There remains little debate that the period before birth sets the stage for subsequent development, yet scant evidence exists showing continuity from characteristics of the individual fetus to characteristics of the child. This report examines, in two studies, whether baseline and evoked fetal neurobehavioral functioning are predictive of features of child temperament and behavior as reported by mothers when offspring were between 7 and 14 years old (M = 10.1 years). Study 1 utilizes data generated from 333 maternal–fetal pairs collected during an undisturbed condition during the second half of gestation in relation to the child temperament dimensions of behavioral inhibition and exuberance. Associations at 32 weeks gestation were detected between all features of fetal neurobehavior and behavioral inhibition. In adjusted models, slower fetal heart rate and less fetal movement were associated with significant unique variance in predicting higher levels of childhood behavioral inhibition. No associations were detected for exuberance. Study 2 focuses on the association of evoked fetal reactivity and recovery to induced maternal arousal with subsequent child behavioral difficulties in a subset of the full sample (n = 130). Greater recovery in fetal heart rate following maternal stimulation was predictive of fewer behavioral difficulties and more prosocial behavior in childhood. Results from both studies provide support for gestational origins of core individual differences that portend childhood outcomes with foundational reactivity and regulatory components.

Experimental animal studies and adult research consistently show that stress exposure and/or psychological symptoms are associated with poorer health and immune functioning. The application to children is not yet clear, however, and we lack developmental models for studies in this area. The objective of this paper was to test the hypothesis that self-reported self-efficacy and depression, two markers of psychological well-being in children, would predict immunity and rate of illnesses. The data are based on a prospective study of 141 healthy, normally developing children aged 7–13 years who were recruited from an ambulatory pediatric setting. Children completed self-efficacy and depression measures and had blood obtained for IL-6 plasma levels and natural killer cell functional assays on three occasions, 6 months apart. Parents maintained weekly child illness diaries over 1 year using a thermometer to record fever. Parent psychiatric symptoms and income were used as covariates. Results indicated that, across the three occasions of measurement collected over the 1-year period, higher perceived self-efficacy was significantly associated with lower plasma interleukin 6 concentrations. There was no overall main effect of depressive symptoms on immune measures; however, for older girls, higher depression was associated with elevated natural killer cell cytotoxicity and an increased rate of total illnesses and febrile illnesses. The findings provide some of the first evidence that psychological processes are associated with immunity and health in a normally developing sample of preadolescents. Furthermore, the pattern of results suggests a modified model of a link between psychological well-being and immunological processes in children. These results build on and expand research on the notion of allostatic load and develop a groundwork for developmental studies in this area.

This study tests competing models of the relation between depression and polysubstance use over the course of adolescence. Participants included a nationwide sample of adolescents (N = 3,604), ages 12 to 17 at study Wave 1, assessed annually for 3 years. Models were tested using cohort-sequential latent growth curve modeling to determine whether depressive symptoms at baseline predicted concurrent and age-related changes in drug use, whether drug use at baseline predicted concurrent and age-related changes in depressive symptoms, and whether initial levels of depression predicted changes in substance use significantly better than vice versa. The results suggest a transactional model such that early polysubstance use promotes early depressive symptoms, which in turn convey elevated risk for increasing polysubstance use over time, which in turn conveys additional risk for future depressive symptoms, even after accounting for gender, ethnicity, and household income. In contrast, early drug use did not portend risk for future depressive symptoms. These findings suggest a complicated pattern of interrelations over time and indicate that many current models of co-occurring polysubstance use and depressive symptoms may not fully account for these associations. Instead, the results suggest a developmental cascade, in which symptoms of one disorder promote symptoms of the other across intrapersonal domains.

Individuals with melancholic major depression exhibit basal hypercortisolism and an attenuated ACTH response to exogenous corticotropin-releasing hormone (CRH) infusion. Given the greater incidence of depression in children of depressed parents, we examined the ACTH and cortisol responses to ovine CRH (oCRH) infusion in 63 adolescent offspring of mothers with major depression, bipolar illness, or no psychiatric illness. Psychiatric and observational assessments of these families had been conducted over the course of 10 years preceding this study. We examined the children's responses to CRH in relation to maternal characteristics and family environment and found the following: (a) cortisol responses were negatively related to chronic family stress and (b) offspring of depressed mothers with an avoidant personality disorder showed an exaggerated ACTH response. In addition, adolescents in late puberty (Tanner 4 and 5) had lower ACTH and cortisol responses to oCRH infusion than those in early puberty. Further, offspring with early histories of mood problems, and those who developed major depressive disorder as young adults, did not exhibit basal hypercortisolism but did show an attenuated ACTH response to CRH. Our results add to the growing body of literature showing the influence of maternal characteristics and environmental factors on hypothalamic–pituitary–adrenal axis patterns in children.We acknowledge the efforts of our predecessors on this project, whose work made this study possible. In addition, we thank Ann Mayfield, Sara Torvik, and Patricia Kasdan for their recruitment efforts and Sue Harris and Hayley Kleitz for their editorial comments on the manuscript. Finally, we thank all of the mothers and their children who have dedicated their time to this study over the course of 20 years.

Bullying has been understudied among preschool children, especially those from Chinese American families. Previous research has also neglected the dimensional effects of psychological control on child bullying development. This study examined two psychological control dimensions, love withdrawal and guilt induction, and their effects on children's bullying aggressive behavior using a longitudinal design. Participants were first-generation Chinese American mothers (N = 133; mean age [Mage] = 37.82) and their preschool children (Mage = 4.48). Chinese immigrant mothers reported their psychologically controlling parenting and teachers rated children's bullying aggressive behaviors in the school setting. Confirmatory factor analyses were conducted to establish the psychometric properties and cross-wave measurement equivalence of the study constructs. Cross-lagged structural equation modeling analysis indicated that maternal love withdrawal prospectively predicted more bullying aggressive behavior, whereas guilt induction predicted less bullying aggressive behavior in children 6 months later. These results held after controlling for the initial level of children's problem behaviors and demographic variables (child age, gender, and maternal education). For child effects, child bullying aggressive behavior predicted more maternal guilt induction over time but not love withdrawal. Our findings highlight the importance of construct specificity and cultural context in understanding associations between parenting and child development.

Early life stress (ELS) is a risk factor for the development of depression in adolescence; the mediating neurobiological mechanisms, however, are unknown. In this study, we examined in early pubertal youth the associations among ELS, cortisol stress responsivity, and white matter microstructure of the uncinate fasciculus and the fornix, two key frontolimbic tracts; we also tested whether and how these variables predicted depressive symptoms in later puberty. A total of 208 participants (117 females; M age = 11.37 years; M Tanner stage = 2.03) provided data across two or more assessment modalities: ELS; salivary cortisol levels during a psychosocial stress task; diffusion magnetic resonance imaging; and depressive symptoms. In early puberty there were significant associations between higher ELS and decreased cortisol production, and between decreased cortisol production and increased fractional anisotropy in the uncinate fasciculus. Further, increased fractional anisotropy in the uncinate fasciculus predicted higher depressive symptoms in later puberty, above and beyond earlier symptoms. In post hoc analyses, we found that sex moderated several additional associations. We discuss these findings within a broader conceptual model linking ELS, emotion dysregulation, and depression across the transition through puberty, and contend that brain circuits implicated in the control of hypothalamic–pituitary–adrenal axis function should be a focus of continued research.

The important implications for developmental psychopathology that derive from advances in psychiatric and behavioral genetics are discussed in relation to a series of mistaken stereotypes: that strong effects mean that environmental influences must be unimportant; that genes provide a limit to potential; that genetic strategies are of no value for studying environmental influences; that nature and nurture are separate; that genes for serious diseases are necessarily bad; that diseases have nothing to do with normal variation; that genetic findings will not help identify diseases; that genetic influences diminish with age; that disorders that run in families must be genetic; that disorders that seem not to run in families cannot be genetic; and that single major genes lead only to specific rare diseases that follow a Mendelian pattern. The reasons why these stereotypes are mistaken are considered in relation to genetic concepts and findings.

There are multiple recent reports of an association between anxious/depressed (A/D) symptomatology and the rate of cerebral cortical thickness maturation in typically developing youths. We investigated the degree to which anxious/depressed symptoms are tied to age-related microstructural changes in cerebral fiber pathways. The participants were part of the NIH MRI Study of Normal Brain Development. Child Behavior Checklist A/D scores and diffusion imaging were available for 175 youths (84 males, 91 females; 241 magnetic resonance imagings) at up to three visits. The participants ranged from 5.7 to 18.4 years of age at the time of the scan. Alignment of fractional anisotropy data was implemented using FSL/Tract-Based Spatial Statistics, and linear mixed model regression was carried out using SPSS. Child Behavior Checklist A/D was associated with the rate of microstructural development in several white matter pathways, including the bilateral anterior thalamic radiation, bilateral inferior longitudinal fasciculus, left superior longitudinal fasciculus, and right cingulum. Across these pathways, greater age-related fractional anisotropy increases were observed at lower levels of A/D. The results suggest that subclinical A/D symptoms are associated with the rate of microstructural development within several white matter pathways that have been implicated in affect regulation, as well as mood and anxiety psychopathology.

This study examines historical variation in individual trajectories of heavy drinking and marijuana use from age 18 to 22. Unlike most studies that have examined cohort differences in drug use, it focuses on differences in both level of use and rates of change (growth). Nearly 39,000 youths from the high school classes of 1976–2004 were surveyed at biennial intervals between the ages of 18 and 22 as part of the national Monitoring the Future study. Between 1976 and 2004, adolescent heavy drinking decreased substantially. However, because the age 18–22 heavy drinking growth rate increased threefold for males and sixfold for females during this period, heavy drinking among 21- to 22-year-olds remained largely stable. The growth rate for marijuana use was more stable across cohorts, and historical declines in use were sizable across the entire 18–22 age band. Generally, historical variation in use was unrelated to college status and living arrangements as well as to historical changes in the distribution of young adult social roles. Findings suggest that historical fluctuations in use were less the result of proximal young adult factors and more the result of historical variation in distal adolescent factors, the effect of which diminished with age, especially for heavy drinking.

This study examined the role of child temperament as moderator of the effect of parenting style on children's externalizing and internalizing behaviors. A series of structural equation models were fit to a representative sample of 2,631 Canadian children from the National Longitudinal Survey of Children and Youth. In addition to testing for the presence of Temperament × Parenting interactions, these models also examined the direct and indirect effects of a number of additional contextual factors such as neighborhood problems, neighborhood cohesion, social support, and maternal depression. The results indicate that exposure to more positive parenting reduces behavior problems in children with difficult/unadaptable temperaments. No moderating effects of temperament on hostile parenting were found. Such results serve to highlight the pivotal role of positive features of the rearing environment as catalysts for the successful adaptation of children with difficult/unadaptable temperaments. The results of this modeling work also serve to emphasize the importance of considering the ways in which more distal factors can affect children's behavioral adaptation by contributing to changes in proximal family processes.

A retrospective longitudinal research design was used to evaluate male adult outcomes associated with four patterns of physical aggression from childhood to adulthood—child-only aggression, child and adult continuity of aggression, adult-onset aggression, and a contrast group with low levels of aggression in childhood and adulthood. The continuity and adult-onset aggression groups had the highest levels of social maladjustment (e.g., marital instability), psychiatric disturbance (e.g., alcohol disorders, major depression), personality dysfunction (e.g., higher prevalence of elevated borderline and narcissistic personality disorder scores), and higher plasma testosterone levels. The child-only aggression group manifested more psychiatric and personality disturbance than the contrast group, but not nearly as much disturbance as the continuity and adult-onset groups. After controlling for age and socioeconomic status (SES) variables, race (White/Black) was typically not a significant predictor of outcome variables. Findings are discussed with regard to life course implications of the physical aggression patterns, and of the support provided for an adult-onset aggressive type.

Through autonomic and affective mechanisms, adverse childhood experiences (ACEs) may disrupt the capacity to regulate negative emotions, increasing craving and exacerbating risk for opioid use disorder (OUD) among individuals with chronic pain who are receiving long-term opioid analgesic pharmacotherapy. This study examined associations between ACEs, heart rate variability (HRV) during emotion regulation, and negative emotional cue-elicited craving among a sample of female opioid-treated chronic pain patients at risk for OUD. A sample of women (N = 36, mean age = 51.2 ± 9.5) with chronic pain receiving long-term opioid analgesic pharmacotherapy (mean morphine equivalent daily dose = 87.1 ± 106.9 mg) were recruited from primary care and pain clinics to complete a randomized task in which they viewed and reappraised negative affective stimuli while HRV and craving were assessed. Both ACEs and duration of opioid use significantly predicted blunted HRV during negative emotion regulation and increased negative emotional cue-elicited craving. Analysis of study findings from a multiple-levels-of-analysis approach suggest that exposure to childhood abuse occasions later emotion dysregulation and appetitive responding toward opioids in negative affective contexts among adult women with chronic pain, and thus this vulnerable clinical population should be assessed for OUD risk when initiating a course of extended, high-dose opioids for pain management.

This study examined the long-term effects of a randomized controlled trial of the Family Check-Up (FCU) intervention initiated at age 2 on inhibitory control in middle childhood and adolescent internalizing and externalizing problems. We hypothesized that the FCU would promote higher inhibitory control in middle childhood relative to the control group, which in turn would be associated with lower internalizing and externalizing symptomology at age 14. Participants were 731 families, with half (n = 367) of the families assigned to the FCU intervention. Using an intent-to-treat design, results indicate that the FCU intervention was indirectly associated with both lower internalizing and externalizing symptoms at age 14 via its effect on increased inhibitory control in middle childhood (i.e., ages 8.5–10.5). Findings highlight the potential for interventions initiated in toddlerhood to have long-term impacts on self-regulation processes, which can further reduce the risk for behavioral and emotional difficulties in adolescence.

This paper questions the assumption that children's social and emotional competence be placed within the developing child, rather than in the interaction of the child with the range of peer social ecologies in which the children might function. This paper presents a new nonstatistical mathematical approach to modeling children's peer social interaction in small groups using nonlinear difference equations in which both an uninfluenced and an influenced regulatory set point of positive minus negative interaction can be separately estimated. Using this model and the estimation procedure, it is possible to estimate what a focal child and the group initially brings to the group interaction and also how these regulatory set points are influenced by the interaction to determine two influenced regulatory set points. Six-person mainstreamed and specialized groups were established involving three types of unacquainted preschool boys: children with and without developmental delays and a language disordered but intellectually normally functioning group, using a methodology that ensured appropriate matching of child and family characteristics. For each 2-week play group, the social interactions of each child were observed during a designated free play period. Handicapped children were observed in either a specialized or mainstreamed setting. The application made of this modeling process in this paper is generating theory to attempt to understand influence processes. Parameters are introduced that reflect uninfluenced target child and group set points, emotional inertia, and influence functions.

Maternal depression is an established risk factor for child conduct problems, but relatively few studies have tested whether children's behavioral problems exacerbate mothers' depression or whether other child behavioral characteristics (e.g., self-regulation) may mediate bidirectional effects between maternal depression and child disruptive behavior. This longitudinal study examined the parallel growth of maternal depressive symptoms and child oppositional behavior from ages 2 to 5; the magnitude and timing of their bidirectional effects; and whether child inhibitory control, a temperament-based self-regulatory mechanism, mediated effects between maternal depression and child oppositionality. A randomized control trial of 731 at-risk families assessed children annually from ages 2 to 5. Transactional models demonstrated positive and bidirectional associations between mothers' depressive symptoms and children's oppositional behavior from ages 2 to 3, with a less consistent pattern of reciprocal relations up to age 5. Mediation of indirect mother–child effects and child evocative effects depended on the rater of children's inhibitory control. Findings are discussed in regard to how child evocative effects and self-regulatory mechanisms may clarify the transmission of psychopathology within families.

Studies in rodents, nonhuman primates, and humans suggest that epigenetic processes mediate between early life experiences and adult phenotype. However, the normal evolution of epigenetic programs during child development, the effect of sex, and the impact of early life adversity on these trajectories are not well understood. This study mapped the genome-wide DNA methylation changes in CD3+ T lymphocytes from rhesus monkeys from postnatal day 14 through 2 years of age in both males and females and determined the impact of maternal deprivation on the DNA methylation profile. We show here that DNA methylation profiles evolve from birth to adolescence and are sex dependent. DNA methylation changes accompany imposed weaning, attenuating the difference between males and females. Maternal separation at birth alters the normal evolution of DNA methylation profiles and targets genes that are also affected by a later stage maternal separation, that is, weaning. Our results suggest that early life events dynamically interfere with the normal developmental evolution of the DNA methylation profile and that these changes are highly effected by sex.

Building upon the transactional model of brain development, we explore the impact of early maternal deprivation on neural development and plasticity in three neural systems: hyperactivity/impulsivity, executive function, and hypothalamic–pituitary–adrenal axis functioning across rodent, nonhuman primate, and human studies. Recognizing the complexity of early maternal–infant interactions, we limit our cross-species comparisons to data from rodent models of artificial rearing, nonhuman primate studies of peer rearing, and the relations between these two experimental approaches and human studies of children exposed to the early severe psychosocial deprivation associated with institutional care. In addition to discussing the strengths and limitations of these paradigms, we present the current state of research on the neurobiological impact of early maternal deprivation and the evidence of sensitive periods, noting methodological challenges. Integrating data across preclinical animal models and human studies, we speculate about the underlying biological mechanisms; the differential impact of deprivation due to temporal factors including onset, offset, and duration of the exposure; and the possibility and consequences of reopening of sensitive periods during adolescence.

A substantial amount of research has demonstrated the deleterious effects of chronic stress on memory. However, much less is known about protective factors. In the current study we test the role of maternal responsiveness in buffering the effects of childhood allostatic load on subsequent adolescent working memory. Allostatic load is a marker of cumulative stress on the body that is caused by mobilization of multiple physiological systems in response to chronic environmental demands. Results of the study suggest that allostatic load negatively affects working memory, but that this effect is significantly attenuated in children with responsive mothers.

Callous–unemotional (CU) behaviors demonstrate meaningful individual differences in early childhood, even in nonclinical samples with low mean levels of CU, but the factors underlying this variation have not been examined. This study investigated genetic and environmental contributions to individual differences and to sources of continuity and change in CU in toddler twins (145 monozygotic, 169 dizygotic) assessed at ages 2 and 3 years. CU, as assessed by the Child Behavior Checklist 1.5–5 (Achenbach & Rescorla, 2000), was moderately stable across age (r = .45, p < .0001). Longitudinal biometric analyses revealed genetic and nonshared environmental influences on CU at both ages, with no significant contribution from shared environmental factors. Stability from age 2 to 3 was due to genetic factors, whereas change was due to both genetic and nonshared environmental influences. This genetic and nonshared environmental change was substantial, suggesting malleability of CU in early childhood. Over 50% of the genetic influences and 100% of the nonshared environmental influences on CU at age 3 were independent of those that operated at age 2. Implications of novel sources of variance across age are discussed.

Although randomized interventions trials have been shown to reduce the incidence of disorganized attachment, no studies to date have identified the mechanisms of change responsible for such reductions. Maternal sensitivity has been assessed in various studies and shown to change with intervention, but in the only study to formally assess mediation, changes in maternal sensitivity did not mediate changes in infant security of attachment (Cicchetti, Rogosch, & Toth, 2006). Primary aims of the current randomized controlled intervention trial in a high-risk population were to fill gaps in the literature by assessing whether the intervention (a) reduced disorganization, (b) reduced disrupted maternal communication, and (c) whether reductions in disrupted maternal communication mediated changes in infant disorganization. The results indicated that, compared to controls (n = 52), both infant disorganization and disrupted maternal communication were significantly reduced in the intervention group (n = 65) that received regular home-visiting during pregnancy and the first year of life. Furthermore, reductions in disrupted maternal communication partially accounted for the observed reductions in infant disorganization compared to randomized controls. The results are discussed in relation to the societal cost effectiveness of early attachment-informed interventions for mothers and infants, as well as the importance of formally assessing underlying mechanisms of change in order to improve and appropriately target preventive interventions.