Data drawn from the in-home subsample of the PROSPER intervention dissemination trial were used to investigate the moderation of intervention effects on underage alcohol use by maternal involvement and candidate genes. The primary gene examined was dopamine receptor D4 (DRD4). Variation in this gene and maternal involvement were hypothesized to moderate the influence of intervention status on alcohol use. The PROSPER data used were drawn from 28 communities randomly assigned to intervention or comparison conditions. Participating youth were assessed in five in-home interviews from sixth to ninth grades. A main effect of sixth-grade pretest maternal involvement on ninth-grade alcohol use was found. Neither intervention status nor DRD4 variation was unconditionally linked to ninth-grade drinking. However, moderation analyses revealed a significant three-way interaction among DRD4 status, maternal involvement, and intervention condition. Follow-up analyses revealed that prevention reduced drinking risk, but only for youth with at least one DRD4 seven-repeat allele who reported average or greater pretest levels of maternal involvement. To determine if this conditional pattern was limited to the DRD4 gene, we repeated analyses using the serotonin transporter linked polymorphic region site near the serotonin transporter gene. The results for this supplemental analysis revealed a significant three-way interaction similar but not identical to that found for DRD4.

Elucidating the mechanisms by which infant birth conditions shape development across lengthy periods is critical for understanding typical and pathological development and for targeted early interventions. This study examined how newborns' regulatory capacities impact 10-year outcomes via the bidirectional influences of child emotion regulation (ER) and reciprocal parenting across early development. Guided by dynamic systems theory, 125 infants were tested at seven time points: birth, 3, 6, 12, and 24 months and 5 and 10 years. Initial regulatory conditions were measured by respiratory sinus arrhythmia (RSA; vagal tone) and neurobehavioral regulation (Brazelton, 1973) at birth. At each assessment between 3 months and 5 years, infant ER was microcoded from age-appropriate paradigms and mother–child reciprocity observed during social interactions. Four regulation-related outcomes were measured at 10 years: child RSA, empathy measured by mother–child conflict discussion and a lab paradigm, accident proneness, and behavior problems. An autoregressive cross-lagged structural model indicated that infant birth conditions impacted 10-year outcomes via three mechanisms. First, child ER and reciprocal parenting were individually stable across development and were each predicted by regulatory birth conditions, describing gradual maturation of ER and reciprocity over time. Second, better ER skills at one time point were related to greater reciprocity at the next time point and vice versa, and these cross-time effects defined a field of individual-context mutual influences that mediated the links between neonatal RSA and 10-year outcomes. Third, direct associations emerged between neonatal regulation and outcome, suggesting that birth conditions may establish a neurobiological milieu that promotes a more mature and resilient system. These mechanisms describe distinct “attractor” states that constrain the system's future options, emphasize the importance of defining behavior-based phenotypes of heterotypic continuity, and suggest that infants may shape their development by initiating unique cascades of individual-context bidirectional effects.

Despite the commonly held belief that there is a high degree of intergenerational continuity in maltreatment, studies to date suggest a mixed pattern of findings. One reason for the variance in findings may be related to the measurement approach used, which includes a range of self-report and official indicators of maltreatment and both cross-sectional and longitudinal designs. This study attempted to shed light on the phenomenon of intergenerational continuity of maltreatment by examining multiple indicators of perpetration of maltreatment in young adults and multiple risk factors across different levels within an individual's social ecology. The sample included 166 women who had been placed in out-of-home care as adolescents (>85% had a substantiated maltreatment incident) and followed into young adulthood, and included three waves of adolescent data and six waves of young adult data collected across 10 years. The participants were originally recruited during adolescence as part of a randomized controlled trial examining the efficacy of the Treatment Foster Care Oregon intervention. Analyses revealed weak to modest associations among the three indicators of perpetration of maltreatment in young adulthood, that is, official child welfare records, self-reported child welfare system involvement, and self-reported maltreatment (r = .03–.51). Further, different patterns of prediction emerged as a function of the measurement approach. Adolescent delinquency was a significant predictor of subsequent self-reported child welfare contact, and young adult partner risk was a significant predictor of perpetration of maltreatment as indexed by both official child welfare records and self-reported child welfare contact. In addition, women who were originally assigned to the intervention condition reported perpetrating less maltreatment during young adulthood. Implications for measurement and interventions related to reducing the risk for intergenerational transmission of risk are discussed.

We used sex, observed parenting quality at 18 months, and three variants of the catechol-O-methyltransferase gene (Val158Met [rs4680], intron1 [rs737865], and 3′-untranslated region [rs165599]) to predict mothers' reports of inhibitory and attentional control (assessed at 42, 54, 72, and 84 months) and internalizing symptoms (assessed at 24, 30, 42, 48, and 54 months) in a sample of 146 children (79 male). Although the pattern for all three variants was very similar, Val158Met explained more variance in both outcomes than did intron1, the 3′-untranslated region, or a haplotype that combined all three catechol-O-methyltransferase variants. In separate models, there were significant three-way interactions among each of the variants, parenting, and sex, predicting the intercepts of inhibitory control and internalizing symptoms. Results suggested that Val158Met indexes plasticity, although this effect was moderated by sex. Parenting was positively associated with inhibitory control for methionine–methionine boys and for valine–valine/valine–methionine girls, and was negatively associated with internalizing symptoms for methionine–methionine boys. Using the “regions of significance” technique, genetic differences in inhibitory control were found for children exposed to high-quality parenting, whereas genetic differences in internalizing were found for children exposed to low-quality parenting. These findings provide evidence in support of testing for differential susceptibility across multiple outcomes.

Prenatal tobacco exposure (PTE) has a well-documented association with disruptive behavior in childhood, but the neurocognitive effects of exposure that underlie this link are not sufficiently understood. The present study was designed to address this gap, through longitudinal follow-up in early childhood of a prospectively enrolled cohort with well-characterized prenatal exposure. Three-year-old children (n = 151) were assessed using a developmentally sensitive battery capturing both cognitive and motivational aspects of self-regulation. PTE was related to motivational self-regulation, where children had to delay approach to attractive rewards, but not cognitive self-regulation, where children had to hold information in mind and inhibit prepotent motor responses. Furthermore, PTE predicted motivational self-regulation more strongly in boys than in girls, and when propensity scores were covaried to control for confounding risk factors, the effect of PTE on motivational self-regulation was significant only in boys. These findings suggest that PTE's impact on neurodevelopment may be greater in boys than in girls, perhaps reflecting vulnerability in neural circuits that subserve reward sensitivity and emotion regulation, and may also help to explain why PTE is more consistently related to disruptive behavior disorders than attention problems.

Here we tested whether there was genetic moderation of effects of early maternal sensitivity on social–emotional and cognitive–linguistic development from early childhood onward and whether any detected Gene × Environment interaction effects proved consistent with differential-susceptibility or diathesis–stress models of Person × Environment interaction (N = 695). Two new approaches for evaluating models were employed with 12 candidate genes. Whereas maternal sensitivity proved to be a consistent predictor of child functioning across the primary-school years, candidate genes did not show many main effects, nor did they tend to interact with maternal sensitivity/insensitivity. These findings suggest that the developmental benefits of early sensitive mothering and the costs of insensitive mothering look more similar than different across genetically different children in the current sample. Although acknowledgement of this result is important, it is equally important that the generally null Gene × Environment results reported here not be overgeneralized to other samples, other predictors, other outcomes, and other candidate genes.

We observed gendered coping strategies and conflict resolution outcomes used by adolescents and parents during a conflict discussion task to evaluate associations with current and later adolescent psychopathology. We studied 137 middle- to upper-middle-class, predominantly Caucasian families of adolescents (aged 11–16 years, 65 males) who represented a range of psychological functioning, including normative, subclinical, and clinical levels of problems. Adolescent coping strategies played key roles both in the extent to which parent–adolescent dyads resolved conflict and in the trajectory of psychopathology symptom severity over a 2-year period. Gender-prototypic adaptive coping strategies were observed in parents but not youth, (i.e., more problem solving by fathers than mothers and more regulated emotion-focused coping by mothers than fathers). Youth–mother dyads more often achieved full resolution of conflict than youth–father dyads. There were generally not bidirectional effects among youth and parents’ coping across the discussion except boys’ initial use of angry/hostile coping predicted fathers’ angry/hostile coping. The child was more influential than the parent on conflict resolution. This extended to exacerbation/alleviation of psychopathology over 2 years: higher conflict resolution mediated the association of adolescents’ use of problem-focused coping with decreases in symptom severity over time. Lower conflict resolution mediated the association of adolescents’ use of angry/hostile emotion coping with increases in symptom severity over time. Implications of findings are considered within a broadened context of the nature of coping and conflict resolution in youth–parent interactions, as well as on how these processes impact youth well-being and dysfunction over time.

In this randomized controlled trial, 508 5-year-old kindergarten children participated, of whom 257 were delayed in literacy skills because they belonged to the lowest quartile of a national standard literacy test. We tested the hypothesis that some children are more susceptible to school-entry educational interventions than their peers due to their genetic makeup, and thus whether the dopamine receptor D4 gene moderated intervention effects. Children were randomly assigned to a control condition or one of two interventions involving computer programs tailored to the literacy needs of delayed pupils: Living Letters for alphabetic knowledge and Living Books for text comprehension. Effects of Living Books met the criteria of differential susceptibility. For carriers of the dopamine receptor D4 gene seven-repeat allele (about one-third of the delayed group), the Living Books program was an important addition to the common core curriculum in kindergarten (effect size d = 0.56), whereas the program did not affect the other children (d = –0.09). The same seven-repeat carriers benefited more from Living Letters than did the noncarriers, as reflected in effect sizes of 0.63 and 0.34, respectively, although such differences did not fulfill the statistical criteria for differential susceptibility. The implications of differential susceptibility for education and regarding the crucial question “what works for whom?” are discussed.

Despite burgeoning evidence linking early exposure to child maltreatment (CM) to deficits in self-regulation, the pathways to strong regulatory development in these children are not well understood, and significant heterogeneity is observed in their outcomes. Experiences of autonomy may play a key role in transmitting self-regulatory capacity across generations and help explain individual differences in maltreatment outcomes. In this study, we investigated multigenerational associations between Generation 1 (G1)–Generation 2 (G2) mothers' early experience of warmth and autonomy in relation to their own mothers and their Generation 3 (G3) children's autonomic physiological regulation in CM (n = 85) and non-CM (n = 128) families. We found that G2 mothers who recalled greater autonomy in their childhood relationship with their G1 mothers had preschool-age G3 children with higher respiratory sinus arrhythmia at baseline when alone while engaged in individual challenge tasks, during social exchanges with their mother in joint challenge tasks, and during the portions of the strange situation procedure when the mother was present. Although no clear mediators of this association emerged, multigenerational links among G1–G2 relations, maternal representations of her child, child behavior, and child respiratory sinus arrhythmia differed by maltreatment status, thus possibly representing important targets for future research and intervention.

The human brain undergoes a remarkable transformation during fetal life and the first postnatal years from a relatively undifferentiated but pluripotent organ to a highly specified and organized one. The outcome of this developmental maturation is highly dependent on a sequence of environmental exposures that can have either positive or negative influences on the ultimate plasticity of the adult brain. Many environmental exposures are beyond the control of the individual, but nutrition is not. An ever-increasing amount of research demonstrates not only that nutrition shapes the brain and affects its function during development but also that several nutrients early in life have profound and long-lasting effects on the brain. Nutrients have been shown to alter opening and closing of critical and sensitive periods of particular brain regions. This paper discusses the roles that various nutrients play in shaping the developing brain, concentrating specifically on recently explicated biological mechanisms by which particularly salient nutrients influence childhood and adult neural plasticity.

The contribution of change over time in parent and child characteristics to parents’ resolution of child's diagnosis was examined among 78 mothers and fathers of children with autism spectrum disorder. Children's characteristics (e.g., mental age and severity of symptoms), parental characteristics (e.g., attachment-related anxiety and stress level), and parents’ resolution of their child's diagnosis (resolved vs. unresolved) were examined at Time 1, and reassessed 3 years later at Time 2. Results indicated a deferential contribution of change in parent and child characteristics among mothers and fathers. An increase in child symptom severity and in maternal attachment-related anxiety, as well as longer durations of time since receiving the diagnosis, significantly predicted maternal resolved status at Time 2. Conversely, none of the changes in children's or paternal characteristics predicted paternal resolved status at Time 2. Results are discussed in relation to child and parental contributions to resolution, the differences in the adjustment and well-being of mothers and fathers of children with autism spectrum disorder, parental growth following receiving the diagnosis, and the need for intervention components specific to parental resolution and attachment-related anxiety.

Resilience and adaptation in the face of early genetic or environmental risk has become a major interest in child psychiatry over recent years. However, we still remain far from an understanding of how developing human brains as a whole adapt to the diffuse and widespread atypical synaptic function that may be characteristic of some common developmental disorders. The first part of this paper discusses four types of whole-brain adaptation in the face of early risk: redundancy, reorganization, niche construction, and adjustment of developmental rate. The second part of the paper applies these adaptation processes specifically to autism. We speculate that key features of autism may be the end result of processes of early brain adaptation, rather than the direct consequences of ongoing neural pathology.

We conducted a developmental analysis of genetic moderation of the effect of the Fast Track intervention on adult externalizing psychopathology. The Fast Track intervention enrolled 891 children at high risk to develop externalizing behavior problems when they were in kindergarten. Half of the enrolled children were randomly assigned to receive 10 years of treatment, with a range of services and resources provided to the children and their families, and the other half to usual care (controls). We previously showed that the effect of the Fast Track intervention on participants' risk of externalizing psychopathology at age 25 years was moderated by a variant in the glucocorticoid receptor gene. Children who carried copies of the A allele of the single nucleotide polymorphism rs10482672 had the highest risk of externalizing psychopathology if they were in the control arm of the trial and the lowest risk of externalizing psychopathology if they were in the treatment arm. In this study, we test a developmental hypothesis about the origins of this for better and for worse Gene × Intervention interaction (G × I): that the observed G × I effect on adult psychopathology is mediated by the proximal impact of intervention on childhood externalizing problems and adolescent substance use and delinquency. We analyzed longitudinal data tracking the 270 European American children in the Fast Track randomized control trial with available genetic information (129 intervention children, 141 control group peers, 69% male) from kindergarten through age 25 years. Results show that the same pattern of for better and for worse susceptibility to intervention observed at the age 25 follow-up was evident already during childhood. At the elementary school follow-ups and at the middle/high school follow-ups, rs10482672 predicted better adjustment among children receiving the Fast Track intervention and worse adjustment among children in the control condition. In turn, these proximal G × I effects early in development mediated the ultimate G × I effect on externalizing psychopathology at age 25 years. We discuss the contribution of these findings to the growing literature on genetic susceptibility to environmental intervention.

Manuck, Craig, Flory, Halder, and Ferrell (2011) reported that a theoretically anticipated effect of family rearing on girls' menarcheal age was genetically moderated by two single nucleotide polymorphisms (SNPs) of the estrogen receptor-α gene. We sought to replicate and extend these findings, studying 210 White females followed from birth. The replication was general because a different measure of the rearing environment was used in this inquiry (i.e., maternal sensitivity) than in the prior one (i.e., family cohesion). Extensions of the work included prospective rather than retrospective measurements of the rearing environment, reports of first menstruation within a year of its occurrence rather than decades later, accounting for some heritability of menarcheal age by controlling for maternal age of menarche, and using a new model-fitting approach to competitively compare diathesis–stress versus differential-susceptibility models of Gene × Environment interaction. The replication/extension effort proved successful in the case of both estrogen receptor-α SNPs, with the Gene × Environment interactions principally reflecting diathesis–stress: lower levels of maternal sensitivity predicted earlier age of menarche for girls homozygous for the minor alleles of either SNP but not for girls carrying other genotypes. Results are discussed in light of the new analytic methods adopted.

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.

Physiological response to stress has been linked to a variety of healthy and pathological conditions. The current study conducted a multilevel examination of interactions among environmental toxins (i.e., neighborhood crime and child maltreatment) and specific genetic polymorphisms of the endothelial nitric oxide synthase gene (eNOS) and GABA(A) receptor subunit alpha-6 gene (GABRA6). One hundred eighty-six children were recruited at age 4. The presence or absence of child maltreatment as well as the amount of crime that occurred in their neighborhood during the previous year were determined at that time. At age 9, the children were brought to the lab, where their physiological response to a cognitive challenge (i.e., change in the amplitude of the respiratory sinus arrhythmia) was assessed and DNA samples were collected for subsequent genotyping. The results confirmed that complex Gene × Gene, Environment × Environment, and Gene × Environment interactions were associated with different patterns of respiratory sinus arrhythmia reactivity. The implications for future research and evidence-based intervention are discussed.

Evocative effects of child characteristics on the quality and quantity of child care were assessed in two studies using longitudinal data from the NICHD Study of Early Child Care. We focus on the influence of child characteristics on two important aspects of the child care experience: language stimulation provided by caregivers and quantity of care. In Study 1, associations between the developmental status of children aged 15 to 54 months and the language stimulation provided by their caregivers were examined using path models, and longitudinal child effects were detected across the earliest time points of the study. In Study 2, the associations among child behavior, temperament, development, and time in care were examined. Little evidence was found for such child effects on time in care. The results are discussed in terms of the effects of child care on child development and implications for developmental processes, particularly for children at greatest risk for developmental delay or psychopathology.

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.

The development of attention has been strongly linked to the regulation of emotion and behavior and has therefore been of particular interest to researchers aiming to better understand precursors to behavioral maladjustment. In the current paper, we utilize a developmental psychopathology and neural plasticity framework to highlight the importance of both intrinsic (i.e., infant neural functioning) and extrinsic (i.e., caregiver behavior) factors for the development of attentional control across the first year. We begin by highlighting the importance of attention for children's emotion regulation abilities and mental health. We then review the development of attention behavior and underscore the importance of neural development and caregiver behavior for shaping attentional control. Finally, we posit that neural activation associated with the development of the executive attention network may be one mechanism through which maternal caregiving behavior influences the development of infants’ attentional control and subsequent emotion regulation abilities known to be influential to childhood psychopathology.

Using a genetic moderation approach, this study examines how an experimental prime of religion impacts self-control in a social context, and whether this effect differs depending on the genotype of an oxytocin receptor gene (OXTR) polymorphism (rs53576). People with different genotypes of OXTR seem to have different genetic orientations toward sociality, which may have consequences for the way they respond to religious cues in the environment. In order to determine whether the influence of religion priming on self-control is socially motivated, we examine whether this effect is stronger for people who have OXTR genotypes that should be linked to greater rather than less social sensitivity (i.e., GG vs. AA/AG genotypes). The results showed that experimentally priming religion increased self-control behaviors for people with GG genotypes more so than people with AA/AG genotypes. Furthermore, this Gene × Religion interaction emerged in a social context, when people were interacting face to face with another person. This research integrates genetic moderation and social psychological approaches to address a novel question about religion's influence on self-control behavior, which has implications for coping with distress and psychopathology. These findings also highlight the importance of the social context for understanding genetic moderation of psychological effects.