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.

How do exposures to stress affect biobehavioral development and, through it, psychiatric and biomedical disorder? In the health sciences, the allostatic load model provides a widely accepted answer to this question: stress responses, while essential for survival, have negative long-term effects that promote illness. Thus, the benefits of mounting repeated biological responses to threat are traded off against costs to mental and physical health. The adaptive calibration model, an evolutionary–developmental theory of stress–health relations, extends this logic by conceptualizing these trade-offs as decision nodes in allocation of resources. Each decision node influences the next in a chain of resource allocations that become instantiated in the regulatory parameters of stress response systems. Over development, these parameters filter and embed information about key dimensions of environmental stress and support, mediating the organism's openness to environmental inputs, and function to regulate life history strategies to match those dimensions. Drawing on the adaptive calibration model, we propose that consideration of biological fitness trade-offs, as delineated by life history theory, is needed to more fully explain the complex relations between developmental exposures to stress, stress responsivity, behavioral strategies, and health. We conclude that the adaptive calibration model and allostatic load model are only partially complementary and, in some cases, support different approaches to intervention. In the long run, the field may be better served by a model informed by life history theory that addresses the adaptive role of stress response systems in regulating alternative developmental pathways.

We hypothesized that presence of the short allele in the promoter region of the serotonin transporter would moderate the effect of early cumulative socioeconomic status (SES) risk on epigenetic change among African American youth. Contrasting hypotheses regarding the shape of the interaction effect were generated using vulnerability and susceptibility frameworks and applied to data from a sample of 388 African American youth. Early cumulative SES risk assessed at 11–13 years based on parent report interacted with presence of the short allele to predict differential methylation assessed at age 19. Across multiple tests, a differential susceptibility perspective rather than a diathesis–stress framework best fit the data for genes associated with depression, consistently demonstrating greater epigenetic response to early cumulative SES risk among short allele carriers. A pattern consistent with greater impact among short allele carriers also was observed using all cytosine nucleotide–phosphate–guanine nucleotide sites across the genome that were differentially affected by early cumulative SES risk. We conclude that the short allele is associated with increased responsiveness to early cumulative SES risk among African American youth, leading to epigenetic divergence for depression-related genes in response to exposure to heightened SES risk among short allele carriers in a “for better” or “for worse” pattern.

This study examined contextual factors (caregiver depression, family resources, ethnicity, and initial levels of youth problem behavior) related to the effectiveness of the Family Check-Up (FCU) and evaluated family processes as a mediator of FCU intervention response and adolescent antisocial behavior. We followed a sample of 180 ethnically diverse youths of families who engaged in the FCU intervention. Family data were collected as part of the FCU assessment, and youth data were collected over 4 years, from sixth through ninth grade. Findings indicated that caregiver depression and minority status predicted greater caregiver motivation to change. In turn, caregiver motivation was the only direct predictor of FCU intervention response during a 1-year period. Growth in family conflict from sixth through eighth grade mediated the link between FCU response and ninth-grade antisocial behavior. This study explicitly tested core aspects of the FCU intervention model and demonstrated that caregiver motivation is a central factor that underlies family response to the FCU. The study also provided support for continued examination of family process mechanisms that account for enduring effects of the FCU and other family-centered interventions.

The co-occurrence of child conduct problems (CPs) and callous–unemotional (CU) traits confers risk for psychopathy. The oxytocin (OXT) system is a likely candidate for involvement in the development of psychopathy. We tested variations in the OXT receptor gene (OXTR) in CP children and adolescents with varying levels of CU traits. Two samples of Caucasian children, aged 4–16 years, who met DSM criteria for disruptive behavior problems and had no features of autism spectrum disorder, were stratified into low versus high CU traits. Measures were the frequencies of nine candidate OXTR polymorphisms (single nucleotide polymorphisms). In Sample 1, high CU traits were associated with single nucleotide polymorphism rs1042778 in the 3′ untranslated region of OXTR and the CGCT haplotype of rs2268490, rs2254298, rs237889, and rs13316193. The association of rs1042778 was replicated in the second rural sample and held across gender and child versus adolescent age groups. We conclude that polymorphic variation of the OXTR characterizes children with high levels of CU traits and CPs. The results are consistent with a hypothesized role of OXT in the developmental antecedents of psychopathy, particularly the differential amygdala activation model of psychopathic traits, and add genetic evidence that high CU traits specify a distinct subgroup within CP children.

The aim of this study was to examine if family system dynamics (e.g., parent mental health, marriage quality, conflict, and cohesion) that have often been overlooked when studying Latino families play a more important role in predicting adolescent internalizing symptoms than acculturation processes. Data comes from the Latino Acculturation and Health Project, a longitudinal investigation of acculturation in Latino families in North Carolina and Arizona (Smokowski & Bacallao, 2006, 2010). Researchers conducted in-depth, community-based interviews with 258 Latino adolescents and 258 of their parents in metropolitan, small-town, and rural areas. Interviews were conducted at four time points at intervals of approximately 6 months. Parent and adolescent ratings of the adolescent's internalizing symptoms were used as the dependent variable in a longitudinal hierarchical linear model with a rater effects structure. Results showed that parent–adolescent conflict and parent mental health (fear/avoidance of social situations and humiliation sensitivity) were significant predictors of adolescent internalizing symptoms. Acculturation scales were not significant predictors; however, internalizing symptoms decreased with time spent in the United States. Females and adolescents from lower socioeconomic status families reported more internalizing symptoms, while participants who had been in the United States longer reported fewer internalizing symptoms. Implications were discussed.

This study examined whether parents’ social information processing was related to their subsequent reports of their harsh discipline. Interviews were conducted with mothers (n = 1,277) and fathers (n = 1,030) of children in 1,297 families in nine countries (China, Colombia, Italy, Jordan, Kenya, the Philippines, Sweden, Thailand, and the United States), initially when children were 7 to 9 years old and again 1 year later. Structural equation models showed that parents’ positive evaluations of aggressive responses to hypothetical childrearing vignettes at Time 1 predicted parents’ self-reported harsh physical and nonphysical discipline at Time 2. This link was consistent across mothers and fathers, and across the nine countries, providing support for the universality of the link between positive evaluations of harsh discipline and parents’ aggressive behavior toward children. The results suggest that international efforts to eliminate violence toward children could target parents’ beliefs about the acceptability and advisability of using harsh physical and nonphysical forms of discipline.

Children born prematurely at very low birth weight (<1500 g) are at increased risk for impairments affecting social functioning, including autism spectrum disorders (e.g., Johnson et al., 2010). In the current study, we used the Happé–Frith animated triangles task (Abell, Happé, & Frith, 2000) to study social attribution skills in this population. In this task, typical viewers attribute intentionality and mental states to shapes, based on characteristics of their movements. Participants included 34 preterm children and 36 full-term controls, aged 8–11 years. Groups were comparable in terms of age at test, gender, handedness, and socioeconomic status; they also performed similarly on tests of selective attention/processing speed and verbal intelligence. Relative to full-term peers, preterm children's descriptions of the animations were less appropriate overall; they also overattributed intentionality/mental states to randomly moving shapes and underattributed intentionality/mental states to shapes that seemed to be interacting socially. Impairments in the ability to infer the putative mental states of triangles from movement cues alone were most evident in children displaying more “autistic-like” traits, and this may reflect atypical development of and/or functioning in, or atypical connections between, parts of the social brain.

A short-term longitudinal study during early childhood (N = 301; 155 girls; M = 44.76 months old, SD = 8.20) investigated the prospective associations between peer victimization and aggression subtypes. Specifically, observations of relational and physical victimization as well as teacher reports of the forms (i.e., relational and physical) and functions (i.e., proactive and reactive) of aggression were collected at two time points during an academic year. Within- and between-group gender differences were examined as part of the preliminary analyses. In order to address key study questions, both directions of effect between peer victimization and aggression subtypes were examined. We found that teacher-reported proactive relational aggression predicted decreases in observed relational victimization over time, whereas reactive relational aggression predicted increases in observed relational victimization over time. Ways in which these and other findings extend the literature are discussed.

Alterations of the glucocorticoid system and of hippocampal volumes have consistently been reported in patients with major depressive disorders (MDD). The aim of the present study was to investigate whether the messenger RNA (mRNA) expression of glucocorticoid inducible genes is associated with changes in the cornu ammonis (CA) and dentate gyrus subfields. Forty-three patients with MDD and 43 healthy controls were recruited and investigated with high resolution magnetic resonance imaging. Hippocampal subfields were measured using freesurfer. Measurement of whole blood mRNA expression of glucocorticoid inducible genes serum and glucocorticoid-regulated kinase 1 (SGK1), FK506 binding protein 5 (FKBP5), and glucocorticoid induced leucine zipper (GILZ) was performed. Patients with MDD had significantly smaller volumes of CA1, CA2/3, CA4/DG, and subiculum compared to healthy controls. In the regression analysis, the factor diagnosis had a significant moderating effect on the association of SGK1 and hippocampal volumes. Patients with low expression of SGK1 had significantly smaller CA2/3 and CA4/DG volumes compared to patients with high expression of SGK1 mRNA and to healthy controls with low/high expression of SGK1, respectively. Therefore, a lack of mRNA expression of glucocorticoid inducible genes in patients with MDD that seems to correspond to a blunted cortisol response is associated with smaller hippocampal CA and dentate gyrus volumes. SGK1 seems to be particularly relevant for stress-related mental disorders.

This study utilized structural equation modeling to examine the associations among parental guilt induction (a form of psychological control), youth cognitive style, and youth internalizing symptoms, with parents and youth participating in a randomized controlled trial of a family-based group cognitive–behavioral preventive intervention targeting families with a history of caregiver depression. The authors present separate models utilizing parent report and youth report of internalizing symptoms. Findings suggest that families in the active condition (family-based group cognitive–behavioral group) relative to the comparison condition showed a significant decline in parent use of guilt induction at the conclusion of the intervention (6 months postbaseline). Furthermore, reductions in parental guilt induction at 6 months were associated with significantly lower levels of youth negative cognitive style at 12 months. Finally, reductions in parental use of guilt induction were associated with lower youth internalizing symptoms 1 year following the conclusion of the intervention (18 months postbaseline).

Neurobehavioral disinhibition (ND) is a complex condition reflecting a wide range of problems involving difficulties with emotion regulation and behavior control. Respiratory sinus arrhythmia (RSA) is a physiological correlate of emotion regulation that has been studied in a variety of at-risk populations; however, there are no studies of RSA in children with ND. Data were drawn from a prospective longitudinal study of prenatal substance exposure that included 1,073 participants. Baseline RSA and RSA reactivity to an attention-demanding task were assessed at 3, 4, 5, and 6 years. ND was assessed at ages 8/9, 11, and 13/14 years via behavioral dysregulation and executive dysfunction composite measures. Greater exposure to early adversity was related to less RSA reactivity at 3 years, increases in RSA reactivity from ages 3 to 6 years, and increased behavioral dysregulation from ages 8/9 to 13/14. RSA reactivity was examined as a moderator of the association between early adversity and changes in ND. A significant Early Adversity × RSA Reactivity quadratic interaction revealed that children with decelerations in RSA reactivity exhibited increases in behavioral dysregulation, regardless of their exposure to early adversity. However, greater exposure to early adversity was related to greater increases in behavioral dysregulation, but only if children exhibited accelerations in RSA reactivity from ages 3 to 6 years. The results contribute to our understanding of how interactions across multiple levels of analysis contribute to the development of ND.

Child conduct problems (CPs) are a robust predictor of adult mental health; the concurrence of callous–unemotional (CU) traits confers specific risk for psychopathy. Psychopathy may be related to disturbances in the oxytocin (OXT) system. Evidence suggests that epigenetic changes in the OXT receptor gene (OXTR) are associated with lower circulating OXT and social–cognitive difficulties. We tested methylation levels of OXTR in 4- to 16-year-old males who met DSM criteria for a diagnosis of oppositional–defiant or conduct disorder and were stratified by CU traits and age. Measures were DNA methylation levels of six CpG sites in the promoter region of the OXTR gene (where a CpG site is a cytosine nucleotide occurs next to a guanine nucleotide in the linear sequence of bases along its lenth, linked together by phosphate binding), and OXT blood levels. High CU traits were associated with greater methylation of the OXTR gene for two cytosine nucleotide and guanine nucleotide phosphate linked sites and lower circulating OXT in older males. Higher methylation correlated with lower OXT levels. We conclude that greater methylation of OXTR characterizes adolescent males with high levels of CU and CPs, and this methylation is associated with lower circulating OXT and functional impairment in interpersonal empathy. The results add genetic evidence that high CU traits specify a distinct subgroup within CP children, and they suggest models of psychopathy may be informed by further identification of these epigenetic processes and their functional significance.

Evidence for the intergenerational transmission of posttraumatic stress disorder (PTSD) is documented in the literature, although the underlying mechanisms are poorly understood. Attachment theory provides a framework for elucidating the ways in which maternal PTSD may increase offspring PTSD vulnerability. The current study utilized two independent prospective data sets to test the hypotheses that (a) maternal PTSD increases the probability of developing an insecure mother–infant attachment relationship and (b) an insecure mother–infant attachment relationship increases the risk of developing PTSD following trauma exposure in later life. In the first study of urban, primarily low-income ethnic/racial minority mothers and infants (N = 45 dyads), elevated maternal PTSD symptoms at 6 months were associated with increased risk for an insecure, particularly disorganized, mother–infant attachment relationship at 13 months. In the second birth cohort of urban, low-income mothers and children (N = 96 dyads), insecure (avoidant or resistant) attachment in infancy was associated in a dose–response manner with increased lifetime risk for a diagnosis of PTSD by adolescence. A history of disorganized attachment in infancy predicted severity of PTSD symptoms, including reexperiencing, avoidance, hyperarousal, and total symptoms, at 17.5 years. In both studies, associations between attachment and PTSD were not attributable to numerous co-occurring risk factors. The findings suggest that promoting positive mother–child relationships in early development, particularly in populations at high risk for trauma exposure, may reduce the incidence of PTSD.

Genetic moderation of the effects of child maltreatment on depression and internalizing symptoms was investigated in a sample of low-income maltreated and nonmaltreated African American children (N = 1,096). Lifetime child maltreatment experiences were independently coded from Child Protective Services records and maternal report. Child depression and internalizing problems were assessed in the context of a summer research camp by self-report on the Children's Depression Inventory and adult counselor report on the Teacher Report Form. DNA was obtained from buccal cell or saliva samples and genotyped for polymorphisms of the following genes: serotonin transporter linked polymorphic region (5-HTTLPR), brain-derived neurotrophic factor (BDNF), norepinephrine transporter, and corticotropin releasing hormone receptor 1. Analyses of covariance with age and gender as covariates were conducted, with maltreatment status and respective polymorphism as main effects and their Gene × Environment (G × E) interactions. Maltreatment consistently was associated with higher Children's Depression Inventory and Teacher Report Form symptoms. The results for child self-report symptoms indicated a G × E interaction for BDNF and maltreatment. In addition, BDNF and triallelic 5-HTTLPR interacted with child maltreatment in a G × G × E interaction. Analyses for counselor report of child anxiety/depression symptoms on the Teacher Report Form indicated moderation of child maltreatment effects by triallelic 5-HTTLPR. These effects were elaborated based on variation in developmental timing of maltreatment experiences. Norepinephrine transporter was found to further moderate the G × E interaction of 5-HTTLPR and maltreatment status, revealing a G × G × E interaction. This G × G × E was extended by consideration of variation in maltreatment subtype experiences. Finally, G × G × E effects were observed for the co-action of BDNF and the corticotropin releasing hormone receptor 1 haplotype. The findings illustrate the variable influence of specific genotypes in G × E interactions based on variation in maltreatment experiences and the importance of a multigenic approach for understanding influences on depression and internalizing symptoms among African American children.

A vast body of literature shows that maternal depression has long-term adverse consequences for children. However, only very few studies have documented the effect of maternal depression on children's ability to process emotional expressions and even fewer incorporated measures of observed maternal sensitivity to further tease apart whether it is the symptoms per se or the associated impact via maternal sensitivity that affects children's developing emotion-processing abilities. In a large community sample of Dutch preschoolers (N = 770), we examined independent and mediated effects of maternal depressive symptoms and sensitivity on children's ability to recognize emotional expressions using a nonverbal and a verbal task paradigm. Maternal depressive symptoms predicted less accurate emotion labeling in children, while maternal sensitivity was associated with more accurate emotion matching, especially for sadness and anger. Maternal sensitivity did not mediate the observed associations between mothers’ depressive symptoms and children's emotion recognition, and effects were similar for boys and girls. Given that maternal depressive symptoms and sensitivity affected nonoverlapping areas of young children's emotion recognition, prevention and intervention efforts should focus on both alleviating maternal depressive symptoms and improving maternal sensitivity at the same time in order to maximize benefit.

The emergence and persistence of conduct problems (CPs) during early childhood is a robust predictor of behavior problems in school and of future maladaptation. In this study we examined the reciprocal influences between observed coercive interactions between children and caregivers, oppositional and aggressive behavior, and growth in parent report of early childhood (ages 2–5) and school-age CPs (ages 7.5 and 8.5). Participants were drawn from the Early Steps multisite randomized prevention trial that includes an ethnically diverse sample of male and female children and their families (N = 731). A parallel-process growth model combining latent trajectory and cross-lagged approaches revealed the amplifying effect of observed coercive caregiver–child interactions on children's noncompliance, whereas child oppositional and aggressive behaviors did not consistently predict increased coercion. The slope and initial levels of child oppositional and aggressive behaviors and the stability of caregiver–child coercion were predictive of teacher-reported oppositional behavior at school age. Families assigned to the Family Check-Up condition had significantly steeper declines in child oppositional and aggressive behavior and moderate reductions in oppositional behavior in school and in coercion at age 3. Results were not moderated by child gender, race/ethnicity, or assignment to the intervention condition. The implications of these findings are discussed with respect to understanding the early development of CPs and to designing optimal strategies for reducing problem behavior in early childhood with families most in need.

The purpose of the present investigation was to examine the association between physiological reactivity to peer stressors and physical and relational aggression. Potential moderation by actual experiences of peer maltreatment (i.e., physical and relational victimization) and gender were also explored. One hundred ninety-six children (M = 10.11 years, SD = 0.64) participated in a laboratory stress protocol during which their systolic blood pressure, diastolic blood pressure, and skin conductance reactivity to recounting a relational stressor (e.g., threats to relationships) and an instrumental stressor (e.g., threats to physical well-being, dominance, or property) were assessed. Teachers provided reports of aggression and victimization. In both boys and girls, physical aggression was associated with blunted physiological reactivity to relational stress and heightened physiological reactivity to instrumental stress, particularly among youth higher in victimization. In girls, relational aggression was most robustly associated with blunted physiological reactivity to relational stressors, particularly among girls exhibiting higher levels of relational victimization. In boys, relational aggression was associated with heightened physiological reactivity to both types of stressors at higher levels of peer victimization and blunted physiological reactivity to both types of stressors at lower levels of victimization. Results underscore the shared and distinct emotional processes underlying physical and relational aggression in boys and girls.