Children entering out-of-home (OoH) care have often experienced multiple forms of maltreatment and are at risk of psychiatric disorder and poor long-term outcome. Recent evidence shows high rates of disinhibited attachment disorder (DAD) among maltreated adolescents in UK OoH care (Kay & Green, 2013). This study aimed to further understand the mechanisms of outcome in this group through investigation of social cognitive functioning. Patterns of theory of mind (ToM) and social information processing were assessed alongside DAD behavior and psychopathology in 63 adolescents in UK OoH care (mean age = 176 months, SD = 22; 48% male; 89% White British) and 69 low-risk comparison adolescents (mean age = 171 months, SD = 17; 46% male; 87% White British). Compared to low risk, OoH adolescents showed a hostile attribution bias and ToM deficit, but this was confounded by language ability. ToM was associated with reduced hostile attribution and responding biases and increased social competence, which was further associated with lower levels of externalizing psychopathology. There was no association between social cognition and core features of DAD. Social cognitive deficits and biases may play a role in the high rates of externalizing psychopathology and relationship functioning difficulties in maltreated samples. Future research should assess alternative cognitive mechanisms for DAD.

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.

The effects of divorce on children's behavioral development have proven to be quite varied across studies, and most developmental and family scholars today appreciate the great heterogeneity in divorce effects. Thus, this inquiry sought to determine whether select dopaminergic genes previously associated with externalizing behavior and/or found to moderate diverse environmental effects (dopamine receptors D2 and D4, catechol-O-methyltransferase) might moderate divorce effects on adolescent self-reported externalizing problems; and, if so, whether evidence of gene–environment (G × E) interaction would prove consistent with diathesis–stress or differential-susceptibility models of environmental action. Data from the first and third wave of the Dutch Tracking Adolescents' Individual Lives Survey (n = 1,134) revealed some evidence of G × E interaction reflecting diathesis–stress but not differential susceptibility. It is intriguing that some evidence pointed to “vantage sensitivity,” which are benefits accruing to those with a specific genotype when their parents remained together, the exact opposite of diathesis–stress. The limits of this work are considered, especially with regard to the conditions for testing differential susceptibility, and future directions are outlined.

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.

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 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.

Throughout the life span, exposure to chronic stress such as child maltreatment is thought to contribute to future dysfunction of the stress response system (SRS) through the process of adaptive calibration. Dysfunction of the SRS is associated with numerous health and behavior problems, so it is important to understand under what conditions and what time frame adaptive calibration occurs. The present study tested for adaptive calibration of the SRS in a sample of maltreated (n = 303) and nonmaltreated (n = 151) youth during the important developmental period of adolescence. Data were used from Waves 2, 3, and 4 of a larger study of the consequences of maltreatment on health and well-being. At each time point, participants underwent the Trier Social Stress Test for Children and provided a baseline and four poststressor saliva samples to measure cortisol reactivity. Adaptive calibration was tested by performing a latent profile analysis using the five samples of salivary cortisol provided at each time point, and testing whether maltreatment status predicted the likelihood of profile membership at Time 2, Time 3, and Time 4. Three cortisol profiles emerged from the data at each time point (blunted, moderate, and elevated), and results indicated that maltreated youth were more likely than nonmaltreated youth to present with the blunted cortisol profile compared to the moderate and elevated profiles at Time 2 and Time 3, even after controlling for recent exposure to violence and trauma. At Time 4, there was no longer a difference in profile membership between maltreated and nonmaltreated youth, suggesting adaptive calibration may be a lengthy process requiring a period of years to become evident. Overall, the findings provide support for adaptive calibration and offer insight into the conditions under which adaptive calibration occurs.

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.

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.

Substantial evidence links socioeconomic status to internalizing and externalizing behavior problems. However, it is unclear how these two categories of behavior problems relate to specific components of socioeconomic status (e.g., income, educational attainment, and occupational prestige) or overall social status. In this study, we conducted a second-order meta-analysis to estimate the average associations of income, education, occupation, and overall socioeconomic status with internalizing and externalizing behavior problems, and to examine if age, sex, and race/ethnicity moderated these associations. Our systematic search in PsycINFO, PubMed, Google Scholar, Web of Science, and ProQuest Dissertations and Theses Global identified 12 meta-analyses (17% unpublished), including approximately 474 primary studies and 327,617 participants. In relation to internalizing, we found small average associations with income, r+ = –.18, 95% confidence interval (CI) [–.31, –.04], and education, r+ = –.12, 95% CI [–.15, –.09]. In relation to externalizing, we found smaller associations with income, r+ = –.02, 95% CI [–.15, .10], education, r+ = –.03, 95% CI [–.16, .10], and overall socioeconomic status, r+ = –.05, 95% CI [–.11, .01], but these CIs included zero. Only sex composition of the samples moderated the latter association. We provide recommendations for best practices and future research directions.

Relations of avoidant personality disorder (AvPD) with shyness and inhibition suggest that a precursor of AvPD is withdrawal. Using a sample of 4.5- to 7-year-olds studied four times, 2 years apart, four and three classes of children differing in trajectories of mother- and teacher-reported withdrawal, respectively, were identified. Mothers and teachers generally did not agree on children's trajectories but the pattern of findings in the two contexts did not differ markedly. The mother-identified high and declining withdrawal class, in comparison with less withdrawn classes, and the teacher-identified high and declining class compared with low withdrawal classes, were associated with relatively high levels of anger and low levels of attentional control and resiliency. The mother-identified moderate and increasing withdrawal class was distinguished from less problematic withdrawal classes by higher anger, lower resiliency, and sometimes, lower attentional control. The teacher-identified low and increasing withdrawal class was distinguished from less problematic withdrawal classes by lower resiliency and lower attentional control. Findings are discussed in terms of the developmental precursors to social withdrawal and avoidant behavior.

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.

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.

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.

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.

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.

Negative emotionality is a distinguishing feature of borderline personality disorder (BPD). However, this person-level characteristic has not been examined as a marker of vulnerability in the development of this disorder. The current study utilized a multimethod approach to examine the interplay between negative emotional reactivity and cumulative exposure to family adversity on the development of BPD symptoms across 3 years (ages 16–18) in a diverse, at-risk sample of adolescent girls (N = 113). A latent variable of negative emotional reactivity was created from multiple assessments at age 16: self-report, emotion ratings to stressors from ecological assessments across 1 week, and observer-rated negative affectivity during a mother–daughter conflict discussion task. Exposure to family adversity was measured cumulatively between ages 5 and 16 from annual assessments of family poverty, single parent household, and difficult life circumstances. The results from latent growth curve models demonstrated a significant interaction between negative emotional reactivity and family adversity, such that exposure to adversity strengthened the association between negative emotional reactivity and BPD symptoms. In addition, family adversity predicted increasing BPD symptoms during late adolescence. These findings highlight negative emotional reactivity as a marker of vulnerability that ultimately increases risk for the development of BPD symptoms.

The prevalence of depression rises steeply during adolescence. Family processes have been identified as one of the important factors that contribute to affect (dys)regulation during adolescence. In this study, we explored the affect expressed by mothers, fathers, and adolescents during a problem-solving interaction and investigated whether the patterns of the affective interactions differed between families with depressed adolescents and families with nondepressed adolescents. A network approach was used to depict the frequencies of different affects, concurrent expressions of affect, and the temporal sequencing of affective behaviors among family members. The findings show that families of depressed adolescents express more anger than families of nondepressed adolescents during the interaction. These expressions of anger co-occur and interact across time more often in families with a depressed adolescent than in other families, creating a more self-sustaining network of angry negative affect in depressed families. Moreover, parents’ angry and adolescents’ dysphoric affect follow each other more often in depressed families. Taken together, these patterns reveal a particular family dynamic that may contribute to vulnerability to, or maintenance of, adolescent depressive disorders. Our findings underline the importance of studying affective family interactions to understand adolescent depression.

The study was based on the assumption that stressors in the lives of pregnant and parenting women are processes that affect prenatal, postpartum, and concurrent maternal hormones and emotions and that these processes affect child temperament. The hypotheses were tested in a group of 67 young mothers and their 3-year-old children. Mothers were clustered into groups based on longitudinal patterns of hormones and emotions at prenatal, postpartum, and 3-year follow-up assessments. The analyses focused on relating maternal patterns of hormones and emotions to the child's temperament at age 3 years. Temperament was assessed by questionnaire and observation of behavior during a challenging situation. Illustrative findings included the following. Verbal aggression and nonverbal aggression were significantly higher in children of mothers in the low prenatal hormone cluster than children of mothers in the high prenatal hormone cluster. Children of mothers in the postpartum low testosterone (T), estradiol (E2), and androstenedione (Δ4-A) and medium cortisol (Cort) cluster (mainly low hormone cluster) exhibited significantly more physical aggression than children of mothers in the medium T and Δ4-A, high E2 and low Cort cluster. Maternal patterns of hormones, emotions, and parenting attitudes and practices were related to multiple aspects of temperament when the children were age 3 years. The findings support the important role of maternal biological and psychological processes in the development of child temperament.