expands on this previous literature by using a genetically-informed, experimental, and long-term longitudinal design to examine trajectories of early-emerging conduct problems and early childhood discriminators of such patterns from the toddler period to adolescence. The sample represents a cohort of 731 toddlers and diverse families recruited based on socioeconomic, child, and family risk, varying in urbanicity and assessed on nine occasions between ages 2 and 14. In addition to examining child, family, and community level discriminators of patterns of emerging conduct problems, we were able to account for genetic susceptibility using polygenic scores and the study's experimental design to determine whether random assignment to the Family Check-Up (FCU) discriminated trajectory groups. In addition, in accord with differential susceptibility theory, we tested whether the effects of the FCU were stronger for those children with higher genetic susceptibility. Results augmented previous findings documenting the influence of child (inhibitory control [IC], gender) and family (harsh parenting, parental depression, and educational attainment) risk. In addition, children in the FCU were overrepresented in the persistent low versus persistent high CP group, but such direct effects were qualified by an interaction between the intervention and genetic susceptibility that was consistent with differential susceptibility. Implications are discussed for early identification and specifically, prevention efforts addressing early child and family risk.

A developmental psychopathology framework, with its emphasis on an interdisciplinary perspective, the interplay between work conducted with normal and atypical populations, and its focus on investigating functioning in multiple domains of development concurrently, possesses significant potential for advancing work on memory and trauma. A brief historical overview of memory and trauma is provided. Significant issues are highlighted that must be confronted in order to advance the understanding of the effects of trauma on memory and the utility of a developmental psychopathology perspective for informing research efforts is examined. The implications of a developmental psychopathology perspective for guiding research, clinical, and social policy initiatives of relevance to trauma and memory are discussed.

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

The study examined the interaction between early maturational timing (measured by premature adrenarche [PA]) and executive functioning and cortisol reactivity on symptoms of psychopathology. The study included 76 girls aged 6 through 8 years (mean = 7.50, SD = 0.85) with PA (n = 40) and on-time adrenarche (n = 36). Girls completed a battery of psychological and neuropsychological tests and blood sampling for cortisol. Parents completed the Child Behavior Checklist. The results demonstrated that girls with PA with lower levels of executive functioning had higher externalizing and anxious symptoms compared to other girls. In addition, girls with PA who demonstrated increases in serum cortisol had higher externalizing symptoms than those with stable patterns. Finally, girls with PA who demonstrated decreases in cortisol reported higher depressive symptoms. The findings from this study provide important information concerning the impact of cognitive functioning and stress reactivity on adjustment to early maturation in girls with PA. The results of this research may inform screening and intervention efforts for girls who may be at greatest risk for emotional and behavioral problems as a result of early maturation.

Exposure to early life adversity is linked to impaired affective, cognitive, and behavioral functioning and increases risk for various psychiatric and medical conditions. Stress-induced increases in pro-inflammatory cytokines may be a biological mechanism of these effects. Few studies have examined cytokine levels in children experiencing early life adversity, and very little research has investigated cytokines or other markers of inflammation in saliva. In the present study, we examined salivary interleukin (IL)-1β and C-reactive protein (CRP) levels in relation to stress exposure in 40 children aged 3 to 5 years who were enrolled in a larger study of early life adversity. Childhood maltreatment status was assessed via review of child welfare records. Contextual stress exposure, traumatic life event history, and symptoms of psychopathology were assessed via caregiver interviews at a home visit. In a subsequent visit, salivary IL-1β and CRP were obtained before and after participation in four emotion-eliciting tasks. The number of past-month contextual stressors, lifetime contextual stressors, and traumatic life events each demonstrated a significant main effect on IL-1β. Baseline IL-1β was positively associated with each of the significant main-effect adversities. Postchallenge IL-1β displayed positive associations with each adversity variable, but these were not significant. CRP was not significantly associated with any of the adversity variables. Given the evidence suggesting the involvement of IL-1β in the neuropathology of psychiatric conditions, these results may have important implications for developmental outcomes.

This study examined physiological correlates (cortisol and α-amylase [AA]) of peer victimization and aggression in a sample of 228 adolescents (45% male, 55% female; 90% African American; M age = 14 years, SD = 1.6 years) who participated in a longitudinal study of stress, physiology, and adjustment. Adolescents were classified into victimization/aggression groups based on patterns with three waves of data. At Wave 3, youth completed the Social Competence Interview (SCI), and four saliva samples were collected prior to, during, and following the SCI. Repeated-measures analyses of variance with victimization/aggression group as the predictor, and physiological measures as outcomes, controlling for time of day, pubertal status, and medication use revealed significant Group × SCI Phase interactions for salivary AA (sAA), but not for cortisol. The results did not differ by sex. For analyses with physical victimization/aggression, aggressive and nonaggressive victims showed increases in sAA during the SCI, nonvictimized aggressors showed a decrease, and the normative contrast group did not show any change. For analyses with relational victimization/aggression, nonaggressive victims were the only group who demonstrated sAA reactivity. Incorporating physiological measures into peer victimization studies may give researchers and clinicians insight into youth's behavior regulation, and help shape prevention or intervention efforts.

Despite substantial recent advancements in psychiatric genetic research, progress in identifying the genetic basis of anxiety disorders has been limited. We review the candidate gene and genome-wide literatures in anxiety, which have made limited progress to date. We discuss several reasons for this hindered progress, including small samples sizes, heterogeneity, complicated comorbidity profiles, and blurred lines between normative and pathological anxiety. To address many of these challenges, we suggest a developmental, multivariate framework that can inform and enhance anxiety phenotypes for genetic research. We review the psychiatric and genetic epidemiological evidence that supports such a framework, including the early onset and chronic course of anxiety disorders, shared genetic risk factors among disorders both within and across time, and developmentally dynamic genetic influences. We propose three strategies for developmentally sensitive phenotyping: examination of early temperamental risk factors, use of latent factors to model underlying anxiety liability, and use of developmental trajectories as phenotypes. Expanding the range of phenotypic approaches will be important for advancing studies of the genetic architecture of anxiety disorders.

This study was designed to examine the nature of object imitation performance in early autism. We hypothesized that imitation would be relatively preserved when behaviors on objects resulted in salient instrumental effects. We designed tasks in which, in one condition, the motor action resulted in a salient, meaningful effect on an object, whereas in the other condition, the same action resulted in a less salient effect because of differing object characteristics. The motor aspects of the tasks did not vary across conditions. Four participant groups of 2- to 5-year-olds were examined: 17 children with early-onset autism, 24 children with regressive onset autism, 22 children with developmental delays, and 22 children with typical development. Groups were matched on nonverbal skills, and differences in verbal development were examined as a moderator of imitative ability. Results revealed an interaction of group by condition, with the combined autism group failing more tasks than the combined comparison groups, and failing more tasks in the less salient condition than in the more salient condition, as hypothesized. Analyses of autism subgroups revealed these effects were primarily because of the regression onset group. Accuracy of motor performance was examined by analyzing errors. Among children passing imitative acts, there were no group differences and no condition effects in the number, type, or pattern of performance errors. Among children passing the tasks, the group with autism did not demonstrate more emulation errors (imitating the goal but not the means) than other groups. There was no evidence that either motor or attentional aspects of the tasks contributed to the poorer imitative performance of the children with autism.

This study examined the links between mothers' frontal EEG asymmetry at rest and during videos of their 5- to 8-month-old infants expressing three emotion states (joy, anger/distress, and neutral interest), mother–infant emotional availability (EA) in the home, mothers' depressive and anxious symptoms, and mothers' emotional experience in response to infant emotion cues. Greater relative right frontal activity at rest was associated with greater maternal anxiety, but was unrelated to EA or mother-reported emotional experience in response to infant emotion cues. A shift toward greater relative right frontal activation in response to infant emotional stimuli was associated with lower maternal anxiety, greater mother–infant EA, and mothers' experience of sadness, concern, irritability, and the absence of joy in response to seeing their own infant in distress. These findings suggest that mothers' in the moment empathetic responding to their infant's emotions, indexed by a shift in frontal EEG asymmetry in response to infant emotional displays, is related to mother–infant EA in the home. Implications for conceptualizing parenting risk are discussed.

Anxious mothers' parenting, particularly transfer of threat information, has been considered important in their children's risk for social anxiety disorder (SAnxD), and maternal narratives concerning potential social threat could elucidate this contribution. Maternal narratives to their preschool 4- to 5-year-old children, via a picture book about starting school, were assessed in socially anxious (N = 73), and nonanxious (N = 63) mothers. Child representations of school were assessed via doll play (DP). After one school term, mothers (Child Behavior Checklist [CBCL]) and teachers (Teacher Report Form) reported on child internalizing problems, and child SAnxD was assessed via maternal interview. Relations between these variables, infant behavioral inhibition, and attachment, were examined. Socially anxious mothers showed more negative (higher threat attribution) and less supportive (lower encouragement) narratives than controls, and their children's DP representations SAnxD and CBCL scores were more adverse. High narrative threat predicted child SAnxD; lower encouragement predicted negative child CBCL scores and, particularly for behaviorally inhibited children, Teacher Report Form scores and DP representations. In securely attached children, CBCL scores and risk for SAnxD were affected by maternal anxiety and threat attributions, respectively. Low encouragement mediated the effects of maternal anxiety on child DP representations and CBCL scores. Maternal narratives are affected by social anxiety and contribute to adverse child outcome.

The present study used a longitudinal and discordant twin design to explore in depth the developmental associations between victimization and loneliness from mid-childhood to young adulthood. The data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 individuals born in England and Wales during 1994–1995. Diverse forms of victimization were considered, differing across context, perpetrator, and timing of exposure. The results indicated that exposure to different forms of victimization was associated with loneliness in a dose–response manner. In childhood, bullying victimization was uniquely associated with loneliness, over and above concurrent psychopathology, social isolation, and genetic risk. Moreover, childhood bullying victimization continued to predict loneliness in young adulthood, even in the absence of ongoing victimization. Within-twin pair analyses further indicated that this longitudinal association was explained by genetic confounds. In adolescence, varied forms of victimization were correlated with young adult loneliness, with maltreatment, neglect, and cybervictimization remaining robust to controls for genetic confounds. These findings indicate that vulnerability to loneliness in victimized young people varies according to the specific form of victimization in question, and also to the developmental period in which it was experienced.

With advancements in the technology of prevention and treatment of childhood anxiety disorders, information regarding our understanding of normal and abnormal child development can be enriched. Typically, research has focused on developing efficacious and effective interventions with less attention devoted to the impact this information may have on the field of developmental psychopathology. By reviewing the results of both treatment and prevention studies, several potential contributions of intervention research to the field can be explored. Results from wait-list or monitoring control groups will be reviewed, providing valuable information regarding the normal trajectory of the anxious child. Outcomes of children receiving the intervention prove that this pathway can be altered and is not impermeable. Furthermore, a review of long-term follow-up studies addresses the question of whether intervention can change the long-term trajectory of an anxiety-disordered child and prevent disorders in later life. Contributions to the etiological understanding of the anxiety disorders will also be reviewed: changes in variables considered important in the etiology and maintenance of disorder can be examined in synchronicity with changes in symptomatology following intervention. An examination of potential developmental predictors of treatment outcome will also contribute to this review, with a focus on the limitations of the current research in gaining a complete understanding of the relationship between developmental level and outcome. Directions regarding future research in the study of interventions for child and adolescent anxiety disorders will be discussed with the aim of promoting further communication between intervention research and the field of developmental psychopathology.

Although animal models and correlational studies support a model of fetal programming as a mechanism in the transmission of risk for psychopathology from parents to children, the experimental studies that are required to empirically test the model with the human prenatal dyad are scarce. With a systematic review and meta-analysis of the literature, we critically examined the evidence regarding the neurobiological and behavioral changes in infants as a function of randomized clinical trials to prevent or reduce maternal depression during pregnancy, treating randomized clinical trials as experiments testing the fetal programming model. Based on 25 articles that met inclusion criteria, we found support for interventions designed to change maternal prenatal mood being associated with changes in offspring functioning, but with a very small effect size. Effect sizes ranged broadly, and were higher for younger children. The findings enhance understanding of putative mechanisms in the transmission of risk from women's prenatal depression to infants’ vulnerabilities to, and early signs of, the development of psychopathology. We note limitations of the literature and suggest solutions to advance understanding of how preventing or treating depression in pregnant women might disrupt the transmission of risk to the infants.

Whereas the basic wiring diagram of the mammalian central nervous system (CNS) is genetically preprogramed, its fine tuning throughout different phases of infancy, childhood, and adulthood are highly experience dependent. The potential neurobiological mechanisms and behavioral effects of such experience-dependent neuroplasticity as a function of stage of development are outlined. A basic thesis of this paper is that mechanisms involved in neuronal learning and memory, such as long-term potentiation (LTP) and long-term depression (LTD), are used and reused not only in the sculpting of the CNS in the initial establishment of connections, but also again in the molding of personality and behavior based on experience. It is postulated that for higher order processes such as emotional memory, such neuroplasticity is occurring at increasingly larger numbers of synapses and cell assemblies with increasing mechanistic complexity and self-organization. Just as overexcitation or deprivation can profoundly affect the development of the visual system, it is postulated that similar phenomena exist in the neural substrates of emotional and cognitive development. In addition, a secondary and potentially more widespread series of ramifications are likely to occur in the higher order and integrative systems, such as secondary and tertiary cortical association areas and prefrontal cortex that become the ultimate integrators of emotion and experience, leading to subsequent actions and plans for the future. This process is, by definition, plastic, and such remodeling is likely to take place not only at the level of the single synapse, but also at higher levels of network integration of which we currently have only the barest glimpse. Nonetheless, beginning to discuss the neurobiology of such self-organizing plastic systems may begin to change our conceptual approaches to psychopathology and open new avenues of therapeutics for the major psychiatric illnesses that are critically dependent on such higher order learning and memory mechanisms.

Associations between low birth weight and prenatal anxiety and later psychopathology may arise from programming effects likely to be adaptive under some, but not other, environmental exposures and modified by sex differences. If physiological reactivity, which also confers vulnerability or resilience in an environment-dependent manner, is associated with birth weight and prenatal anxiety, it will be a candidate to mediate the links with psychopathology. From a general population sample of 1,233 first-time mothers recruited at 20 weeks gestation, a sample of 316 stratified by adversity was assessed at 32 weeks and when their infants were aged 29 weeks (N = 271). Prenatal anxiety was assessed by self-report, birth weight from medical records, and vagal reactivity from respiratory sinus arrhythmia during four nonstressful and one stressful (still-face) procedure. Lower birth weight for gestational age predicted higher vagal reactivity only in girls (interaction term, p = .016), and prenatal maternal anxiety predicted lower vagal reactivity only in boys (interaction term, p = .014). These findings are consistent with sex differences in fetal programming, whereby prenatal risks are associated with increased stress reactivity in females but decreased reactivity in males, with distinctive advantages and penalties for each sex.

Attachment theory and family systems perspectives were used to explore the intergenerational origins of an overinvolved, symbiotic parenting pattern that hampers children's emerging autonomy. Consistent with principles of developmental psychopathology, the same underlying relationship disturbance was expected to manifest differently at different times in the developmental process. Specifically, links among maternal intrusiveness during infancy, overprotection during childhood, and mother-child role-reversal during young adulthood were explored. Forty-nine maternal grandmothers, mothers, and firstborn infants were visited in the mothers' homes when the infants were 6 and 9 months old. Grandmothers' memories of overprotection were related to observational ratings of high boundary dissolution and low positive affectivity with the mothers. No significant relationships were found between mothers' past and current relationships with the grandmothers. Yet, mothers' memories of overprotection during childhood or their current participation in unaffectionate, enmeshed, and role-reversed relationships with their mothers forecast their intrusive care with their own infants. Moreover, mothers' memories of overprotection related to their beliefs that others cannot be trusted and these beliefs were related, in turn, to observations of their intrusive care at 9 months. The implications of understanding the origins of maternal intrusiveness for developing prevention programs are discussed.

In this prospective study of upper middle class youth, we document frequency of alcohol and drug use, as well as diagnoses of abuse and dependence, during early adulthood. Two cohorts were assessed as high school seniors and then annually across 4 college years (New England Study of Suburban Youth younger cohort [NESSY-Y]), and across ages 23–27 (NESSY older cohort [NESSY-O]; ns = 152 and 183 at final assessments, respectively). Across gender and annual assessments, results showed substantial elevations, relative to norms, for frequency of drunkenness and using marijuana, stimulants, and cocaine. Of more concern were psychiatric diagnoses of alcohol/drug dependence: among women and men, respectively, lifetime rates ranged between 19%–24% and 23%–40% among NESSY-Os at age 26; and 11%–16% and 19%–27% among NESSY-Ys at 22. Relative to norms, these rates among NESSY-O women and men were three and two times as high, respectively, and among NESSY-Y, close to one among women but twice as high among men. Findings also showed the protective power of parents’ containment (anticipated stringency of repercussions for substance use) at age 18; this was inversely associated with frequency of drunkenness and marijuana and stimulant use in adulthood. Results emphasize the need to take seriously the elevated rates of substance documented among adolescents in affluent American school communities.