The Detection of Environmental Influences on Academic Achievement Appears to Depend on the Analytic Approach.

One long-standing analytic approach in adoption studies is to examine correlations between features of adoptive homes and outcomes of adopted children (hereafter termed 'measured environment correlations') to illuminate environmental influences on those associations. Although results from such studies have almost uniformly suggested modest environmental influences on adopted children's academic achievement, other work has indicated that adopted children's achievement is routinely higher than that of their reared-apart family members, often substantially so. We sought to understand this discrepancy. We examined academic achievement and literacy-promotive features of the home in 424 yoked adoptive/biological families participating in the Early Growth and Development Study (EGDS; i.e., adopted children, adoptive mothers, birth mothers, and biological siblings of the adopted children remaining in the birth homes) using an exhaustive modeling approach. Results indicated that, as anticipated, adopted children scored up to a full standard deviation higher on standardized achievement tests relative to their birth mothers and reared-apart biological siblings. Moreover, these achievement differences were associated with differences in the literacy-promotive features of the adoptive and birth family homes, despite minimal measured environment correlations within adoptive families. A subsequent simulation study highlighted noise in measured environmental variables as an explanation for the decreased utility of measured environment correlations. We conclude that the field's heavy focus on measured environment correlations within adoptive families may have obscured detection of specific environmental effects on youth outcomes, and that future adoption studies should supplement their measured environment analyses with mean differences between reared-apart relatives.

Disentangling genetic and environmental influences on early language development: The interplay of genetic propensity for negative emotionality and surgency, and parenting behavior effects on early language skills in an adoption study.

Parenting and children's temperament are important influences on language development. However, temperament may reflect prior parenting, and parenting effects may reflect genes common to parents and children. In 561 U.S. adoptees (57% male) and their birth and rearing parents (70% and 92% White, 13% and 4% African American, and 7% and 2% Latinx, respectively), this study demonstrated how genetic propensity for temperament affects language development, and how this relates to parenting. Genetic propensity for negative emotionality inversely predicted language at 27 months (ß = -.15) and evoked greater maternal warmth (ß = .12), whereas propensity for surgency positively predicted language at 4.5 years (ß = .20), especially when warmth was low. Parental warmth (ß = .15) and sensitivity (ß = .19) further contributed to language development, controlling for common gene effects.

The pernicious role of stress on intergenerational continuity of psychopathology.

Development and Psychopathology has been a premier resource for understanding stressful childhood experiences and the intergenerational continuity of psychopathology. Building on that tradition, we examined the unique and joint influences of maternal stress on children's effortful control (age 7) and externalizing behavior (age 11) as transmitted via genetics, the prenatal environment, and the postnatal environment. The sample included N = 561 adopted children and their biological and adoptive parents. Path models identified a direct effect of biological mother life stress on children's effortful control (ß = -.08) and an indirect effect of her life stress on child externalizing behavior via effortful control (ß = .52), but no main or indirect effects of biological parent psychopathology, prenatal stress, or adoptive mother adverse childhood experiences (ACES). Adoptive mother ACES amplified the association between biological mother life stress and child effortful control (ß = -.08), externalizing behavior (ß = 1.41), and the indirect effect via effortful control, strengthening associations when adoptive mothers reported average or high ACES during their own childhoods. Results suggest that novel study designs are needed to enhance the understanding of how life stress gets "under the skin" to affect psychopathology in the offspring of adults who have experienced stress.

Incidence rates of childhood asthma with recurrent exacerbations in the US Environmental influences on Child Health Outcomes (ECHO) program.

BACKGROUND: Descriptive epidemiological data on incidence rates (IRs) of asthma with recurrent exacerbations (ARE) are sparse. OBJECTIVES: This study hypothesized that IRs for ARE would vary by time, geography, age, and race and ethnicity, irrespective of parental asthma history. METHODS: The investigators leveraged data from 17,246 children born after 1990 enrolled in 59 US with 1 Puerto Rican cohort in the Environmental Influences on Child Health Outcomes (ECHO) consortium to estimate IRs for ARE. RESULTS: The overall crude IR for ARE was 6.07 per 1000 person-years (95% CI: 5.63-6.51) and was highest for children aged 2-4 years, for Hispanic Black and non-Hispanic Black children, and for those with a parental history of asthma. ARE IRs were higher for 2- to 4-year-olds in each race and ethnicity category and for both sexes. Multivariable analysis confirmed higher adjusted ARE IRs (aIRRs) for children born 2000-2009 compared with those born 1990-1999 and 2010-2017, 2-4 versus 10-19 years old (aIRR = 15.36; 95% CI: 12.09-19.52), and for males versus females (aIRR = 1.34; 95% CI 1.16-1.55). Black children (non-Hispanic and Hispanic) had higher rates than non-Hispanic White children (aIRR = 2.51; 95% CI 2.10-2.99; and aIRR = 2.04; 95% CI: 1.22-3.39, respectively). Children born in the Midwest, Northeast and South had higher rates than those born in the West (P < .01 for each comparison). Children with a parental history of asthma had rates nearly 3 times higher than those without such history (aIRR = 2.90; 95% CI: 2.43-3.46). CONCLUSIONS: Factors associated with time, geography, age, race and ethnicity, sex, and parental history appear to influence the inception of ARE among children and adolescents.

The Environmental Influences on Child Health Outcomes (ECHO)-Wide Cohort.

The Environmental Influences on Child Health Outcomes (ECHO)-Wide Cohort Study (EWC), a collaborative research design comprising 69 cohorts in 31 consortia, was funded by the National Institutes of Health (NIH) in 2016 to improve children's health in the United States. The EWC harmonizes extant data and collects new data using a standardized protocol, the ECHO-Wide Cohort Data Collection Protocol (EWCP). EWCP visits occur at least once per life stage, but the frequency and timing of the visits vary across cohorts. As of March 4, 2022, the EWC cohorts contributed data from 60,553 children and consented 29,622 children for new EWCP data and biospecimen collection. The median (interquartile range) age of EWCP-enrolled children was 7.5 years (3.7-11.1). Surveys, interviews, standardized examinations, laboratory analyses, and medical record abstraction are used to obtain information in 5 main outcome areas: pre-, peri-, and postnatal outcomes; neurodevelopment; obesity; airways; and positive health. Exposures include factors at the level of place (e.g., air pollution, neighborhood socioeconomic status), family (e.g., parental mental health), and individuals (e.g., diet, genomics).

Using the Flanker Task to Examine Genetic and Environmental Contributions in Inhibitory Control Across the Preschool Period.

The limited research exploring genetic and environmental influences on inhibitory control (IC) in preschoolers has relied on parent ratings or simple delay tasks and has produced mixed results. The present study uses a cognitively-challenging Flanker task to examine genetic and environmental contributions to the development of early IC in a longitudinal sample of 310 same-sex twin pairs (123 MZ; 187 DZ; 51% female) assessed at ages 3, 4 and 5 years. IC was significantly heritable at each age (a2: age 3 = .36; age 4 = .36; age 5 = .35). Stability was entirely accounted for by genetic influences, and change was explained by genetic and nonshared environmental factors. No significant shared environmental influences were observed.

Genetic and environmental influences on temperament development across the preschool period.

BACKGROUND: Preschoolers' temperament characteristics are associated with children's long-term development. Such links underscore the importance of understanding factors that shape temperament during preschool. This is the first study to examine genetic and environmental sources of developmental growth in three temperament dimensions: surgency, negative affectivity, and effortful control, during the preschool period. METHODS: Biometric latent growth curve modeling was used to examine genetic, shared, and nonshared environmental contributions to the invariant level of and developmental growth in temperament, using a sample of 310 same-sex twin pairs (MZ = 123, DZ = 187) assessed at 3, 4, and 5 years of age. Temperament was assessed using primary caregiver's report on the Child Behavior Questionnaire-Short Form. RESULTS: All three temperament dimensions demonstrated linear increases from ages 3 to 5 years. The invariant levels of all three temperament dimensions were explained by genetic and nonshared environmental factors. Growth in surgency was fully explained by nonshared environmental factors, while growth in negative affectivity was mainly explained by genetic factors. Growth in effortful control was explained by genetic and nonshared environmental factors, although neither were significant due to large bootstrap standard errors. For negative affectivity and effortful control, the genetic factors that contributed to developmental growth were independent from those associated with their invariant levels. CONCLUSIONS: Collectively, these findings indicate that both genetic and nonshared environmental factors play important roles in the invariant levels of temperament. Findings also accord a critical role of children's nonshared environment in the development of surgency and to a lesser extent negative affectivity and effortful control. It is also notable that novel genetic effects contribute to developmental growth in negative affectivity and effortful control as children age, emphasizing the importance of integrating developmental models in genetic research.

Developmental trajectories of behavioral inhibition from infancy to age seven: The role of genetic and environmental risk for psychopathology.

The present study leveraged data from a longitudinal adoption study of 361 families recruited between 2003 and 2010 in the United States. We investigated how psychopathology symptoms in birth parents (BP; Mage  = 24.1 years; 50.5-62.9% completed high school) and adoptive parents (AP; Mage  = 37.8 years; 80.9% completed college; 94% mother-father couples) influenced children's behavioral inhibition (BI) trajectories. We used latent growth models of observed BI at 18 and 27 months, and 4.5 and 7 years in a sample of adopted children (Female = 42%, White = 57%, Black = 11%, Multi-racial = 21%, Latinx = 9%). BI generally decreased over time, yet there was substantial variability in these trajectories. Neither BP nor AP psychopathology symptoms independently predicted systematic differences in BI trajectories. Instead, we found that AP internalizing symptoms moderated the effects of BP psychopathology on trajectories of BI, indicating a gene by environment interaction.

The Role of Childhood Asthma in Obesity Development: A Nationwide US Multicohort Study.

RATIONALE: Asthma and obesity often co-occur. It has been hypothesized that asthma may contribute to childhood obesity onset. OBJECTIVES: To determine if childhood asthma is associated with incident obesity and examine the role of asthma medication in this association. METHODS: We studied 8,716 children between ages 6 and 18.5 years who were nonobese at study entry participating in 18 US cohorts of the Environmental influences on Child Health Outcomes program (among 7,299 children with complete covariate data mean [SD] study entry age = 7.2 [1.6] years and follow up = 5.3 [3.1] years). MEASUREMENTS AND MAIN RESULTS: We defined asthma based on caregiver report of provider diagnosis. Incident obesity was defined as the first documented body mass index ≥95th percentile for age and sex following asthma status ascertainment. Over the study period, 26% of children had an asthma diagnosis and 11% developed obesity. Cox proportional hazards models with sex-specific baseline hazards were fitted to assess the association of asthma diagnosis with obesity incidence. Children with asthma had a 23% (95% confidence intervals [CI] = 4, 44) higher risk for subsequently developing obesity compared with those without asthma. A novel mediation analysis was also conducted to decompose the total asthma effect on obesity into pathways mediated and not mediated by asthma medication use. Use of asthma medication attenuated the total estimated effect of asthma on obesity by 64% (excess hazard ratios = 0.64; 95% CI = -1.05, -0.23). CONCLUSIONS: This nationwide study supports the hypothesis that childhood asthma is associated with later risk of obesity. Asthma medication may reduce this association and merits further investigation as a potential strategy for obesity prevention among children with asthma.

Early manifestations of intellectual performance: Evidence that genetic effects on later academic test performance are mediated through verbal performance in early childhood.

Intellectual performance is highly heritable and robustly predicts lifelong health and success but the earliest manifestations of genetic effects on this asset are not well understood. This study examined whether early executive function (EF) or verbal performance mediate genetic influences on subsequent intellectual performance, in 561 U.S.-based adoptees (57% male) and their birth and adoptive parents (70% and 92% White, 13% and 4% African American, 7% and 2% Latinx, respectively), administered measures in 2003-2017. Genetic influences on children's academic performance at 7 years were mediated by verbal performance at 4.5 years (ß = .22, 95% CI [0.08, 0.35], p = .002) and not via EF, indicating that verbal performance is an early manifestation of genetic propensity for intellectual performance.

Intergenerational transmission of psychopathology: An examination of symptom severity and directionality.

The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32-60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11-22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins' symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins' symptom directionality. Both comorbid problems and preponderance of symptoms of a particular - internalizing versus externalizing - spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.

Developmental profiles of child behavior problems from 18 months to 8 years: The protective effects of structured parenting vary by genetic risk.

Some children are more affected by specific family environments than others, as a function of differences in their genetic make-up. However, longitudinal studies of genetic moderation of parenting effects during early childhood have not been conducted. We examined developmental profiles of child behavior problems between 18 months and age 8 in a longitudinal parent-offspring sample of 361 adopted children. In toddlerhood (18 months), observed structured parenting indexed parental guidance in service of task goals. Biological parent psychopathology served as an index of genetic influences on children's behavior problems. Four profiles of child behavior problems were identified: low stable (11%), average stable (50%), higher stable (29%), and high increasing (11%). A multinominal logistic regression analysis indicated a genetically moderated effect of structured parenting, such that for children whose biological mother had higher psychopathology, the odds of the child being in the low stable group increased as structured parenting increased. Conversely, for children whose biological mother had lower psychopathology, the odds of being in the low stable group was reduced when structured parenting increased. Results suggest that increasing structured parenting is an effective strategy for children at higher genetic risk for psychopathology, but may be detrimental for those at lower genetic risk.

Parenting in the Context of the Child: Genetic and Social Processes.

The focus on the role of parenting in child development has a long-standing history. When measures of parenting precede changes in child development, researchers typically infer a causal role of parenting practices and attitudes on child development. However, this research is usually conducted with parents raising their own biological offspring. Such research designs cannot account for the effects of genes that are common to parents and children, nor for genetically influenced traits in children that influence how they are parented and how parenting affects them. The aim of this monograph is to provide a clearer view of parenting by synthesizing findings from the Early Growth and Development Study (EGDS). EGDS is a longitudinal study of adopted children, their birth parents, and their rearing parents studied across infancy and childhood. Families (N = 561) were recruited in the United States through adoption agencies between 2000 and 2010. Data collection began when adoptees were 9 months old (males = 57.2%; White 54.5%, Black 13.2%, Hispanic/Latinx 13.4%, Multiracial 17.8%, other 1.1%). The median child age at adoption placement was 2 days (M = 5.58, SD = 11.32). Adoptive parents were predominantly in their 30s, White, and coming from upper-middle- or upper-class backgrounds with high educational attainment (a mode at 4-year college or graduate degree). Most adoptive parents were heterosexual couples, and were married at the beginning of the project. The birth parent sample was more racially and ethnically diverse, but the majority (70%) were White. At the beginning of the study, most birth mothers and fathers were in their 20s, with a mode of educational attainment at high school degree, and few of them were married. We have been following these family members over time, assessing their genetic influences, prenatal environment, rearing environment, and child development. Controlling for effects of genes common to parents and children, we confirmed some previously reported associations between parenting, parent psychopathology, and marital adjustment in relation to child problematic and prosocial behavior. We also observed effects of children's heritable characteristics, characteristics thought to be transmitted from parent to child by genetic means, on their parents and how those effects contributed to subsequent child development. For example, we found that genetically influenced child impulsivity and social withdrawal both elicited harsh parenting, whereas a genetically influenced sunny disposition elicited parental warmth. We found numerous instances of children's genetically influenced characteristics that enhanced positive parental influences on child development or that protected them from harsh parenting. Integrating our findings, we propose a new, genetically informed process model of parenting. We posit that parents implicitly or explicitly detect genetically influenced liabilities and assets in their children. We also suggest future research into factors such as marital adjustment, that favor parents responding with appropriate protection or enhancement. Our findings illustrate a productive use of genetic information in prevention research: helping parents respond effectively to a profile of child strengths and challenges rather than using genetic information simply to identify some children unresponsive to current preventive interventions.

Gene × Environment Interactions in the Development of Preschool Effortful Control, and Its Implications for Childhood Externalizing Behavior.

This study examined the role of gene × environment interaction (G × E) in the development of effortful control (EC) and externalizing symptoms (EXT). Participants included 361 adopted children, and their Adoptive Parents (APs) and Birth Mothers (BMs), drawn from the Early Growth and Development Study. The primary adoptive caregivers' (AP1) laxness and overreactivity were assessed when children were 27-months-old, and used as indices of environmental influences on EC. Heritable influences on child EC were assessed by the BMs' personality characteristics (emotion dysregulation, agreeableness). Secondary adoptive caregivers (AP2) reported on children's EC at 54 months, and EXT at 7 years. Interactions between BM characteristics and AP1 laxness were related to EC and indirectly predicted EXT via EC. Parental laxness and EC were positively associated if children had high heritable risk for poor EC (BM high emotion dysregulation or low agreeableness), but negatively associated if children had low heritable risk for poor EC (BM low emotion dysregulation or high agreeableness). BM agreeableness also moderated associations between AP1 overreactivity and effortful control, and yielded a similar pattern of results. Our findings suggest that G × E is an important first step in the development of EXT via its effect on EC. Consistent with "goodness of fit" models, heritable tendencies can affect which parenting practices best support EC development.

The role of child negative emotionality in parenting and child adjustment: Gene-environment interplay.

BACKGROUND: Evocative gene-environment correlation (rGE) describes a process through which children's heritable characteristics influence their rearing environments. The current study examined whether heritable influences on parenting and children's behavioural outcomes operate through child negative emotionality. METHOD: Using data from the Early Growth and Development Study, we examined associations among adoptive parent reports of child anger and sadness at 4.5 years, adoptive parents' hostile and warm parenting at 6 years and child behavioural problems and social competence at age 7. Birth parent temperament was included to test whether child effects on parents reflect evocative gene-environment correlation (rGE). RESULTS: Child anger at 4.5 years evoked hostile parenting from adoptive parents at 6 years, which was subsequently related to child problem behaviours at 7 years. Evocative rGE effects were identified for adoptive parents' hostile parenting. CONCLUSIONS: By employing a genetically informed design, we found that birth parent temperament was related to child negative emotionality. Adoptive parents were sensitive to child negative emotionality, and this sensitivity was linked to the child's later adjustment.

Examining reciprocal associations between parent depressive symptoms and child internalizing symptoms on subsequent psychiatric disorders: An adoption study.

INTRODUCTION: The dynamic interplay between parent depressive symptoms and child internalizing behavior over time is not well understood. METHODS: We used data from a prospective parent-offspring adoption design (N = 561) to examine associations between adoptive parent depressive symptoms and child internalizing behavior when children were ages 18 months, 27 months, 4.5 years, and 6 years, and subsequent child psychiatric disorder symptoms when children were between the ages of 6-8 years. Models also accounted for the contributions of birth parent psychopathology, birth mother depressive symptoms during pregnancy, and infant negative emotionality. Bidirectional associations between adoptive parent depressive symptoms and child internalizing behavior were examined using a random-intercept cross-lagged panel model. RESULTS: There was evidence for associations between child internalizing behavior and adoptive parent depressive symptoms over time, with mothers' depressive symptoms being a more salient risk factor for child internalizing behavior than fathers'. We found one significant cross-lagged association from adoptive mother depressive symptoms at child age 18 months to child internalizing behavior at age 27 months. Infant negative emotionality (i.e., emotional liability) at age 9 months predicted both child internalizing behavior and adoptive parent depressive symptoms. CONCLUSION: Results suggest that postnatal maternal depressive symptoms confer specific risks for child internalizing behaviors in toddlerhood and childhood and depressive symptoms in childhood.

Using an adoption design to test genetically based differences in risk for child behavior problems in response to home environmental influences.

Differential susceptibility theory (DST) posits that individuals differ in their developmental plasticity: some children are highly responsive to both environmental adversity and support, while others are less affected. According to this theory, "plasticity" genes that confer risk for psychopathology in adverse environments may promote superior functioning in supportive environments. We tested DST using a broad measure of child genetic liability (based on birth parent psychopathology), adoptive home environmental variables (e.g., marital warmth, parenting stress, and internalizing symptoms), and measures of child externalizing problems (n = 337) and social competence (n = 330) in 54-month-old adopted children from the Early Growth and Development Study. This adoption design is useful for examining DST because children are placed at birth or shortly thereafter with nongenetically related adoptive parents, naturally disentangling heritable and postnatal environmental effects. We conducted a series of multivariable regression analyses that included Gene × Environment interaction terms and found little evidence of DST; rather, interactions varied depending on the environmental factor of interest, in both significance and shape. Our mixed findings suggest further investigation of DST is warranted before tailoring screening and intervention recommendations to children based on their genetic liability or "sensitivity."

Psychopathology Symptoms are Associated with Prenatal Health Practices in Pregnant Women with Heavy Smoking Levels.

PURPOSE: Smoking during pregnancy may be linked to other problematic prenatal health behaviors in women. We examined interrelationships among prenatal smoking, prenatal health behaviors and mental health. The objective of this study was to examine factors that may contribute to variations in prenatal health practices among women who smoke during pregnancy. METHODS: Birth mothers from an adoption study (N = 912) were interviewed about prenatal smoking, health behaviors, and mental health symptoms at 5 months postpartum. RESULTS: One-quarter of participants (N = 222) reported smoking 6 or more cigarettes daily for at least 1 trimester. For mothers who smoked more than 6 cigarettes daily, higher levels of antisocial behaviors (ß = - .14, p = .03) and depressive symptoms (ß = - .17, p = .03) were associated with less frequent prenatal folate use; antisocial behaviors and depressive symptoms were not associated for prenatal folate use among women who did not smoke more than 6 cigarettes daily. For mothers who did not smoke more than 6 cigarettes daily, more depressive symptoms were associated with fewer prenatal care visits (ß = .12, p = .01). Antisocial behaviors and anxiety symptoms were not associated with prenatal care visits in either group of mothers. CONCLUSIONS FOR PRACTICE: Maternal antisocial behaviors and depressive symptoms during pregnancy may be markers for poorer adherence to recommendations for folate supplementation among women who smoke 6 or more cigarettes daily during pregnancy, independent of adequacy of prenatal care.

Examining the Role of Genetic Risk and Longitudinal Transmission Processes Underlying Maternal Parenting and Psychopathology and Children's ADHD Symptoms and Aggression: Utilizing the Advantages of a Prospective Adoption Design.

Although genetic factors may contribute to initial liability for ADHD onset, there is growing evidence of the potential importance of the rearing environment on the developmental course of ADHD symptomatology. However, associations between family-level variables (maternal hostility, maternal depressive symptoms) and child behaviors (developmental course of ADHD and aggression) may be explained by genes that are shared by biologically related parents and children. Furthermore, ADHD symptoms and aggression commonly co-occur: it is important to consider both simultaneously to have a better understanding of processes underlying the developmental course of ADHD and aggression. To addresses these issues, we employed a longitudinal genetically sensitive parent-offspring adoption design. Analyses were conducted using Cohort I (n = 340) of the Early Growth and Development Study with cross-validation analyses conducted with Cohort II (n = 178). Adoptive mother hostility, but not depression, was associated with later child ADHD symptoms and aggression. Mothers and their adopted children were genetically unrelated, removing passive rGE as a possible explanation. Early child impulsivity/activation was associated with later ADHD symptoms and aggression. Child impulsivity/activation was also associated with maternal hostility, with some evidence for evocative gene-environment correlation processes on adoptive mother depressive symptoms. This study provides novel insights into family-based environmental influences on child ADHD and aggression symptoms, independent of shared parental genetic factors, implications of which are further explicated in the discussion.

Child Effects on Parental Negativity: The Role of Heritable and Prenatal Factors.

This study examined two possible mechanisms, evocative gene-environment correlation and prenatal factors, in accounting for child effects on parental negativity. Participants included 561 children adopted at birth, and their adoptive parents and birth parents within a prospective longitudinal adoption study. Findings indicated child effects on parental negativity, such that toddlers' negative reactivity at 18 months was positively associated with adoptive parents' over-reactive and hostile parenting at 27 months. Furthermore, we found that child effects on parental negativity were partially due to heritable (e.g., birth mother [BM] internalizing problems and substance use) and prenatal factors (e.g., BM illicit drug use during pregnancy) that influence children's negative reactivity at 18 months. This study provides critical evidence for "child on parent" effects.