Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.

Ninety-four low- and middle-income preschoolers (48 boys, 46 girls) were recruited from two sites in a large southwestern city. Children's positive attributions of peer intent, social problem-solving decisions, and attributions of peers' feelings about the provocation were evaluated from individual interviews. In addition, children's anger perception accuracy and their global emotion situation knowledge were assessed. Teachers and their assistants reported on the children's social competence, internalizing and externalizing behavior, and the degree to which children were physically and relationally victimized. Social competence was a negative predictor of relational and physical victimization, and externalizing behavior was a positive predictor of both types of victimization. Anger perception accuracy was negatively related to physical victimization, and global emotion situation knowledge and attributions of sorrow to provoking peers were positive predictors. Results support a conceptual framework that emphasizes the importance of social and emotion-related social cognitive variables for understanding young children's peer-related victimization.The authors thank the children and families for their participation and the preschool teachers for their cooperation. Thanks are also due to the many undergraduate and graduate students who helped with this research. Special thanks to Kimberly Estep and Courtney Hunter for their help with data collection and coding.

This article examines the relationship between coparenting and family-level processes during preschool and peer relationship outcomes in middle childhood, and the hypothesis that children's ability to regulate emotion (as indexed by basal vagal tone and the ability to suppress vagal tone) may moderate this relationship. We predicted that high vagal tone and a greater ability to suppress vagal tone would buffer children from the effects of negative coparenting and family processes. Results indicated that hostile–withdrawn coparenting predicted higher levels of conflicted play and lower levels of positive peer conversation. Vagal suppression also moderated the relationship between hostile–withdrawn coparenting and peer conflict. For children who were unable to suppress vagal tone, hostile–withdrawn coparenting was associated with higher levels of peer conflict, while for children who were able to suppress vagal tone there was no relationship hostile–withdrawn coparenting and peer conflict. The relationship between hostile–withdrawn coparenting and positive peer conversation was also moderated by children's ability to suppress vagal tone. For children who were unable to suppress vagal tone, there was no relationship between hostile–withdrawn coparenting and positive peer conversation, while for those who were able to suppress vagal tone, hostile–withdrawn coparenting was associated with less positive peer conversation. Cohesive family-level processes also predicted positive conversation in play at age 9 after controlling for positive conversation at age 5; however, this relationship was not moderated by vagal suppression. Basal vagal tone also did not function as a moderator of relations between hostile–withdrawn coparenting and peer play. Results are discussed in terms of the effects of negative coparenting on children with different patterns of modulating physiological arousal.This research was supported by a research grant from the National Institute of Mental Health to the second author (1 R01 49141). The authors thank the families involved for their participation.

Viewing social rejection from same-age peers as a source of stress for children, the current study sought to determine the most appropriate model of the effects of temporary versus consistent experiences with rejection for both short-term and long-term internalizing problems. Adopting a cross-sectional longitudinal design, the sociometric status of children in the first year of the study (when the children were in the first, second, or third grades), and then again in the next school year (when children were in the second, third, or fourth grades) was assessed to determine which children were rejected by their peers. Internalizing outcome measures were administered in the third and sixth years of follow-up. Results indicated that, for boys, the Threshold Model best represented the stressful effects of rejection. That is, only boys who were exposed to rejection for 2 consecutive years demonstrated both short-term and long-term internalizing problems in subsequent years. For girls, however, there appeared to be few significant differences among those who never experienced rejection, who had only temporary experiences with rejection, and girls who were consistently exposed to rejection. Results are discussed in terms of the significance of a Threshold Model as well as possible explanations for these gender differences.

Many children meet criteria for multiple Diagnostic and Statistical Manual (DSM) categories, such as oppositional defiant disorder (ODD) and conduct disorder (CD). If each disorder has been well validated as a separate entity, statistically significant co-occurrence of different disorders may be highly informative. However, ODD and CD have not been well validated as separate entities. The very high rate of overlap between diagnoses of ODD and CD may therefore arise artifactually from the lack of a valid distinction between them, rather than from potentially informative comorbidity between two different disorders. Empirical research strongly supports a distinction between two syndromes that correspond to subsets of the DSM-III-R criteria for CD. Designated as delinquent behavior and aggressive behavior, these syndromes have been found to differ in biological correlates, heritability, developmental stability, course, response to interventions, and long-term outcomes. At this stage of our knowledge, empirically based assessment and taxonomic methods can be especially useful for distinguishing between syndromes, deriving norms, doing longitudinal studies, and detecting patterns of comorbidity. These methods do not preclude categorical taxa, which can be formed by imposing cutpoints on the distributions of syndrome scores. Categorical taxa can also be formed by cluster analyzing profiles of syndrome scores. Accelerated longitudinal designs can bring multiple analyses to bear on empirically derived syndromes to test complex developmental relations more quickly and powerfully than can traditional longitudinal designs. Follow-ups of high-risk groups can identify variables that predict good versus poor outcomes if standardized baseline and outcome measures are used. Interventions for conduct problems should be designed to counteract the risk factors found to predict poor long-term outcomes.

The influences of three risk factors (insecure attachment, maternal depressive symptoms, and economic risk) on children's depressive symptomatology were examined. Subjects were 85 children from a range of income levels; all subjects were between 7 and 9 years of age. Children's depressive symptomatology was assessed with the Dimensions of Depression Profile for Children and Adolescents. Results indicated that children at high economic risk were more likely to exhibit depressive symptomatology than were children at low economic risk. Security of attachment was significantly related to children's depressive symptomatology. In addition, a significant relation was noted between children's depressive symptomatology and the depressive symptomatology of their mothers. Contrary to expectations, no significant relation was found between maternal depressive symptomatology and security of attachment. A multiple regression analysis revealed that security of attachment, maternal depressive symptomatology, and economic risk accounted for 47% of the variability in children's depression scores. Secure attachment served as a buffer; economic risk was associated with depressive symptoms only among insecurely attached children.

The development of joint attention skills is a major milestone of infancy. Recent research suggests that the development of these skills may be affected by disorganized (D) attachment. This hypothesis was examined in a longitudinal study of attachment and joint attention skill development in a sample of infants at risk for developmental–behavioral morbidity. The results revealed that toddlers with D classifications initiated joint attention with an experimenter significantly less often than did secure, or even other insecure, toddlers. However, no group differences in the capacity to respond to the joint attention bids of others were observed in this study. These data suggest that a disturbance in the tendency to initiate episodes of joint attention with others may be indicative of early social–cognitive and social–emotional disturbance among infants affected by disorganized attachment status. Theory and research is reviewed to suggest that an early impairment in joint attention facility may make a significant contribution to risk for negative cognitive and emotional outcomes among these infants.

The question of whether and how the effects of cultural trauma can be transmitted intergenerationally from parents to offspring, or even to later generations, has evoked interest and controversy in academic and popular forums. Recent methodological advances have spurred investigations of potential epigenetic mechanisms for this inheritance, representing an exciting area of emergent research. Epigenetics has been described as the means through which environmental influences “get under the skin,” directing transcriptional activity and influencing the expression or suppression of genes. Over the past decade, this complex environment–biology interface has shown increasing promise as a potential pathway for the intergenerational transmission of the effects of trauma. This article reviews challenges facing research on cultural trauma, biological findings in trauma and posttraumatic stress disorder, and putative epigenetic mechanisms for transmission of trauma effects, including through social, intrauterine, and gametic pathways. Implications for transmission of cultural trauma effects are discussed, focused on the relevance of cultural narratives and the possibilities of resilience and adaptivity.

This study examined the relationship between paternal alcoholism and toddler behavior problems from 18 to 36 months of age, as well as the potential moderating effects of 12-month infant–mother attachment security on this relationship. Children with alcoholic fathers had higher levels of internalizing and externalizing behavior than children of nonalcoholic fathers. Simple effects testing of an interaction effect of child age, group, and attachment security with mothers on externalizing behavior suggested that at 24 and 36 months of age mother–infant attachment security moderated the relationship between alcohol group status and externalizing behavior. Namely, within the alcohol group, those children with secure relationships with their mothers had significantly lower externalizing than insecure children of alcoholics. A similar pattern was noted for internalizing behavior at 36 months of age. Implications for intervention are discussed.The authors thank the parents and infants who participated in this study and the research staff who were responsible for conducting numerous assessments with these families. This study was made possible by grants from NIAAA (1RO1 AA-10042-01A1) and NIDA (1K21DA00231-01A1).

Previous research supports gene–environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene–environment–environment interaction (G × E × E; specifically, gene–EA–proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 single nucleotide polymorphism rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). The results are consistent with the notion that EA exposure results in neurobiological and cognitive–emotional consequences (e.g., altered hypothalamic–pituitary–adrenal axis functioning), leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms.

Premorbid risk for major depressive disorder (MDD) and predictors of an earlier onset and recurrent course were examined in two studies in a large, community-based sample of parents and offspring, prospectively assessed from late childhood into adulthood. In Study 1 (N = 2,764 offspring and their parents), parental psychiatric status, offspring personality at age 11, and age 11 offspring internalizing and externalizing symptoms predicted the subsequent development of MDD, as did poor quality parent–child relationships, poor academic functioning, early pubertal development, and childhood maltreatment by age 11. Parental MDD and adult antisocial behavior, offspring negative emotionality and disconstraint, externalizing symptoms, and childhood maltreatment predicted an earlier onset of MDD, after accounting for course; lower positive emotionality, trait anxiety, and childhood maltreatment predicted recurrent MDD, after accounting for age of onset. In Study 2 (N = 7,146), we examined molecular genetic risk for MDD by extending recent reports of associations with glutamatergic system genes. We failed to confirm associations with MDD using either individual single nucleotide polymorphism based tests or gene-based analyses. Overall, results speak to the pervasiveness of risk for MDD, as well as specific risk for early onset MDD; risk for recurrent MDD appears to be largely a function of its often earlier onset.

We investigate the role of distal, proximal, and child risk factors as predictors of reading readiness and attention and behavior in children at risk of dyslexia. The parents of a longitudinal sample of 251 preschool children, including children at family risk of dyslexia and children with preschool language difficulties, provided measures of socioeconomic status, home literacy environment, family stresses, and child health via interviews and questionnaires. Assessments of children's reading-related skills, behavior, and attention were used to define their readiness for learning at school entry. Children at family risk of dyslexia and children with preschool language difficulties experienced more environmental adversities and health risks than controls. The risks associated with family risk of dyslexia and with language status were additive. Both home literacy environment and child health predicted reading readiness while home literacy environment and family stresses predicted attention and behavior. Family risk of dyslexia did not predict readiness to learn once other risks were controlled and so seems likely to be best conceptualized as representing gene–environment correlations. Pooling across risks defined a cumulative risk index, which was a significant predictor of reading readiness and, together with nonverbal ability, accounted for 31% of the variance between children.

This study examined the relation between maternal and filial attributions and the aggressiveness of their interactions. We also examined whether or not certain setting conditions (e.g., maternal and child depression, maternal and child negative life events, marital conflict, socioeconomic status) predispose some mothers and children to make negative attributions and interact coercively. One hundred four mothers and sons (age 7–9 years) from married and divorced families participated. They completed questionnaire and interview data and were observed while participating in two gamelike tasks (e.g., Trouble, Etch-a-Sketch). Both maternal and child attributions were significantly related to their coercive interactions. The most aggressive dyads were those in which both mothers and sons perceived hostile intent in the other. The relations between attributions and coercive interactions were found to be moderated by marital conflict, and maternal education, such that the association between attributions and coercive behavior, was stronger when marital conflict was low and the mothers were better educated.

Mothers who scored zero on the Beck Depression Inventory (N = 25) were compared to “depressed” mothers (high scores on the Beck) (N = 39) and nondepressed mothers (N = 98) during face-to-face interactions with their 5-month-old infants. The interaction videotapes were rated on the Interaction Rating Scales and were coded second-by-second for attentive/affective behavior states. The zero Beck mothers and their infants received lower ratings and were in less positive behavior states (alone or together) than the high scoring Beck “depressed” mother/infant dyads and even more frequently than the nondepressed mother/infant dyads. The lower activity levels, lesser expressivity, and less frequent vocalizing were suggestive of “depressed” behavior in both the mothers and their infants. In addition, the infants of the zero Beck mothers had lower vagal tone and lower growth percentiles (weight, length, and head circumference) than the infants of nondepressed mothers, although they did not differ from the infants of depressed mothers on these measures. These data suggest that mothers who report no depressive symptoms may present as much, if not greater risk, for their infants than mothers who do report depressive symptoms on the Beck Depression Inventory.

Contrary to the standard assumption that psychopathology stems from developmental immaturity (retardation, fixation, regression), people diagnosed with psychopathology typically develop along distinctive pathways in which they build complex, advanced skills. These pathways are based on adaptation to trauma, such as maltreatment, or to problems in affective–cognitive regulation, such as those in autism. They do not fit normative developmental frameworks. Research has characterized several types of distinctive pathways, especially those arising from maltreatment; they are marked by normal developmental complexity but distinctive affective–cognitive organization. In one study sexually abused depressed adolescent girls admitted for treatment in a mental hospital described themselves-in-relationships with age-appropriate, complex developmental levels equal to those of both nonabused depressed girls and other adolescents. At the same time, they showed a powerful negativity bias contrasting with the positivity biases of other girls. Many of them produced dramatic switches in affective–cognitive organization across assessments contrasting with the similar organization showed by other girls. In another study toddlers from maltreating families showed a consistent negativity bias in play and representations of interactions. We show how to portray these distinctive developmental pathways through the example of Hidden Family Violence, in which people dissociate their private violent world from their public, good-citizen world.

Epigenetic modifications to the genome are a key mechanism involved in the biological encoding of experience. Animal studies and a growing body of literature in humans have shown that early adversity is linked to methylation of the gene for the glucocorticoid receptor (GR), which is a key regulator of the hypothalamic–pituitary–adrenal axis as well as a broad range of physiological systems including metabolic and immune function. One hundred eighty-four families participated, including n = 74 with child welfare documentation of moderate-severe maltreatment in the past 6 months. Children ranged in age from 3 to 5 years, and were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors, and a composite variable assessed the number exposures to these adversities. Methylation of regions 1D, 1F, and 1H of the GR gene was measured via sodium bisulfite pyrosequencing. The composite measure of adversity was positively correlated with methylation at exons 1D and 1F in the promoter of the GR gene. Individual stress measures were significantly associated with a several CpG sites in these regions. GR gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children.

Efforts to differentiate between the developmental sequelae of childhood emotional abuse and childhood emotional neglect are critical to both research and practice efforts. As an oft-identified mechanism of the effects of child maltreatment on later adjustment, emotion dysregulation represents a key potential pathway. The present study explored a higher order factor model of specific emotion regulation skills, and the extent to which these skill sets would indicate distinct developmental pathways from unique emotional maltreatment experiences to multidomain adjustment. A sample of 500 ethnoracially diverse college students reported on their experiences. A two-factor model of emotion regulation skills based on subscales of the Difficulties in Emotion Regulation Scale was revealed. Significant indirect effects of childhood emotional abuse on psychopathology and problems in social relationships were found through response-focused difficulties in emotion regulation, whereas a significant indirect effect of childhood emotional neglect on problems in social relationships was found through antecedent-focused difficulties in emotion regulation. These results are consistent with theoretical models and empirical evidence suggesting differential effects of childhood emotional abuse and emotional neglect, and provide an important indication for developing targeted interventions focusing on specific higher order emotion dysregulation skill clusters.

The co-occurring development of internalizing and externalizing problems were examined in an inception cohort of 392 children diagnosed with autism spectrum disorder at age 3 who were assessed on four occasions. Results indicated that internalizing and externalizing problems were stable over time and highly comorbid. Joint trajectory analysis suggested that 13% of the sample followed a dual high-risk trajectory. High risk was not found to be associated with intellectual ability or autism spectrum disorder symptom severity but was linked to lower income and gender: more girls than boys were found in the high/stable internalizing problems trajectory. The results suggest that 1 in 4 preschoolers followed a trajectory of internalizing or externalizing problems (or a combination of the two) that could be characterized as clinically elevated.

In this paper we discuss the contribution of neural activity-dependent factors to shaping the brain in normal and pathologic development, and we discuss factors that determine the likelihood of recovery from the experience of abnormal neural activity during development.

Analysis of longitudinal data for 145 children [51 healthy, 40 with cystic fibrosis (CF), and 54 with congenital heart disease (CHD)] was conducted: (a) to ascertain whether behavioral problems evident in older medically compromised children would be reported as early as 2–3 years-of-age; and (b) to test theoretical predictions concerning the role of infant-mother attachment in the etiology of behavior problems. As predicted, children with a medical diagnosis received higher scores from parents on the Child Behavior Checklist (CBCL), primarily on the Internalizing scale. Reports of somatic symptoms did not account for this effect. Contrary to predictions, children with CHD were reported to have more behavior problems than those with CF. Secure attachment was associated with lower CBCL scores for internalizing problems regardless of medical status. The increase in behavior problem reports associated with insecure attachment was shown to reflect an effect of avoidance rather than insecurity per se. The importance of distinguishing effects of different types of insecurity and the need for meta-analytic strategies to do so is emphasized.