Early adversity increases risk for child mental health difficulties. Stressors in the home environment (e.g., parental mental illness, household socioeconomic challenges) may be particularly impactful. Attending out-of-home childcare may buffer or magnify negative effects of such exposures. Using a longitudinal observational design, we leveraged data from the NIH Environmental influences on Child Health Outcomes Program to test whether number of hours in childcare, defined as 1) any type of nonparental care and 2) center-based care specifically, was associated with child mental health, including via buffering or magnifying associations between early exposure to psychosocial and socioeconomic risks (age 0–3 years) and later internalizing and externalizing symptoms (age 3–5.5 years), in a diverse sample of N = 2,024 parent–child dyads. In linear regression models, childcare participation was not associated with mental health outcomes, nor did we observe an impact of childcare attendance on associations between risk exposures and symptoms. Psychosocial and socioeconomic risks had interactive effects on internalizing and externalizing symptoms. Overall, the findings did not indicate that childcare attendance positively or negatively influenced child mental health and suggested that psychosocial and socioeconomic adversity may need to be considered as separate exposures to understand child mental health risk in early life.

Although new mothers are at risk of heightened vulnerability for depressive symptoms, there is limited understanding regarding changes in maternal depressive symptoms over the course of the postpartum and early childhood of their child’s life among rural, low-income mothers from diverse racial backgrounds. This study examined distinct trajectories of depressive symptoms among rural low-income mothers during the first five years of their child’s life, at 6, 15, 24, and 58 months, using data from the Family Life Project (N = 1,292). Latent class growth analysis identified four distinct trajectories of maternal depressive symptoms, including Low-decreasing (50%; n = 622), Low-increasing (26%; n = 324), Moderate-decreasing (13%; n = 156), and Moderate-increasing (11%; n = 131) trajectories. Multinomial logistic regression demonstrated that higher perceived financial strain and intimate partner violence, and lower social support predicted higher-risk trajectories (Low-increasing, Moderate-decreasing, and Moderate-increasing) relative to the Low-decreasing trajectory. Compared to the Low-decreasing trajectory, lower neighborhood safety/quietness predicted to the Low-increasing trajectory. Moreover, lower social support predicted the Moderate-increasing trajectory, the highest-risk trajectory, compared to those in Moderate-decreasing. The current analyses underscore the heterogeneity on patterns of depressive symptoms among rural, low-income mothers, and that the role of both proximal and broader contexts contributing to distinct trajectories of maternal depressive symptoms over early childhood.

We identified family risk profiles at 6 months using socioeconomic status (SES) and maternal mental health indicators with data from the Family Life Project (N = 1,292). We related profiles to executive function (EF) at 36 months (intercept) and growth in EF between 36 and 60 months. Latent profile analysis revealed five distinct profiles, characterized by different combinations of SES and maternal mental health symptoms. Maternal sensitivity predicted faster growth in EF among children in the profile characterized by deep poverty and the absence of maternal mental health symptoms. Maternal sensitivity also predicted higher EF intercept but slower EF growth among children in the profile characterized by deep poverty and maternal mental health symptoms, and children in the near poor (low SES), mentally healthy profile. Maternal sensitivity also predicted higher EF intercept but had no effect on growth in EF in the near poor, mentally distressed profile. In contrast, maternal sensitivity did not predict the intercept or growth of EF in the privileged SES/mentally healthy profile. Our findings using a person-centered approach provide a more nuanced understanding of the role of maternal sensitivity in the growth of EF, such that maternal sensitivity may differentially affect the growth of EF in various contexts.

One pathway by which environments of socioeconomic risk are thought to affect cognitive development is through stress physiology. The biological systems underpinning stress and attention undergo a sensitive period of development during infancy. Psychobiological theory emphasizes a dynamic pattern of context-dependent development, however, research has yet to examine how basal cortisol and attention dynamically covary across infancy in ecologically valid contexts. Thus, to address these gaps, we leveraged longitudinal, multilevel analytic methods to disentangle between- from within-person associations of hypothalamic–pituitary–adrenal (HPA) axis activity and executive attention behaviors across infancy. We use data from a large longitudinal sample (N = 1,292) of infants in predominantly low-income, nonurban communities at 7-, 15-, and 24-months of age. Using multilevel models, we investigated longitudinal associations of infant attention and basal cortisol levels and examined caregiving behaviors as moderators of this relationship. Results indicated a negative between- and within-person association between attention and cortisol across infancy and a within-person moderation by caregiver responsiveness. In other words, on the within-person level, higher levels of cortisol were concomitantly associated with lower infant attention across the first 2 years of life. However, variation in the caregiver's level of responsiveness either buffered or sensitized the executive attention system to the negative effects of physiological stress.

Environmental adversity increases child susceptibility to disrupted developmental outcomes, but the mechanisms by which adversity can shape development remain unclear. A translational cross-species approach was used to examine stress-mediated pathways by which poverty-related adversity can influence infant social development. Findings from a longitudinal sample of low-income mother–infant dyads indicated that infant cortisol (CORT) on its own did not mediate relations between early-life scarcity-adversity exposure and later infant behavior in a mother-child interaction task. However, maternal CORT through infant CORT served as a mediating pathway, even when controlling for parenting behavior. Findings using a rodent “scarcity-adversity” model indicated that pharmacologically blocking pup corticosterone (CORT, rodent equivalent to cortisol) in the presence of a stressed mother causally prevented social transmission of scarcity-adversity effects on pup social behavior. Furthermore, pharmacologically increasing pup CORT without the mother present was not sufficient to disrupt pup social behavior. Integration of our cross-species results suggests that elevated infant CORT may be necessary, but without elevated caregiver CORT, may not be sufficient in mediating the effects of environmental adversity on development. These findings underscore the importance of considering infant stress physiology in relation to the broader social context, including caregiver stress physiology, in research and interventional efforts.

This study used repeated measures data to identify developmental profiles of elevated risk for ADHD (i.e., six or more inattentive and/or hyperactive-impulsive symptoms), with an interest in the age at which ADHD risk first emerged. Risk factors that were measured across the first 3 years of life were used to predict profile membership. Participants included 1,173 children who were drawn from the Family Life Project, an ongoing longitudinal study of children's development in low-income, nonmetropolitan communities. Four heuristic profiles of ADHD risk were identified. Approximately two thirds of children never exhibited elevated risk for ADHD. The remaining children were characterized by early childhood onset and persistent risk (5%), early childhood limited risk (10%), and middle childhood onset risk (19%). Pregnancy and delivery complications and harsh-intrusive caregiving behaviors operated as general risk for all ADHD profiles. Parental history of ADHD was uniquely predictive of early onset and persistent ADHD risk, and low primary caregiver education was uniquely predictive of early childhood limited ADHD risk. Results are discussed with respect to how changes to the age of onset criterion for ADHD in DSM5 may affect etiological research and the need for developmental models of ADHD that inform ADHD symptom persistence and desistance.

Adverse effects of early exposure to parental mood disturbance on child adjustment have been documented for both mothers and fathers, but are rarely examined in tandem. Other under-researched questions include effects of changes over time in parental well-being, similarities and contrasts between effects of parental mood disturbance on children's internalizing versus externalizing problems, and potential mediating effects of couple relationship quality. The current study involved 438 couples who reported symptoms of depression and anxiety at each of four time points (i.e., last trimester of pregnancy and 4, 14, and 24 months postbirth). Mothers and fathers also rated their couple relationship quality and their child's socioemotional adjustment at 14 months, as well as internalizing and externalizing problems at 24 months. Latent growth models indicated direct effects of (a) maternal prenatal well-being on externalizing problems at 24 months, and (b) paternal prenatal well-being on socioemotional problems at 14 months. Internalizing symptoms at 24 months showed only indirect associations with parental well-being, with couple relationship quality playing a mediating role. Our findings highlight the importance of prenatal exposure to parental mood disturbance and demonstrate that, even in a low-risk sample, poor couple relationship quality explains the intergenerational stability of internalizing problems.

Children reared in impoverished environments are at risk for enduring psychological and physical health problems. Mechanisms by which poverty affects development, however, remain unclear. To explore one potential mechanism of poverty's impact on social–emotional and cognitive development, an experimental examination of a rodent model of scarcity-adversity was conducted and compared to results from a longitudinal study of human infants and families followed from birth (N = 1,292) who faced high levels of poverty-related scarcity-adversity. Cross-species results supported the hypothesis that altered caregiving is one pathway by which poverty adversely impacts development. Rodent mothers assigned to the scarcity-adversity condition exhibited decreased sensitive parenting and increased negative parenting relative to mothers assigned to the control condition. Furthermore, scarcity-adversity reared pups exhibited decreased developmental competence as indicated by disrupted nipple attachment, distress vocalization when in physical contact with an anesthetized mother, and reduced preference for maternal odor with corresponding changes in brain activation. Human results indicated that scarcity-adversity was inversely correlated with sensitive parenting and positively correlated with negative parenting, and that parenting fully mediated the association of poverty-related risk with infant indicators of developmental competence. Findings are discussed from the perspective of the usefulness of bidirectional–translational research to inform interventions for at-risk families.

Children who grow up in poverty are more likely to experience chronic stressors that generate “wear” on stress regulatory systems including the hypothalamus–pituitary–adrenal (HPA) axis. This can have long-term consequences for health and well-being. Prior research has examined the role of proximal family and home contributions to HPA axis functioning. However, there is evidence to suggest that more distal levels of context, including neighborhoods, also matter. Prior evidence has primarily focused on adolescents and adults, with little evidence linking the neighborhood context with HPA activity in infancy and toddlerhood. We tested whether neighborhood disadvantage (indexed by US Census data) was associated with basal salivary cortisol levels at 7, 15, and 24 months of child age in a large sample of families (N = 1,292) residing in predominately low-income and rural communities in the United States. Multilevel models indicated that neighborhood disadvantage was positively associated with salivary cortisol levels and that this effect emerged across time. This effect was moderated by the race/ethnicity of children such that the association was only observed in White children in our sample. Findings provide preliminary evidence that the neighborhood context is associated with stress regulation during toddlerhood, elucidating a need for future work to address possible mechanisms.

Theory suggests that early experiences may calibrate the “threshold activity” of the hypothalamus–pituitary–adrenal axis in childhood. Particularly challenging or particularly supportive environments are posited to manifest in heightened physiological sensitivity to context. Using longitudinal data from the Family Life Project (N = 1,292), we tested whether links between maternal sensitivity and hypothalamus–pituitary–adrenal axis activity aligned with these predictions. Specifically, we tested whether the magnitude of the within-person relation between maternal sensitivity and children's cortisol levels, a proxy for physiological sensitivity to context, was especially pronounced for children who typically experienced particularly low or high levels of maternal sensitivity over time. Our results were consistent with these hypotheses. Between children, lower levels of mean maternal sensitivity (7–24 months) were associated with higher mean cortisol levels across this period (measured as a basal sample collected at each visit). However, the magnitude and direction of the within-person relation was contingent on children's average levels of maternal sensitivity over time. Increases in maternal sensitivity were associated with contemporaneous cortisol decreases for children with typically low-sensitive mothers, whereas sensitivity increases were associated with cortisol increases for children with typically high-sensitive mothers. No within-child effects were evident at moderate levels of maternal sensitivity.

The following prospective longitudinal study considers the ways that protracted exposure to verbal and physical aggression between parents may take a substantial toll on emotional adjustment for 1,025 children followed from 6 to 58 months of age. Exposure to chronic poverty from infancy to early childhood as well as multiple measures of household chaos were also included as predictors of children's ability to recognize and modulate negative emotions in order to disentangle the role of interparental conflict from the socioeconomic forces that sometimes accompany it. Analyses revealed that exposure to greater levels of interparental conflict, more chaos in the household, and a higher number of years in poverty can be empirically distinguished as key contributors to 58-month-olds' ability to recognize and modulate negative emotion. Implications for models of experiential canalization of emotional processes within the context of adversity are discussed.

This paper examined the relation of early environmental adversity associated with poverty to child resting or basal level of cortisol in a prospective longitudinal sample of 1135 children seen at 7, 15, 24, 35, and 48 months of age. We found main effects for poor housing quality, African American ethnicity, and low positive caregiving behavior in which each was uniquely associated with an overall higher level of cortisol from age 7 to 48 months. We also found that two aspects of the early environment in the context of poverty, adult exits from the home and perceived economic insufficiency, were related to salivary cortisol in a time-dependent manner. The effect for the first of these, exits from the home, was consistent with the principle of allostatic load in which the effects of adversity on stress physiology accumulate over time. The effect for perceived economic insufficiency was one in which insufficiency was associated with higher levels of cortisol in infancy but with a typical but steeper decline in cortisol with age at subsequent time points.

This study prospectively examined the effect of intimate partner violence (IPV) on adrenocortical reactivity and recovery during early childhood. The sample (n = 1102 mother–infant dyads; 49.2% male) was racially diverse and from predominantly low-income, rural communities. To measure IPV exposure mothers completed the Conflicts Tactics Scale, and her caretaking behaviors were observed when her child was approximately 7, 15, and 24 months of age. Children's saliva samples, later assayed for cortisol, were collected around challenge tasks designed to elicit emotional reactivity. IPV was related to a trajectory of increased cortisol reactivity from infancy to toddlerhood. By contrast, the trajectory for non-IPV-exposed children decreased in cortisol reactivity across 7 to 24 months of age. At the 24-month assessment, on average, toddlers did not exhibit a cortisol reaction; however, those exposed to high levels of violence continued to have reactivity. Accumulative levels of IPV across the first 2 years of life predicted cortisol reactivity at 24 months of age. Early (7-month) sensitive maternal behavior moderated this relationship, so that only children exposed to both early insensitivity and high accumulated IPV exhibited increased reactivity at the 24-month assessment. Findings are discussed in relation to the risky family framework.

Despite their potentially central role in fostering school readiness, executive function (EF) skills have received little explicit attention in the design and evaluation of school readiness interventions for socioeconomically disadvantaged children. The present study examined a set of five EF measures in the context of a randomized-controlled trial of a research-based intervention integrated into Head Start programs (Head Start REDI). Three hundred fifty-six 4-year-old children (17% Hispanic, 25% African American; 54% girls) were followed over the course of the prekindergarten year. Initial EF predicted gains in cognitive and social–emotional skills and moderated the impact of the Head Start REDI intervention on some outcomes. The REDI intervention promoted gains on two EF measures, which partially mediated intervention effects on school readiness. We discuss the importance of further study of the neurobiological bases of school readiness, the implications for intervention design, and the value of incorporating markers of neurobiological processes into school readiness interventions.

This paper examines interrelations between biological and social influences on the development of self-regulation in young children and considers implications of these interrelations for the promotion of self-regulation and positive adaptation to school. Emotional development and processes of emotion regulation are seen as influencing and being influenced by the development of executive cognitive functions, including working memory, inhibitory control, and mental flexibility important for the effortful regulation of attention and behavior. Developing self-regulation is further understood to reflect an emerging balance between processes of emotional arousal and cognitive regulation. Early childhood educational programs that effectively link emotional and motivational arousal with activities designed to exercise and promote executive functions can be effective in enhancing self-regulation, school readiness, and school success.

Family systems theory proposes that an individual's functioning depends on interactive processes within the self and within the context of dyadic family subsystems. Previous research on these processes has focused largely on behavioral, cognitive, and psychophysiological properties of the individual and the dyad. The goals of this study were to explore genetic and environmental interactions within the family system by examining how the dopamine receptor D2 gene (DRD2) A1+ polymorphism in mothers and children relates to maternal sensitivity, how maternal and child characteristics might mediate those effects, and whether maternal sensitivity moderates the association between DRD2 A1+ and child affective problems. Evidence is found for an evocative effect of child polymorphism on parenting behavior, and for a moderating effect of child polymorphism on the association between maternal sensitivity and later child affective problems. Findings are discussed from a family systems perspective, highlighting the role of the family as a context for gene expression in both mothers and children.

The target article provides a thoughtful review and synthesis of studies examining the neural basis of cognitive abilities associated with intelligence test performance. In its attempt to present a new or generative theory of the neural basis for intelligence, however, the review faces specific limits to its theoretical model that relate to processes of development and the role of automaticity in cognition.

This target article considers the relation of fluid cognitive functioning to general intelligence. A neurobiological model differentiating working memory/executive function cognitive processes of the prefrontal cortex from aspects of psychometrically defined general intelligence is presented. Work examining the rise in mean intelligence-test performance between normative cohorts, the neuropsychology and neuroscience of cognitive function in typically and atypically developing human populations, and stress, brain development, and corticolimbic connectivity in human and nonhuman animal models is reviewed and found to provide evidence of mechanisms through which early experience affects the development of an aspect of cognition closely related to, but distinct from, general intelligence. Particular emphasis is placed on the role of emotion in fluid cognition and on research indicating fluid cognitive deficits associated with early hippocampal pathology and with dysregulation of the hypothalamic-pituitary-adrenal axis stress-response system. Findings are seen to be consistent with the idea of an independent fluid cognitive construct and to assist with the interpretation of findings from the study of early compensatory education for children facing psychosocial adversity and from behavior genetic research on intelligence. It is concluded that ongoing development of neurobiologically grounded measures of fluid cognitive skills appropriate for young children will play a key role in understanding early mental development and the adaptive success to which it is related, particularly for young children facing social and economic disadvantage. Specifically, in the evaluation of the efficacy of compensatory education efforts such as Head Start and the readiness for school of children from diverse backgrounds, it is important to distinguish fluid cognition from psychometrically defined general intelligence.

Primary issues raised by the commentaries on the target article relate to (1) the need to differentiate distinct but overlapping aspects of fluid cognition, and (2) the implications that this differentiation may hold for conceptions of general intelligence. In response, I outline several issues facing researchers concerned with differentiation of human cognitive abilities and suggest that a revised and expanded theory of intelligence is needed to accommodate an increasingly diverse and varied empirical base.

This study examined the relation of negative emotionality in infancy to child social and cognitive developmental outcomes among low birth weight (LBW) preterm infants participating in the Infant Health and Development Program (IHDP), a comprehensive compensatory education intervention beginning in infancy and lasting through age 3 years. In this analysis, intervention effects at age 36 months on maternal report of child behavior as assessed by the Child Behavior Checklist externalizing and internalizing scales and on intelligence as measured by the Stanford–Binet scale were largest among children characterized by higher levels of negative emotionality in infancy. Findings indicate that for LBW preterm infants characterized by negative emotionality at age 12 months the intervention was associated with a twofold decrease in the occurrence of clinically meaningful levels of behavior problems at age 3 years and a fourfold decrease in the occurrence of a high-risk profile in which both internalizing and externalizing scores are in the clinically meaningful range. The intervention was also associated with a fivefold decrease in the occurrence of IQ ≤ 75 at age 3 years among children with higher levels of negative emotionality and heavier LBW (2001–2500 g). However, specific aspects of temperamental difficulty such as fearfulness and anger were related to internalizing and externalizing, respectively, in both the intervention and control groups. Findings are consistent with research linking negative emotionality in infancy with social and cognitive developmental outcomes in early childhood among normal birth weight infants. Results suggest the need for further attention to child temperament in early intervention research.