The purpose of this study was to determine whether five subcomponents of
children's externalizing behavior showed distinctive patterns of
long-term growth and predictive correlates. We examined growth in
teachers' ratings of overt aggression, covert aggression, oppositional
defiance, impulsivity/inattention, and emotion dysregulation across three
developmental periods spanning kindergarten through Grade 8 (ages 5–13
years). We also determined whether three salient background characteristics,
family socioeconomic status, child ethnicity, and child gender, differentially
predicted growth in discrete categories of child externalizing symptoms across
development. Participants were 543 kindergarten-age children (52% male,
81% European American, 17% African American) whose problem
behaviors were rated by teachers each successive year of development through
Grade 8. Latent growth curve analyses were performed for each component scale,
contrasting with overall externalizing, in a piecewise fashion encompassing
three developmental periods: kindergarten–Grade 2, Grades 3–5,
and Grades 6–8. We found that most subconstructs of externalizing
behavior increased significantly across the early school age period relative to
middle childhood and early adolescence. However, overt aggression did not show
early positive growth, and emotion dysregulation significantly increased across
middle childhood. Advantages of using subscales were most clear in relation to
illustrating different growth functions between the discrete developmental
periods. Moreover, growth in some discrete subcomponents was differentially
associated with variations in family socioeconomic status and ethnicity. Our
findings strongly affirmed the necessity of adopting a developmental approach to
the analysis of growth in children's externalizing behavior and provided
unique data concerning similarities and differences in growth between
subconstructs of child and adolescent externalizing behavior.
The present study examined the specificity of autobiographical memory in adolescents and adults with versus without child sexual abuse (CSA) histories. Eighty-five participants, approximately half of whom per age group had experienced CSA, were tested on the Autobiographical Memory Interview. Individual difference measures, including for trauma-related psychopathology, were also administered. Findings revealed developmental differences in the relation between autobiographical memory specificity and CSA. Even with depression statistically controlled, reduced memory specificity in CSA victims relative to controls was observed among adolescents but not among adults. A higher number of Posttraumatic Stress Disorder criteria met predicted more specific childhood memories in participants who reported CSA as their most traumatic life event. These findings contribute to the scientific understanding of childhood trauma and autobiographical memory functioning and underscore the importance of considering the role of age and degree of traumatization within the study of autobiographical memory.
In recent years, translational research involving humans and animals has uncovered biological and physiological pathways that explain associations between early adverse circumstances and long-term mental and physical health outcomes. In this article, we summarize the human and animal literature demonstrating that epigenetic alterations in key biological systems, the hypothalamus–pituitary–adrenal axis and immune system, may underlie such disparities. We review evidence suggesting that changes in DNA methylation profiles of the genome may be responsible for the alterations in hypothalamus–pituitary–adrenal axis and immune system trajectories. Using some preliminary data, we demonstrate how explorations of genome-wide and candidate-gene DNA methylation profiles may inform hypotheses and guide future research efforts in these areas. We conclude our article by discussing the many important future directions, merging perspectives from developmental psychology, molecular genetics, neuroendocrinology, and immunology, that are essential for furthering our understanding of how early adverse circumstances may shape developmental trajectories, particularly in the areas of stress reactivity and physical or mental health.
Previous studies have documented that smoking during pregnancy (SDP) is associated with offspring externalizing problems, even when measured covariates were used to control for possible confounds. However, the association may be due to non-measured environmental and genetic factors that increase risk for offspring externalizing problems. The current project used the National Longitudinal Survey of Youth and their children, ages 4–10 years, to explore the relations between SDP and offspring conduct problems (CP), oppositional-defiant problems (ODP), and attention deficit hyperactivity problems (ADHP) using methodological and statistical controls for confounds. When offspring were compared to their own siblings who differed in their exposure to prenatal nicotine, there was no effect of SDP on offspring CP and ODP. This suggests that SDP does not have a causal effect on offspring CP and ODP. There was a small association between SDP and ADHP, consistent with a causal effect of SDP, but the magnitude of the association was greatly reduced by methodological and statistical controls. Genetically informed analyses suggest that unmeasured environmental variables influencing both SDP and offspring externalizing behaviors account for the previously observed associations. That is, the current analyses imply that important unidentified environmental factors account for the association between SDP and offspring externalizing problems, not teratogenic effects of SDP.
smoking during pregnancy; conduct problems; externalizing problems; ADHD; children of twins; causation
Temperament, effortful control, and problem behaviors at 4.5 years were assessed in 72 children classified as exuberant, inhibited, and low-reactive as 2-year-olds. Exuberant toddlers were more positive, socially responsive to novel persons, less shy, and rated as having more problem behaviors including externalizing and internalizing behaviors, than other children as preschoolers. Two forms of effortful control, the ability to delay a response and the ability to produce a subdominant response, were associated with fewer externalizing behaviors, while expressing more negative affect (relative to positive/neutral affect) when disappointed was related to more internalizing behaviors. Interaction effects implicated high levels of unregulated emotion during disappointment as a risk factor for problem behaviors in exuberant children.
temperament; externalizing; internalizing; exuberant; inhibited; toddlers
Early parent–child attachment has been extensively explored as a contributor to children’s future adaptive or antisocial outcomes, but the specific developmental mechanisms remain to be fully understood. We examined long-term indirect developmental sequelae of early security in two longitudinal community samples followed from infancy to early school age: the Family Study (102 mothers, fathers, and infants) and the Parent–Child Study (112 mothers and infants). Constructs at multiple levels (child characteristics, parent–child security, parental discipline, and child antisocial outcomes) were assessed using a range of methods (extensive behavioral observations in a variety of settings, informants’ ratings). Both studies supported the proposed model of infant attachment as a potent catalyst that moderates future developmental socialization trajectories, despite having few long-term main effects. In insecure dyads, a pattern of coercion emerged between children who were anger prone as toddlers and their parents, resulting in parents’ increased power-assertive discipline. Power assertion in turn predicted children’s rule-breaking conduct and a compromised capacity to delay in laboratory paradigms, as well as oppositional, disruptive, callous, and aggressive behavior rated by parents and teachers at early school age. This causal chain was absent in secure dyads, where child anger proneness was unrelated to power assertion, and power assertion was unrelated to antisocial outcomes. Early insecurity appeared to act as a catalyst for the parent–child dyad embarking on a mutually adversarial path toward antisocial outcomes, whereas security defused such a maladaptive dynamic. The possible mechanisms of those effects were proposed.
This study was designed to examine the prospective relations of life stress and genetic status with increases in drug use. African Americans (N = 399) in rural Georgia (Wave 1 mean age = 17 years) provided 3 waves of data across 27.5 months and a saliva sample from which the dopamine receptor gene DRD4 was genotyped. Multilevel growth curve modeling analysis indicated that emerging adults manifested the highest escalations in drug use when they reported high life stress and carried an allele of DRD4 with 7 or more repeats (7+R allele). In addition, emerging adults who reported high life stress and carried the 7+R allele evinced the largest increases in two proximal risk factors for drug use, affiliations with drug-using companions and drug use vulnerability cognitions. Furthermore, when the G×E effects on increases in affiliations with drug-using companions and vulnerability cognitions were entered into the model forecasting drug use, the life stress × DRD4 status interaction on drug use became nonsignificant in the presence of the risk mechanisms. This finding provides an example of “second generation” G×E interaction research in which the interaction's effects on proximal risk mechanisms account for its effects on outcomes.
African Americans; drug use; early adulthood; genetics; stress
Children born to older fathers are at higher risk to develop severe psychopathology (e.g., schizophrenia and bipolar disorder), possibly due to increased de novo mutations during spermatogenesis with older paternal age. Since severe psychopathology is correlated with antisocial behavior, we examined possible associations between advancing paternal age and offspring violent offending.
Interlinked Swedish national registers provided information on fathers’ age at childbirth and violent criminal convictions in all offspring born 1958–1979 (n=2,359,921). We used ever committing a violent crime and number of violent crimes as indices of violent offending. The data included information on multiple levels; we compared differentially exposed siblings in within-family analyses to rigorously test causal influences.
In the entire population, advancing paternal age predicted offspring violent crime according to both indices. Congruent with a causal effect, this association remained for rates of violent crime in within-family analyses. However, in within-analyses, we found no association with ever committing a violent crime, suggesting that factors shared by siblings (genes and environment) confounded this association. Life-course-persistent criminality has been proposed to have a partly biological etiology; our results agree with a stronger biological effect (i.e., de novo mutations) on persistent violent offending.
Paternal age; Violent criminality; De novo mutations; Sibling comparison
Gene-environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N = 627, M age = 11.27). Variants in three genes, TPH1, 5-HTTLPR, and MAOA uVNTR, were examined. In addition to child maltreatment status, we also considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer-, and adult counselor-reports. In a series of ANCOVAs, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all forms of report. Genetic effects operated primarily in the context of gene-environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms of TPH1, 5-HTTLPR, and MAOA were each related to heightened self-report of antisocial behavior; the interaction of 5-HTTLPR and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype. TPH1 and 5-HTTLPR interacted with maltreatment subtype to predict peer-report of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. TPH1 and 5-HTTLPR polymorphisms also moderated the effects of maltreatment subtype on adult report of antisocial behavior; again genetic effects were strongest for children who were abused. Additionally, TPH1 moderated the effect of developmental timing of maltreatment and chronicity on adult report of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.
The additive and interactive relations of parenting styles (authoritative and authoritarian parenting) and child temperament (anger/frustration, sadness, and effortful control) to children’s internalizing problems were examined in a 3.8-year longitudinal study of 425 Chinese children (6 – 9 years) from Beijing. At Wave 1, parents self-reported on their parenting styles, and parents and teachers rated child temperament. At Wave 2, parents, teachers, and children rated children’s internalizing problems. Structural equation modeling indicated that the main effect of authoritative parenting, and the interactions of authoritarian parenting × effortful control and authoritative parenting × anger/frustration (parents’ reports only) prospectively and uniquely predicted internalizing problems. The above results did not vary by child sex and remained significant after controlling for co-occurring externalizing problems. These findings suggest that: a) children with low effortful control may be particularly susceptible to the adverse effect of authoritarian parenting, and b) the benefit of authoritative parenting may be especially important for children with high anger/frustration.
temperament; parenting styles; internalizing problems
Research on ethnic-minority youths’ mental health has rarely examined developmental trajectories for the same ethnic group in contexts where they are a minority vs. where they are the majority, or mechanisms accounting for differences in trajectories across such contexts. This study examines Puerto Rican youth residing in two contexts -- one in which they are in their home culture of Puerto Rico, and one in which they are a minority group, in New York. We explore the relationship between social context, minority status, risk, resilience, and trajectories of internalizing symptoms after adjusting for factors related to migration. We found that youths’ reports of internalizing symptoms declined over time. Youth in New York had higher levels of internalizing symptoms than youth in Puerto Rico, but similar trajectories. Differences in internalizing symptoms across the two social contexts were accounted for by experiences of discrimination and exposure to violence. Parental monitoring was associated with fewer internalizing symptoms across the two sites, although this effect diminished over time. Contrary to what was expected, family religiosity was associated with higher levels of internalizing symptoms. This association was stronger in the New York than in the Puerto Rico site.
internalizing symptoms; ethnic minorities; early adolescents; risk and resilience
Prenatal exposure to maternal stress, anxiety, and depression can have lasting effects on infant development with consequences for risk of psychopathology. Though the impact of prenatal maternal distress has been well documented, the potential mechanisms through which maternal psychosocial variables shape development have yet to be fully elucidated. Advances in molecular biology have highlighted the role of epigenetic mechanisms in regulating gene activity, neurobiology, and behavior and the potential role of environmentally-induced epigenetic variation in linking early life exposures to long-term biobehavioral outcomes. In this review, we discuss evidence illustrating the association between maternal prenatal distress and both fetal and infant developmental trajectories and the potential role of epigenetic mechanisms in mediating these effects. Postnatal experiences may have a critical moderating influence on prenatal effects, and here we review findings illustrating prenatal-postnatal interplay and the developmental and epigenetic consequences of postnatal mother-infant interactions. The in utero environment is regulated by placental function and there is emerging evidence that the placenta is highly susceptible to maternal distress and a target of epigenetic dysregulation. Integrating studies of prenatal exposures, placental function, and postnatal maternal care with the exploration of epigenetic mechanisms may provide novel insights into the pathophysiology induced by maternal distress.
prenatal stress; maternal depression; DNA methylation; development; epigenetic
Gene–environment correlations (rGE) have been demonstrated in behavioral genetic studies, but rGE have proven elusive in molecular genetic research. Significant gene–environment correlations may be difficult to detect because potential moderators could reduce correlations between measured genetic variants and the environment. Molecular genetic studies investigating moderated rGE are lacking. This study examined associations between child catechol-O-methyltransferase genotype and aspects of positive parenting (responsiveness and warmth), and whether these associations were moderated by parental personality traits (neuroticism and extraversion) among a general community sample of third, sixth, and ninth graders (N = 263) and their parents. Results showed that parent personality traits moderated the rGE association between youths’ genotype and coded observations of positive parenting. Parents with low levels of neuroticism and high levels of extraversion exhibited greater sensitive responsiveness and warmth, respectively, to youth with the valine/valine genotype. Moreover, youth with this genotype exhibited lower levels of observed anger. There was no association between the catechol-O-methyltransferase genotype and parenting behaviors for parents high on neuroticism and low on extraversion. Findings highlight the importance of considering moderating variables that may influence child genetic effects on the rearing environment. Implications for developmental models of maladaptive and adaptive child outcomes, and interventions for psychopathology, are discussed within a developmental psychopathology framework.
Relations between political violence and child adjustment are matters of international concern. Past research demonstrates the significance of community, family and child psychological processes in child adjustment, supporting study of inter-relations between multiple social ecological factors and child adjustment in contexts of political violence. Testing a social ecological model, 300 mothers and their children (M= 12.28 years, SD = 1.77) from Catholic and Protestant working class neighborhoods in Belfast, Northern Ireland completed measures of community discord, family relations, and children’s regulatory processes (i.e., emotional security) and outcomes. Historical political violence in neighborhoods based on objective records (i.e., politically motivated deaths) were related to family members’ reports of current sectarian and non-sectarian antisocial behavior. Interparental conflict and parental monitoring and children’s emotional security about both the community and family contributed to explanatory pathways for relations between sectarian antisocial behavior in communities and children’s adjustment problems. The discussion evaluates support for social ecological models for relations between political violence and child adjustment and its implications for understanding relations in other parts of the world.
Political violence and children; social ecological model; community violence; marital conflict; emotional security
Although neurodevelopmental impairment is a risk factor for poor cognitive and behavioral outcomes, associations between early and later functioning are only moderate in magnitude, and it is likely that other factors intervene to modify this trajectory. The current study tested the hypothesis that sensitive, stimulating caregiving would promote positive behavioral and cognitive outcomes among children who were at risk based on the results of a neurodevelopmental screener and a temperament inventory. The sample comprised 1,720 infants and toddlers from the National Survey of Child and Adolescent Well-Being, a longitudinal study of children who were involved with child welfare services. Children were first assessed between 3 and 24 months of age and subsequently 18 months later. Children who experienced improvements in the amount of sensitive, stimulating caregiving they received had positive cognitive and behavioral outcomes 18 months later, despite early levels of neurodevelopmental risk. The association between changes in caregiving quality and changes in children’s functioning was stronger for children who were removed from the care of their biological parents before the follow-up assessment than for children who remained in the care of biological parents, suggesting a causal role for caregiving quality on children’s outcomes.
Within an allostatic load framework, the effect of gene by environment (GxE) interactions on diurnal cortisol regulation and internalizing symptomatology were investigated. Variation in the CRHR1 TAT haplotype and 5-HTTLPR was determined in a sample of maltreated (n = 238, 21.4% with early physical and sexual abuse) and nonmaltreated (n = 255) children (M age = 10.08) participating in a summer research camp. Internalizing and depressive symptoms were assessed by other- and self-report. GxE effects for CRHR1 and maltreatment and early abuse on diurnal cortisol regulation were observed; CRHR1 variation was related to cortisol dysregulation only among maltreated children. Early abuse and high internalizing symptoms also interacted to predict atypical diurnal cortisol regulation. The interaction of CRHR1, 5-HTTLPR, and child maltreatment (GxGxE) identified a subgroup of maltreated children with high internalizing symptoms who shared the same combination of the two genes. The findings support an allostatic load perspective on the effects of the chronic stress associated with child maltreatment on cortisol regulation and internalizing symptomatology as moderated by genetic variation.
This study examined the childhood history of maltreatment, peer relations, and externalizing problems among individuals who manifested low, moderate, or high symptom levels of paranoid personality disorder (PPD) in adolescence. Participants included 174 children who attended a longitudinal summer camp research program between the ages of 9 to 12. Multiple sources of information (self-, peer-, and counselor-reports) were utilized. Subsequently, they participated in a personality disorder assessment during adolescence (Mean age =15.30). The results indicated that children who manifested higher levels of PPD symptoms in adolescence had higher odds of having a history of child maltreatment. Children who manifested high levels of PPD symptoms in adolescence showed a faster growth rate for peer bullying and externalizing problems in childhood. In addition, their peers rated them as less cooperative, less likely to be leaders, and more likely to initiate fights. These finding suggested that children who manifested elevated PPD symptoms in adolescence had shown early signs of behavioral disturbances in childhood, some of which gradually worsened as they approach adolescence.
This study examined the role of maternal psychopathology and maternal warmth as mediators of the association between prenatal cocaine and other substance exposure and toddler behavior problems. It was also hypothesized that infant cortisol reactivity and environmental risk may moderate these associations. Participants were 220 caregiver–infant dyads (119 cocaine exposed, 101 not cocaine exposed; 49% boys). Mother–infant dyads were recruited at delivery with assessments at 4–8 weeks and 7, 13, and 18 months of child ages. Results yielded no direct associations between prenatal cocaine/other substance exposure and toddler behavior problems, but significant indirect associations between prenatal cigarette/alcohol exposure and toddler behavior problems at 18 months. With regard to moderation, results indicated an indirect association between prenatal cocaine exposure and toddler behavior problems via lower maternal warmth for children with higher, but not lower, cortisol reactivity at 7 months. Results suggest potential pathways to toddler behavior problems among children at high biological risk.
This study examined the prospective relations of adolescents’ perceptions of discrimination and their genetic status with increases in conduct problems. Participants were 461 African American youths residing in rural Georgia (M age, wave 1 = 15.5 years) who provided three waves of data and a saliva sample from which a polymorphism in the SCL6A4 (5-HTT) gene promoter known as the 5-HTTLPR was genotyped. Data analyses using growth curve modeling indicated that perceived discrimination was significantly related to the slope of conduct problems. As hypothesized, interactions between perceived discrimination and genetic status emerged for male but not female youths. Compared with those carrying two copies of the long allele variant of 5-HTTLPR, male youths carrying one or two copies of its short allele variant evinced higher rates of conduct problems over time when they perceived high levels of racial discrimination. These findings are consistent with resilience and differential susceptibility propositions stating that genes can both foster sensitivity to adverse events and confer protection from those events.
African American; conduct problems; discrimination; gender; genetics
The family is one of the primary contexts of child development. Marital and parent–child conflict (family conflict) are common and predict a wide range of negative behavioral and emotional outcomes in children. Thus, an important task for developmental researchers is to identify the processes through which family conflict contributes to children's psychological maladjustment, as well as vulnerability and protective factors in the context of family conflict. In the current paper, we aim to advance a conceptual model that focuses on indices of children's autonomic nervous system (ANS) functioning that increase vulnerability or provide protection against psychological maladjustment in the context of family conflict. In doing so, we provide a selective review that reflects the state of the science linking family conflict, children's ANS activity, and child psychological adjustment, and offer directions and guidance for future research. Our hope is to accelerate research at the intersection of family conflict and ANS functioning to advance understanding of risk and resilience among children.
Researchers have long been interested in whether particular temperamental traits in childhood connote risk for depressive disorders. For example, children characterized as having high negative emotionality (NE; sadness, fear, anger) and low positive emotionality (PE; anhedonia, listlessness, and lack of enthusiasm) are hypothesized to be at risk for depression. Few studies, however, have examined whether (and how) these two temperamental dimensions interact to confer risk. In a sample of 329 preschoolers, the present study addressed this question by examining the relation between PE and NE and asymmetry in resting EEG activity in frontal and posterior regions, which are putative biomarkers for depression. Using a laboratory battery to define temperament, we found an interaction of PE and NE on posterior asymmetry. Specifically, when PE was high, NE was associated with greater relative right activity. When PE was low, NE was not related to posterior asymmetry. These results were driven by differences in EEG activity in right posterior regions, an area associated with emotional processing and arousal, and were specific to girls. We found no relation between temperament and frontal asymmetry. These findings suggest that, at least for girls, PE and NE may have an interactive effect on risk for depression.
This is a report on the research design and findings of a 23-year longitudinal study of the impact of intrafamilial sexual abuse on female development. The conceptual framework integrated concepts of psychological adjustment with theory regarding how psychobiological factors might impact development. Participants included 6- to 16-year-old females with substantiated sexual abuse and a demographically similar comparison group. A cross-sequential design was used and six assessments have taken place, with participants at median age 11 at the first assessment and median age 25 at the sixth assessment. Mothers of participants took part in the early assessments and offspring took part at the sixth assessment. Results of many analyses, both within circumscribed developmental stages and across development, indicated that sexually abused females (on average) showed deleterious sequelae across a host of biopsychosocial domains including: earlier onsets of puberty, cognitive deficits, depression, dissociative symptoms, maladaptive sexual development, hypothalamic–pituitary–adrenal attenuation, asymmetrical stress responses, high rates of obesity, more major illnesses and healthcare utilization, dropping out of high school, persistent psottraumatic stress disorder, self-mutilation, Diagnostic and Statistical Manual of Mental Disorders diagnoses, physical and sexual revictimization, premature deliveries, teen motherhood, drug and alcohol abuse, and domestic violence. Offspring born to abused mothers were at increased risk for child maltreatment and overall maldevelopment. There was also a pattern of considerable within group variability. Based on this complex network of findings, implications for optimal treatments are elucidated. Translational aspects of extending observational research into clinical practice are discussed in terms that will likely have a sustained impact on several major public health initiatives.
We examined Genotype × Environment (G × E) interactions between children’s genotypes (the serotonin transporter linked promoter region [5-HTTLPR] gene) and maternal responsive care observed at 15, 25, 38, and 52 months on three aspects of children’s competence at 67 months: academic skills and school engagement, social functioning with peers, and moral internalization that encompassed prosocial moral cognition and the moral self. Academic and social competence outcomes were reported by both parents, and moral internalization was observed in children’s narratives elicited by hypothetical stories and in a puppet interview. Analyses revealed robust G × E interactions, such that children’s genotype moderated the effects of maternal responsive care on all aspects of children’s competence. Among children with a short 5-HTTLPR allele (ss/sl), those whose mothers were more responsive were significantly more competent than those whose mothers were less responsive. Responsiveness had no effect for children with two long alleles (ll). For academic and social competence, the G × E interactions resembled the diathesis–stress model: ss/sl children of unresponsive mothers had particularly unfavorable outcomes, but ss/sl children of responsive mothers had no worse outcomes than ll children. For moral internalization, the G × E interaction reflected the differential susceptibility model: whereas ss/sl children of unresponsive mothers again had particularly unfavorable outcomes, ss/sl children of responsive mothers had significantly better outcomes than ll children.
In this investigation, gene-environment interaction effects in predicting resilience in adaptive functioning among maltreated and nonmaltreated low-income children (N = 595) were examined. A multi-component index of resilient functioning was derived and levels of resilient functioning were identified. Variants in four genes, 5-HTTLPR, CRHR1, DRD4 -521C/T, and OXTR, were investigated. In a series of ANCOVAs, child maltreatment demonstrated a strong negative main effect on children’s resilient functioning, whereas no main effects for any of the genotypes of the respective genes were found. However, gene-environment interactions involving genotypes of each of the respective genes and maltreatment status were obtained. For each respective gene, among children with a specific genotype, the relative advantage in resilient functioning of nonmaltreated compared to maltreated children was stronger than was the case for nonmaltreated and maltreated children with other genotypes of the respective gene. Across the four genes, a composite of the genotypes that more strongly differentiated resilient functioning between nonmaltreated and maltreated children provided further evidence of genetic variations influencing resilient functioning in nonmaltreated children, whereas genetic variation had a negligible effect on promoting resilience among maltreated children. Additional effects were observed for children based on the number of subtypes of maltreatment children experienced, as well as for abuse and neglect subgroups. Finally, maltreated and nonmaltreated children with high levels of resilience differed in their average number of differentiating genotypes. These results suggest that differential resilient outcomes are based on the interaction between genes and developmental experiences.
Child neglect is the most prevalent form of child maltreatment in the United States, and poses a serious public health concern. Children who survive such episodes go on to experience long-lasting psychological and behavioral problems, including higher rates of post-traumatic stress disorder symptoms, depression, alcohol and drug abuse, attention-deficit/hyperactivity disorder, and cognitive deficits. To date, most research into the causes of these life-long problems has focused on well-established targets such as stress responsive systems, including the hypothalamus–pituitary–adrenal axis. Using the maternal separation and early weaning model, we have attempted to provide comprehensive molecular profiling of a model of early-life neglect in an organism amenable to genomic manipulation: the mouse. In this article, we report new findings generated with this model using chromatin immunoprecipitation sequencing, diffuse tensor magnetic resonance imaging, and behavioral analyses. We also review the validity of the maternal separation and early weaning model, which reflects behavioral deficits observed in neglected humans including hyperactivity, anxiety, and attentional deficits. Finally, we summarize the molecular characterization of these animals, including RNA profiling and label-free proteomics, which highlight protein translation and myelination as novel pathways of interest.