This investigation examined the extent to which polymorphisms of the serotonin transporter linked promoter region (5-HTTLPR) and the dopamine receptor D4 (DRD4) genes differentially influenced the development of attachment security and disorganization in maltreated and nonmaltreated infants at age 13 months, and the extent to which the efficacy of preventive interventions to promote attachment security were influenced by genetic variation. The sample consisted of 106 infants from maltreating families, participating in a randomized control trial evaluating the efficacy of two interventions, child–parent psychotherapy and psychoeducational parenting intervention, and 47 infants from nonmaltreating families. DNA samples were genotyped for polymorphisms of 5-HTTLPR, DRD4 exon III variable number tandem repeat, and DRD4-521. Attachment organization at age 1 and at age 2 was assessed with the Strange Situation for all participants, prior to and following the completion of the interventions. High rates of disorganized attachment were observed in the maltreatment compared to the nonmaltreatment group, and both interventions resulted in increased rates of attachment security at age 2. Genetic variation did not influence improvement in attachment organization among maltreated infants. Among maltreated infants, genetic variation had minimal effect on attachment organization. In contrast, among nonmaltreated infants, 5-HTTLPR and DRD4 polymorphisms influenced attachment security and disorganization at age 2 and the stability of attachment disorganization over time.

This study employed event-related potentials (ERPs) to investigate the neural correlates of facial affect processing in maltreated and nonmaltreated children at 42 months of age. ERPs elicited while children passively viewed standardized pictures of female models posing angry, happy, and neutral facial expressions were examined, and differences between maltreated (N = 46) and nonmaltreated (N = 25) children were reported. Three occipital components (P1, N170, and P400) and four frontal–central components (N150, P240, Nc, and a positive slow wave [PSW]) were identified. Findings revealed that maltreated children had greater P1 and P400 amplitude in response to angry facial affect compared to other emotions, and compared to nonmaltreated children. N170 amplitude was greater in response to happy compared to angry in the maltreated group. For the P240 component, maltreated children had greater amplitude in response to angry facial expressions relative to happy, whereas children in the nonmaltreated group had greater P240 amplitude in response to happy relative to angry facial affect. Further, the nonmaltreated group had greater PSW amplitude in response to angry facial affect, whereas those in the maltreated group showed greater PSW amplitude to happy facial expressions. The results provided further support for the hypothesis that the experience of maltreatment and the predominantly negative emotional tone in maltreating families alters the functioning of neural systems associated with the identification and processing of facial emotion. These results exemplify the importance of early preventive interventions focused on emotion for children who have experienced maltreatment early in life.

Children in the birth to 5 age range are disproportionately exposed to traumatic events relative to older children, but they are underrepresented in the trauma research literature as well as in the development and implementation of effective clinical treatments and in public policy initiatives to protect maltreated children. Children from ethnic minority groups and those living in poverty are particularly affected. This paper discusses the urgent need to address the needs of traumatized young children and their families through systematic research, clinical, and public policy initiatives, with specific attention to underserved groups. The paper reviews research findings on early childhood maltreatment and trauma, including the role of parental functioning, the intergenerational transmission of trauma and psychopathology, and protective contextual factors in young children's response to trauma exposure. We describe the therapeutic usefulness of a simultaneous treatment focus on current traumatic experiences and on the intergenerational transmission of relational patterns from parent to child. We conclude with a discussion of the implications of current knowledge about trauma exposure for clinical practice and public policy and with recommendations for future research.

Children's trauma-related mental health problems are widespread, largely untreated and constitute significant barriers to academic achievement and attainment. Translational research has begun to identify school-based interventions to prevent violence, trauma and psychopathology. We describe in detail the findings to date on research evaluating one such intervention, the Reading, Writing, Respect, and Resolution (4Rs) Program. The 4Rs Program has led to modest positive impacts on both classrooms and children after 1 year that appear to cascade to more impacts in other domains of children's development after 2 years. This research strives not only to translate research into practice but also translate practice into research. However, considerable challenges must be met for such research to inform prevention strategies at population scale.

The purpose of the present research was to examine Deese–Roediger–McDermott false memory for trauma-related and nontrauma-related lists in adolescents and adults with and without documented histories of child sexual abuse (CSA). Individual differences in psychopathology and adult attachment were also explored. Participants were administered free recall and recognition tests after hearing CSA, negative, neutral, and positive Deese–Roediger–McDermott lists. In free recall, CSA and negative lists produced the most false memory. In sharp contrast, for recognition, CSA lists enjoyed the highest d′ scores. CSA-group adolescents who evinced greater posttraumatic stress disorder (PTSD) symptoms had higher rates of false memory compared to (a) non-CSA group adolescents with higher PTSD symptom scores (free recall), and (b) CSA-group adolescents with lower PTSD symptom scores (recognition). Regression analyses revealed that individuals with higher PTSD scores and greater fearful-avoidant attachment tendencies showed less proficient memory monitoring for CSA lists. Implications for trauma and memory development and for translational research are discussed.

The ability to effectively regulate emotions and a secure attachment style are critical for maintaining mental health across the life span. The experience of childhood maltreatment interferes with normal development of emotional regulation and dramatically increases risk for a wide range of psychiatric disorders in adulthood. The central nervous system oxytocin systems are critically involved in mediating social attachment and buffering psychophysiological responses to stress. We therefore investigated the impact of childhood maltreatment and an oxytocin receptor (OXTR) single nucleotide polymorphism (rs53576) and their interaction on emotional dysregulation and attachment style in adulthood in a sample of low-income, African American men and women recruited from primary care clinics of an urban, public hospital. Consistent with prior research, we found that the severity of childhood maltreatment was associated with increased levels of emotional dysregulation in adulthood. Childhood maltreatment was also positively associated with ratings of disorganized/unresolved adult attachment style and negatively associated with ratings of secure adult attachment style. There was no direct association between rs53576 and emotional dysregulation or ratings of adult attachment style. However, there were significant interactions between rs53576 and childhood maltreatment in predicting level of adult emotional dysregulation and attachment style. Specifically, G/G genotype carriers were at risk for increased emotional dysregulation when exposed to three or more categories of childhood abuse. In addition, G/G genotype carriers exhibited enhanced disorganized adult attachment style when exposed to severe childhood abuse compared to A/A and A/G carriers. Our findings suggest that A allele carriers of OXTR rs53576 are resilient against the effects of severe childhood adversity, by protection against emotional dysregulation and disorganized attachment.

This is a report on the research design and findings of a 23-year longitudinal study of the impact of intrafamilial sexual abuse on female development. The conceptual framework integrated concepts of psychological adjustment with theory regarding how psychobiological factors might impact development. Participants included 6- to 16-year-old females with substantiated sexual abuse and a demographically similar comparison group. A cross-sequential design was used and six assessments have taken place, with participants at median age 11 at the first assessment and median age 25 at the sixth assessment. Mothers of participants took part in the early assessments and offspring took part at the sixth assessment. Results of many analyses, both within circumscribed developmental stages and across development, indicated that sexually abused females (on average) showed deleterious sequelae across a host of biopsychosocial domains including: earlier onsets of puberty, cognitive deficits, depression, dissociative symptoms, maladaptive sexual development, hypothalamic–pituitary–adrenal attenuation, asymmetrical stress responses, high rates of obesity, more major illnesses and healthcare utilization, dropping out of high school, persistent posttraumatic stress disorder, self-mutilation, Diagnostic and Statistical Manual of Mental Disorders diagnoses, physical and sexual revictimization, premature deliveries, teen motherhood, drug and alcohol abuse, and domestic violence. Offspring born to abused mothers were at increased risk for child maltreatment and overall maldevelopment. There was also a pattern of considerable within group variability. Based on this complex network of findings, implications for optimal treatments are elucidated. Translational aspects of extending observational research into clinical practice are discussed in terms that will likely have a sustained impact on several major public health initiatives.

The effects of childhood abuse are diverse, and although pathology is not the only outcome, psychiatric illness, including posttraumatic stress disorder (PTSD), can develop. However, adult PTSD is less common among those who experienced single-event traumas as children than it is among those who experienced childhood abuse. In addition, PTSD is more common among adults than children who experienced childhood abuse. Such evidence raises doubt about the direct, causal link between childhood trauma and adult PTSD. The experience of childhood trauma, and in particular abuse, has been identified as a risk factor for subsequent development of PTSD following exposure to adult trauma, and a substantial literature identifies revictimization as a factor that plays a pivotal role in this trajectory. The literature on the developmental effects of childhood abuse and pathways to revictimization, when considered in tandem with the biological effects of early stress in animal models, may provide some explanations for this. Specifically, it seems possible that permanent sensitization of the hypothalamic–pituitary–adrenal axis and behavioral outcomes are a consequence of childhood abuse, and these combine with the impact of retraumatization to sustain, perpetuate, and amplify symptomatology of those exposed to maltreatment in childhood.

This article delineates parallel frameworks that grew out of the research on risk and resilience over the past four decades, a framework for research and a framework for practice, and then discusses the promise of an emerging synthesis. The research framework defined the meaning, models, and methods that successfully guided four waves of research to date on the nature and processes involved in human resilience. The applied framework emerged in response to urgent needs of children and families faced by adversity and those charged with helping them, resulting in guidelines for translating the unfolding but incomplete research evidence into action. The application of a resilience approach transformed practice in many fields concerned with promoting resilience in people at risk for problems, revolutionizing the mission, models, measures, and methods of practice to align with the emphasis on positive adaptation and strengths defining a resilience-based approach. Yet these interventions rarely translated back to inform and refine resilience theory in ways that would accelerate progress to promote resilience more effectively. The concluding section on translational synergy discusses the potential for a synthesis of basic and applied resilience frameworks as the next steps toward realizing the original objective and promise of resilience science.

The maternal experience of stressful events during pregnancy has been associated with a number of adverse consequences for behavioral development in offspring, but the measurement and interpretation of prenatal stress varies among reported studies. The Raine Study recruited 2900 pregnancies and recorded life stress events experienced by 18 and 34 weeks' gestation along with numerous sociodemographic data. The mother's exposure to life stress events was further documented when the children were followed-up in conjunction with behavioral assessments at ages 2, 5, 8, 10, and 14 years using the Child Behavior Checklist. The maternal experience of multiple stressful events during pregnancy was associated with subsequent behavioral problems for offspring. Independent (e.g., death of a relative, job loss) and dependent stress events (e.g., financial problems, marital problems) were both significantly associated with a greater incidence of mental health morbidity between age 2 and 14 years. Exposure to stressful events in the first 18 weeks of pregnancy showed similar associations with subsequent total and externalizing morbidity to events reported at 34 weeks of gestation. These results were independent of postnatal stress exposure. Improved support for women with chronic stress exposure during pregnancy may improve the mental health of their offspring in later life.

We investigated the effects of timing and the course of maternal perinatal depressive symptoms on mother–infant hypothalamic–pituitary–adrenal (HPA) response profiles during an attachment stressor, as well as on within-dyad synchrony of stress profiles: coordination of HPA and sympathetic nervous system and infant–mother HPA attunement. Mothers (n = 86) completed the Center for Epidemiological Studies Depression Scale during pregnancy (Time 1 [T1]) and at 5 months (T2) and 18 months (T3) postnatal. At T3 mother–infant dyads completed the Strange Situation, and four saliva samples collected from both mothers and infants were assayed for cortisol and α-amylase. Hierarchical linear modeling was used to predict mother–infant cortisol response trajectories and within-dyad synchronies by main and interactive effects of T1–T3 Center for Epidemiological Studies Depression Scale scores. Main effects of earlier (T1, T2) depressive symptoms predicted mothers' cortisol trajectories and coordination, and interactions of T1 with postnatal (T2 and T3) symptoms predicted infants' cortisol trajectories, coordination, and attunement. Decomposition of interactions revealed more marked effects on infant cortisol trajectories when the mother shifted from higher to lower depressive symptoms (or vice versa) across the perinatal period. Shifts from lower to higher symptoms also predicted inverse coordination of cortisol with salivary α-amylase and greater attunement of infant with mother cortisol. Implications for the development and transmission of stress dysregulation are discussed.

This study examined the role of maternal psychopathology and maternal warmth as mediators of the association between prenatal cocaine and other substance exposure and toddler behavior problems. It was also hypothesized that infant cortisol reactivity and environmental risk may moderate these associations. Participants were 220 caregiver–infant dyads (119 cocaine exposed, 101 not cocaine exposed; 49% boys). Mother–infant dyads were recruited at delivery with assessments at 4–8 weeks and 7, 13, and 18 months of child ages. Results yielded no direct associations between prenatal cocaine/other substance exposure and toddler behavior problems, but significant indirect associations between prenatal cigarette/alcohol exposure and toddler behavior problems at 18 months. With regard to moderation, results indicated an indirect association between prenatal cocaine exposure and toddler behavior problems via lower maternal warmth for children with higher, but not lower, cortisol reactivity at 7 months. Results suggest potential pathways to toddler behavior problems among children at high biological risk.

Researchers have long been interested in whether particular temperamental traits in childhood connote risk for depressive disorders. For example, children characterized as having high negative emotionality (NE; sadness, fear, anger) and low positive emotionality (PE; anhedonia, listlessness, and lack of enthusiasm) are hypothesized to be at risk for depression. Few studies, however, have examined whether (and how) these two temperamental dimensions interact to confer risk. In a sample of 329 preschoolers, the present study addressed this question by examining the relation between PE and NE and asymmetry in resting EEG activity in frontal and posterior regions, which are putative biomarkers for depression. Using a laboratory battery to define temperament, we found an interaction of PE and NE on posterior asymmetry. Specifically, when PE was high, NE was associated with greater relative right activity. When PE was low, NE was not related to posterior asymmetry. These results were driven by differences in EEG activity in right posterior regions, an area associated with emotional processing and arousal, and were specific to girls. We found no relation between temperament and frontal asymmetry. These findings suggest that, at least for girls, PE and NE may have an interactive effect on risk for depression.

The current study explored longitudinal associations between interparental aggression, the development of child attention skills, and early childhood behavior problems in a diverse sample of 636 families living in predominately low-income, nonmetropolitan communities. The results of latent-variable, cross-lagged longitudinal models revealed that maternal-reported interparental aggression in infancy predicted reduced observed attention skills in toddlerhood; no association was observed, however, between attention in infancy and interparental aggression during the toddler years. Further, reduced toddler attention and high interparental aggression were both associated with increased risk for attention-deficit/hyperactivity disorder symptoms and conduct problems at 3 years of age. Processes largely operated in similar ways regardless of child gender or low-income status, although a few differences were observed. Overall, the results suggest that interparental aggression undermines attention development, putting children's early behavioral adjustment at risk.

Parent–child dyadic rigidity and negative affect contribute to children's higher levels of externalizing problems. The present longitudinal study examined whether the opposite constructs of dyadic flexibility and positive affect predicted lower levels of externalizing behavior problems across the early childhood period. Mother–child (N = 163) and father–child (n = 94) dyads engaged in a challenging block design task at home when children were 3 years old. Dynamic systems methods were used to derive dyadic positive affect and three indicators of dyadic flexibility (range, dispersion, and transitions) from observational coding. We hypothesized that the interaction between dyadic flexibility and positive affect would predict lower levels of externalizing problems at age 5.5 years as rated by mothers and teachers, controlling for stability in externalizing problems, task time, child gender, and the child's effortful control. The hypothesis was supported in predicting teacher ratings of child externalizing from both mother–child and father–child interactions. There were also differential main effects for mothers and fathers: mother–child flexibility was detrimental and father–child flexibility was beneficial for child outcomes. Results support the inclusion of adaptive and dynamic parent–child coregulation processes in the study of children's early disruptive behavior.

The goal of the study was to examine several factors that may explain the development of anxiety symptoms in middle childhood. Using data from the NICHD Study of Early Child Care (n = 1,364 families), we examined mother–child relationships, other aspects of family context, and child characteristics as predictors of anxiety in preadolescence. Latent growth curve analyses revealed that children who were more anxious at the beginning of middle childhood had been more behaviorally inhibited as preschoolers, and in middle childhood lived in families who experienced more negative life events and had mothers who were more anxious. Children who became more anxious across middle childhood were less behaviorally inhibited as preschoolers and in middle childhood perceived less security in their attachments to their mothers, experienced more negative life events, and had mothers who were more anxious. The findings illustrate the need to include a broad set of risk factors in etiological models of anxiety. In addition, the evidence for cumulative effects suggests several possible points of intervention with anxious children and their parents.

We examined Genotype × Environment (G × E) interactions between children's genotypes (the serotonin transporter linked promoter region [5-HTTLPR] gene) and maternal responsive care observed at 15, 25, 38, and 52 months on three aspects of children's competence at 67 months: academic skills and school engagement, social functioning with peers, and moral internalization that encompassed prosocial moral cognition and the moral self. Academic and social competence outcomes were reported by both parents, and moral internalization was observed in children's narratives elicited by hypothetical stories and in a puppet interview. Analyses revealed robust G × E interactions, such that children's genotype moderated the effects of maternal responsive care on all aspects of children's competence. Among children with a short 5-HTTLPR allele (ss/sl), those whose mothers were more responsive were significantly more competent than those whose mothers were less responsive. Responsiveness had no effect for children with two long alleles (ll). For academic and social competence, the G × E interactions resembled the diathesis–stress model: ss/sl children of unresponsive mothers had particularly unfavorable outcomes, but ss/sl children of responsive mothers had no worse outcomes than ll children. For moral internalization, the G × E interaction reflected the differential susceptibility model: whereas ss/sl children of unresponsive mothers again had particularly unfavorable outcomes, ss/sl children of responsive mothers had significantly better outcomes than ll children.

This study examined the prospective relations of adolescents' perceptions of discrimination and their genetic status with increases in conduct problems. Participants were 461 African American youths residing in rural Georgia (Wave 1 mean age = 15.5 years) who provided three waves of data and a saliva sample from which a polymorphism in the SCL6A4 (serotonin transporter [5-HTT]) gene polymorphism known as the 5-HTT linked promoter region (5-HTTLPR) was genotyped. Data analyses using growth curve modeling indicated that perceived discrimination was significantly related to the slope of conduct problems. As hypothesized, interactions between perceived discrimination and genetic status emerged for male but not female youths. Compared with those carrying two copies of the long allele variant of 5-HTTLPR, male youths carrying one or two copies of its short allele variant evinced higher rates of conduct problems over time when they perceived high levels of racial discrimination. These findings are consistent with resilience and differential susceptibility propositions stating that genes can both foster sensitivity to adverse events and confer protection from those events.

This study focuses on the association between language skills and core cognitive processes relative to the duration of institutionalization in children adopted from orphanages abroad. Participants in the adoptive group (n = 46) had arrived in the United States between the ages of 2 and 84 months (mean = 24 months), and had been living in the United States for 1–9 years. Drawing on both experimental and standardized assessments, language skills of the international adoptees differed as a function of length of time spent in an institution and from those of 24 nonadopted controls. Top-down cognitive assessments including measures of explicit memory and cognitive control differed between adopted and nonadopted children, yet differences between groups in bottom-up implicit learning processes were unremarkable. Based on the present findings, we propose a speculative model linking language and cognitive changes to underlying neural circuitry alterations that reflect the impact of chronic stress, due to adoptees' experience of noncontingent, nonindividualized caregiving. Thus, the present study provides support for a relationship between domain-general cognitive processes and language acquisition, and describes a potential mechanism by which language skills are affected by institutionalization.