The acute effects of community violence on young children's regulatory, behavioral, and developmental outcomes in a low-income urban sample in Brazil.

BACKGROUND: Existing research on the impacts of adversity on young children's psychological well-being has largely focused on household-level risk factors using observational methods in high-income countries. This study leverages natural variation in the timing and location of community homicides to estimate their acute effects on the regulatory, behavioral, and developmental outcomes of Brazilian 3-year-olds. METHODS: We compared the outcomes of children who were assessed soon after a recent neighborhood homicide to those of children from the same residential neighborhoods who had not recently experienced community violence. Our sample included 3,241 3-year-olds (Mage = 41.05 months; 53% female; 45% caregiver education less than middle school; 26% receiving a public assistance program) from seven neighborhoods in São Paulo, Brazil. Child outcome measures included parent reports of effortful control and behavior problems as well as direct assessments of children's developmental (cognitive, language, and motor) skills. Community homicides were measured using police records. RESULTS: Recent exposure to community homicides was associated with lower effortful control, higher behavior problems, and lower overall developmental performance for children (d = .05-.20 standard deviations; p = ns - <.001). Effects were consistent across subgroups based on sociodemographic characteristics and environmental supports, but generally largest when community violence exposure was geographically proximal (within 600 m of home) and recent (within 2 weeks prior to assessment). CONCLUSIONS: Results highlight the pervasive effects that community violence can have on young children as well as the need to expand support to mitigate these effects and prevent inequities early in life.

Long-term mental health cost of the Great Chinese Famine.

The Great Chinese Famine (1959-1961) claimed tens of millions of lives. This study aims to causally examine the long-term mental health cost it imposed on those who survived. To estimate the nationwide total mental health cost, we use a novel dataset to measure the famine intensity of every prefecture-level region, match it to a nationally representative survey, and then identify the long-term effects of the famine on the depression of rural residents then in the early years of their lives. Difference-in-differences estimates reveal that a one-standard-deviation rise in the experienced famine intensity increased a standard measure of depression by about 0.039 and 0.064 if the individual experienced the famine at ages 0-2 and 3-5, respectively. This translates into roughly 7.99 million cases of severe depressive symptoms caused by the famine, which is likely an undercount. Examining the mechanisms behind the large effects, we find that important roles were played by starvation experience and childhood maltreatment, as well as the primary mediators including other health outcomes, economic status, and social relationship. Our findings shed light on how large-scale food security failures impact the mental well-being of the survivors.

Mother's and children's ADHD genetic risk, household chaos and children's ADHD symptoms: A gene-environment correlation study.

BACKGROUND: Chaotic home environments may contribute to children's attention-deficit hyperactivity disorder (ADHD) symptoms. However, ADHD genetic risk may also influence household chaos. This study investigated whether children in chaotic households had more ADHD symptoms, if mothers and children with higher ADHD genetic risk lived in more chaotic households, and the joint association of genetic risk and household chaos on the longitudinal course of ADHD symptoms across childhood. METHODS: Participants were mothers and children from the Environmental Risk (E-Risk) Longitudinal Twin Study, a UK population-representative birth cohort of 2,232 twins. Children's ADHD symptoms were assessed at ages 5, 7, 10 and 12 years. Household chaos was rated by research workers at ages 7, 10 and 12, and by mother's and twin's self-report at age 12. Genome-wide ADHD polygenic risk scores (PRS) were calculated for mothers (n = 880) and twins (n = 1,999); of these, n = 871 mothers and n = 1,925 children had information on children's ADHD and household chaos. RESULTS: Children in more chaotic households had higher ADHD symptoms. Mothers and children with higher ADHD PRS lived in more chaotic households. Children's ADHD PRS was associated with household chaos over and above mother's PRS, suggesting evocative gene-environment correlation. Children in more chaotic households had higher baseline ADHD symptoms and a slower rate of decline in symptoms. However, sensitivity analyses estimated that gene-environment correlation accounted for a large proportion of the association of household chaos on ADHD symptoms. CONCLUSIONS: Children's ADHD genetic risk was independently associated with higher levels of household chaos, emphasising the active role of children in shaping their home environment. Our findings suggest that household chaos partly reflects children's genetic risk for ADHD, calling into question whether household chaos directly influences children's core ADHD symptoms. Our findings highlight the importance of considering parent and child genetic risk in relation to apparent environmental exposures.

Early life experience and sex influence acoustic repertoire use in wild-born, but hand-reared, captive cheetahs (Acinonyx jubatus).

Early deprivation of adult influence is known to have long-lasting effects on social abilities, notably communication skills, as adults play a key role in guiding and regulating the behavior of youngsters, including acoustic repertoire use in species in which vocal production is not learned. Cheetahs grow up alongside their mother for 18 months, thus maternal influences on the development of social skills are likely to be crucial. Here, we investigated the impact of early maternal deprivation on vocal production and use in 12 wild-born cheetahs, rescued and subsequently hand-reared either at an early (less than 2 months) or a later stage of development. We could distinguish 16 sound types, produced mostly singly but sometimes in repeated or multitype sound sequences. The repertoire of these cheetahs did not differ fundamentally from that described in other studies on adult cheetahs, but statistical analyses revealed a concurrent effect of both early experience and sex on repertoire use. More specifically, early-reared males were characterized by a high proportion of Purr, Meow, and Stutter; early-reared females Mew, Growl, Hoot, Sneeze, and Hiss; late-reared males Meow, Mew, Growl, and Howl; and late-reared females mostly Meow. Our study demonstrates therefore the long-term effects of maternal deprivation on communication skills in a limited-vocal learner and its differential effect according to sex, in line with known social differences and potential differential maternal investment. More generally, it emphasizes the critical importance to consider the past history of the subjects (e.g., captive/wild-born, mother/hand-reared, early/late-mother-deprived, etc.) when studying social behavior, notably acoustic communication.

Myelin and oligodendrocyte lineage cell dysfunctions: New players in the etiology and treatment of depression and stress-related disorders.

Depressive disorders are complex, multifactorial disorders that have been traditionally attributed exclusively to neuronal abnormalities. However, recent studies have increased our understanding of the contribution of glial cells-and particularly of oligodendroglia-to the pathogenesis and treatment outcome of depression and stress-related disorders. This review scrutinizes recent studies focusing on the neurosupportive functions exerted by myelin and oligodendrocyte lineage cells and their disruption in depression and stress-related disorders. It also illustrates how myelin and oligodendroglia respond to antidepressants and non-pharmacological treatment alternatives and proposes oligodendroglia-directed approaches as novel therapeutic options for depressive disorders.

Associations of perceived adverse lifetime experiences with brain structure in UK Biobank participants.

BACKGROUND: Adversity experiences (AEs) are major risk factors for psychiatric illness, and ample evidence suggests that adversity-related changes in brain structure enhance this vulnerability. To achieve greater understanding of the underlying biological pathways, increased convergence among findings is needed. Suggested future directions may benefit from the use of large population samples which may contribute to achieving this goal. We addressed mechanistic pathways by investigating the associations between multiple brain phenotypes and retrospectively reported AEs in early life (child adversity) and adulthood (partner abuse) in a large population sample, using a cross-sectional approach. METHODS: The UK Biobank resource was used to access imaging-derived phenotypes (IDPs) from 6,751 participants (aged: M = 62.1, SD = 7.2, range = 45-80), together with selected reports of childhood AEs and adult partner abuse. Principal component analysis was used to reduce the dimensionality of the data prior to multivariate tests. RESULTS: The data showed that participants who reported experiences of childhood emotional abuse ('felt hated by family member as a child') had smaller cerebellar and ventral striatum volumes. This result was also depicted in a random subset of participants; however, we note small effect sizes ( ηp2  < .01), suggestive of modest biological changes. CONCLUSIONS: Using a large population cohort, this study demonstrates the value of big datasets in the study of adversity and using automatically preprocessed neuroimaging phenotypes. While retrospective and cross-sectional characteristics limit interpretation, this study demonstrates that self-perceived adversity reports, however nonspecific, may still expose neural consequences, identifiable with increased statistical power.

Editorial: Are our kids getting a fair deal?

With the patchy but increasing roll-out of the COVID-19 vaccine, and as the world begins to emerge in a bumpy fashion from strict lock-downs, the frightening experience of overwhelmed hospitals and alarmingly high mortality rates from COVID-19, we are beginning to take stock of the huge toll from the pandemic. One of the oft-voiced concerns is the impact on mental health, particularly for vulnerable children and adolescents, but how much of a problem is there really? Are we facing a crisis?

Annual Research Review: Critical windows - the microbiota-gut-brain axis in neurocognitive development.

The gut microbiota is a vast, complex, and fascinating ecosystem of microorganisms that resides in the human gastrointestinal tract. As an integral part of the microbiota-gut-brain axis, it is now being recognized that the microbiota is a modulator of brain and behavior, across species. Intriguingly, periods of change in the microbiota coincide with the development of other body systems and particularly the brain. We hypothesize that these times of parallel development are biologically relevant, corresponding to 'sensitive periods' or 'critical windows' in the development of the microbiota-gut-brain axis. Specifically, signals from the microbiota during these periods are hypothesized to be crucial for establishing appropriate communication along the axis throughout the life span. In other words, the microbiota is hypothesized to act like an expected input to calibrate the development of the microbiota-gut-brain axis. The absence or disruption of the microbiota during specific developmental windows would therefore be expected to have a disproportionate effect on specific functions or potentially for regulation of the system as a whole. Evidence for microbial modulation of neurocognitive development and neurodevelopmental risk is discussed in light of this hypothesis, finishing with a focus on the challenges that lay ahead for the future study of the microbiota-gut-brain axis during development.

Practitioner Review: Twenty years of research with adverse childhood experience scores - Advantages, disadvantages and applications to practice.

BACKGROUND: Adverse childhood experience (ACE) scores have become a common approach for considering childhood adversities and are highly influential in public policy and clinical practice. Their use is also controversial. Other ways of measuring adversity - examining single adversities, or using theoretically or empirically driven methods - might have advantages over ACE scores. METHODS: In this narrative review we critique the conceptualisation and measurement of ACEs in research, clinical practice, public health and public discourse. RESULTS: The ACE score approach has the advantages - and limitations - of simplicity: its simplicity facilitates wide-ranging applications in public policy, public health and clinical settings but risks over-simplistic communication of risk/causality, determinism and stigma. The other common approach - focussing on single adversities - is also limited because adversities tend to co-occur. Researchers are using rapidly accruing datasets on ACEs to facilitate new theoretical and empirical approaches but this work is at an early stage, e.g. weighting ACEs and including severity, frequency, duration and timing. More research is needed to establish what should be included as an ACE, how individual ACEs should be weighted, how ACEs cluster, and the implications of these findings for clinical work and policy. New ways of conceptualising and measuring ACEs that incorporate this new knowledge, while maintaining some of the simplicity of the current ACE questionnaire, could be helpful for clinicians, practitioners, patients and the public. CONCLUSIONS: Although we welcome the current focus on ACEs, a more critical view of their conceptualisation, measurement, and application to practice settings is urgently needed.

Research Review: Intergenerational transmission of disadvantage: epigenetics and parents' childhoods as the first exposure.

BACKGROUND: For decades, economists and sociologists have documented intergenerational transmission of socioeconomic disadvantage, demonstrating that economic, political, and social factors contribute to 'inherited hardship'. Drawing on biological factors, the developmental origins of adult health and disease model posits that fetal exposure to maternal prenatal distress associated with socioeconomic disadvantage compromises offspring's neurodevelopment, affecting short- and long-term physical and mental health, and thereby psychosocial standing and resources. Increasing evidence suggests that mother-to-child influence occurs prenatally, in part via maternal and offspring atypical HPA axis regulation, with negative effects on the maturation of prefrontal and subcortical neural circuits in the offspring. However, even this in utero timeframe may be insufficient to understand biological aspects of the transmission of factors contributing to disadvantage across generations. METHODS: We review animal studies and emerging human research indicating that parents' childhood experiences may transfer epigenetic marks that could impact the development of their offspring independently of and in interaction with their offspring's perinatal and early childhood direct exposures to stress stemming from socioeconomic disadvantage and adversity. RESULTS: Animal models point to epigenetic mechanisms by which traits that could contribute to disadvantage may be transmitted across generations. However, epigenetic pathways of parental childhood experiences influencing child outcomes in the next generation are only beginning to be studied in humans. With a focus on translational research, we point to design features and methodological considerations for human cohort studies to be able to test the intergenerational transmission hypothesis, and we illustrate this with existing longitudinal studies. CONCLUSIONS: Epigenetic intergenerational transmission, if at play in human populations, could have policy implications in terms of reducing the continuation of disadvantage across generations. Further research is needed to address this gap in the understanding of the perpetuation of compromised lives across generations.

Early adversity and learning: implications for typical and atypical behavioral development.

BACKGROUND: Children who experience early adversity often develop emotion regulatory problems, but little is known about the mechanisms that mediate this relation. We tested whether general associative learning processes contribute to associations between adversity, in the form of child maltreatment, and negative behavioral outcomes. METHODS: Eighty-one participants between 12 and 17 years of age were recruited for this study and completed a probabilistic learning Task. Forty-one of these participants had been exposed to physical abuse, a form of early adversity. Forty additional participants without any known history of maltreatment served as a comparison group. All participants (and their parents) also completed portions of the Youth Life Stress Interview to understand adolescent's behavior. We calculated measures of associative learning, and also constructed mathematical models of learning. RESULTS: We found that adolescents exposed to high levels of adversity early in their lives had lower levels of associative learning than comparison adolescents. In addition, we found that impaired associative learning partially explained the higher levels of behavioral problems among youth who suffered early adversity. Using mathematical models, we also found that two components of learning were specifically affected in children exposed to adversity: choice variability and biases in their beliefs about the likelihood of rewards in the environment. CONCLUSIONS: Participants who had been exposed to early adversity were less able than their peers to correctly learn which stimuli were likely to result in reward, even after repeated feedback. These individuals also used information about known rewards in their environments less often. In addition, individuals exposed to adversity made decisions early in the learning process as if rewards were less consistent and occurred more at random. These data suggest one mechanism through which early life experience shapes behavioral development.

FKBP5 genotype and early life stress exposure predict neurobehavioral outcomes for preterm infants.

PROBLEM: This study evaluated the relationship between stressful early life neonatal intensive care unit (NICU) experiences, genetic variation of a stress response-associated gene (FKBP5), and neurobehavioral outcomes. METHOD: The impact of genetic variation and stress experience on neurobehavioral outcomes was examined for 41 preterm infants. Statistical analyses explored the main effects of FKBP5 genotype and NICU stress experience, as well as their interaction on infant neurobehavioral development prior to discharge. RESULTS: Statistical analyses demonstrated a relationship between both FKPB5 genotype and stress related to NICU care that were independently associated with neurobehavioral outcomes; indicating a main effect of genotype and a main effect of stress on neurodevelopment. Additionally, we found an interaction between the minor allele genotype and NICU stress potentially associated with less favorable developmental progress at discharge. IMPLICATIONS: Evidence of genetic and environmental risk factors for neurodevelopmental impairment suggests the need for improved evidence-based practice initiatives to protect those most vulnerable to the combination of genetic susceptibility to stress and medical fragility.

Naturalistic rodent models of chronic early-life stress.

A close association between early-life experience and cognitive and emotional outcomes is found in humans. In experimental models, early-life experience can directly influence a number of brain functions long-term. Specifically, and often in concert with genetic background, experience regulates structural and functional maturation of brain circuits and alters individual neuronal function via large-scale changes in gene expression. Because adverse experience during sensitive developmental periods is often associated with neuropsychiatric disease, there is an impetus to create realistic models of distinct early-life experiences. These can then be used to study causality between early-life experiential factors and cognitive and emotional outcomes, and to probe the underlying mechanisms. Although chronic early-life stress has been linked to the emergence of emotional and cognitive disorders later in life, most commonly used rodent models of involve daily maternal separation and hence intermittent early-life stress. We describe here a naturalistic and robust chronic early-life stress model that potently influences cognitive and emotional outcomes. Mice and rats undergoing this stress develop structural and functional deficits in a number of limbic-cortical circuits. Whereas overt pathological memory impairments appear during adulthood, emotional and cognitive vulnerabilities emerge already during adolescence. This naturalistic paradigm, widely adopted around the world, significantly enriches the repertoire of experimental tools available for the study of normal brain maturation and of cognitive and stress-related disorders including depression, autism, post-traumatic stress disorder, and dementia.

Neonatal handling: an overview of the positive and negative effects.

As one of the first rodent models designed to investigate the effects of early-life experiences, the neonatal handling paradigm has helped us better understand how subtle changes in the infant environment can powerfully drive neurodevelopment of the immature brain in typical or atypical trajectories. Here, we review data from more than 50 years demonstrating the compelling effects of neonatal handling on behavior, physiology, and neural function across the lifespan. Moreover, we present data that challenge the classical view of neonatal handling as an animal model that results only in positive/beneficial outcomes. Indeed, the overall goal of this review is to offer the suggestion that the effects of early-life experiences-including neonatal handling-are nuanced rather than unidirectional. Both beneficial and negative outcomes may occur, depending on the parameters of testing, sex of the subject, and neurobehavioral system analyzed.

Long-run Relations between Childhood Shocks and Health in Late Adulthood-Evidence from the Survey of Health, Ageing, and Retirement in Europe.

In this article, we address the long-run associations between childhood shocks and health in late adulthood. Applying a life-course approach and data from SHARE, we estimate direct and indirect relations of shocks like relocation, dispossession, or hunger and health outcomes after 50 years of age. Having lived in a children's home, in a foster family, or having suffered a period of hunger turn out to be the most detrimental. Using a finite mixture model, which allows to classify the correlations between shocks and later health into a priori unknown groups, we show that some adverse shocks show opposite relations for specific groups. (JEL codes: J1, I12, J13).

Early-life diet does not affect preference for fish in herring gulls (Larus argentatus).

Urban populations of herring gulls (Larus argentatus) are increasing and causing human-wildlife conflict by exploiting anthropogenic resources. Gulls that breed in urban areas rely on varying amounts of terrestrial anthropogenic foods (e.g., domestic refuse, agricultural and commercial waste) to feed themselves. However, with the onset of hatching, many parent gulls switch to sourcing more marine than anthropogenic or terrestrial foods to provision their chicks. Although anthropogenic foods may meet chick calorific requirements for growth and development, some such foods (e.g., bread) may have lower levels of protein and other key nutrients compared to marine foods. However, whether this parental switch in chick diet is driven by chicks' preference for marine foods, or whether chicks' food preferences are shaped by the food types provisioned by their parents, remains untested. This study tests whether chick food preferences can be influenced by their provisioned diet by experimentally manipulating the ratio of time for which anthropogenic and marine foods were available (80:20 and vice versa) in the rearing diets of two treatment groups of rescued herring gull chicks. Each diet was randomly assigned to each of the 27 captive-reared chicks for the duration of the study. We tested chicks' individual food preferences throughout their development in captivity using food arrays with four food choices (fish, cat food, mussels and brown bread). Regardless of the dietary treatment group, we found that all chicks preferred fish and almost all refused to eat most of the bread offered. Our findings suggest that early-life diet, manipulated by the ratio of time the different foods were available, did not influence gull chicks' food preferences. Instead, chicks developed a strong and persistent preference for marine foods, which appears to match adult gulls' dietary switch to marine foods upon chick hatching and may reinforce the provisioning of marine foods during chick development. However, whether chicks in the wild would refuse provisioned foods, and to a sufficient extent to influence parental provisioning, requires further study. Longitudinal studies of urban animal populations that track wild individuals' food preferences and foraging specialisations throughout life are required to shed light on the development and use of anthropogenic resource exploitation.

Multiple behavioral mechanisms shape development in a highly social cichlid fish.

Early-life social experiences shape adult phenotype, yet the underlying behavioral mechanisms remain poorly understood. We manipulated early-life social experience in the highly social African cichlid fish Astatotilapia burtoni to investigate the effects on behavior and stress axis function in juveniles. Juveniles experienced different numbers of social partners in stable pairs (1 partner), stable groups (6 fish; 5 partners), and socialized pairs (a novel fish was exchanged every 5 days; 5 partners). Treatments also differed in group size (groups vs. pairs) and stability (stable vs. socialized). We then measured individual behavior and water-borne cortisol to identify effects of early-life experience. We found treatment differences in behavior across all assays: open field exploration, social cue investigation, dominant behavior, and subordinate behavior. Treatment did not affect cortisol. Principal components (PC) analysis revealed robust co-variation of behavior across contexts, including with cortisol, to form behavioral syndromes sensitive to early-life social experience. PC1 (25.1 %) differed by social partner number: juveniles with more partners (groups and socialized pairs) were more exploratory during the social cue investigation, spent less time in the territory, and were more interactive as dominants. PC5 (8.5 %) differed by stability: socialized pairs were more dominant, spent less time in and around the territory, were more socially investigative, and had lower cortisol than stable groups or pairs. Observations of the home tanks provided insights into the social experiences that may underlie these effects. These results contribute to our understanding of how early-life social experiences are accrued and exert strong, lasting effects on phenotype.

Expression of bond-related behaviors affects titi monkey responsiveness to oxytocin and vasopressin treatments.

Social bonds influence physiology and behavior, which can shape how individuals respond to physical and affective challenges. Coppery titi monkey (Plecturocebus cupreus) offspring form selective bonds with their fathers, making them ideal for investigating how father-daughter bonds influence juveniles' responses to oxytocin (OT) and arginine-vasopressin (AVP) manipulations. We quantified the expression of father-daughter bond-related behaviors in females (n = 10) and gave acute intranasal treatments of saline, low/medium/high OT, low/high AVP, or an OT receptor antagonist (OTA) to subjects prior to a parent preference test. While females spent more time in proximity to their parents than strangers, we found a large degree of individual variation. Females with greater expression of bonding behaviors responded to OT treatments in a dose-dependent manner. Subjects also spent less time in proximity to strangers when treated with High OT (p = 0.003) and Low OT (p = 0.007), but more time when treated with High AVP (p = 0.007), Low AVP (p = 0.009), and OTA (p = 0.001). Findings from the present study suggest that variation in the expression of bond-related behaviors may alter responsiveness to OT and AVP, increasing engagement with unfamiliar social others. This enhanced sociality with strangers may promote the formation of pair bonds with partners.

Pathways From Early Life Adversities to Youth Marginalization: A Longitudinal Study of Youth Not in Education, Employment, or Training.

PURPOSE: Youth who are Not in Education, Employment, or Training (NEET) are at risk for numerous long-term occupational, social, and mental health-related sequelae. The aim of the present study was to investigate mediated pathways from early life risk factors to NEET status in early adulthood, with a particular focus on the role of the family environment during adolescence. METHODS: Participants were 6,403 respondents from the National Longitudinal Survey of Children and Youth, who were aged 10-11 years in cycles 1 (1994-1995) to 4 (2000-2001). Parents reported on indicators of early life adversity as well as parent-child conflict at age 12-13. Adolescents reported on their mental health and behaviour at age 14-15. NEET status was assessed at age 24 using tax information from the linked T1 Family File. Indirect pathways from childhood exposures, through adolescent factors, to NEET status in young adulthood were assessed via mediation analysis. RESULTS: At age 10/11, living with a single parent, low household income, stressful life events, and having a parent with a chronic condition were associated with greater likelihood of being NEET at age 24; parents' social support was negatively associated with NEET. These associations were mediated through parental depression at age 10/11, parent-child conflict at age 12/13, and adolescent mental health and behaviour at age 14/15. DISCUSSION: Our results add to a large body of literature linking family stressors, parental depression, parent-child interaction, and adolescent behaviour symptoms, suggesting a chain of influence through these factors toward young adult marginalization from the labour market.

Chd8 haploinsufficiency impacts rearing experience in C57BL/6 mice.

Mutations in CHD8 are one of the highest genetic risk factors for autism spectrum disorder. Studies in mice that investigate underlying mechanisms have shown Chd8 haploinsufficient mice display some trait disruptions that mimic clinical phenotypes, although inconsistencies have been reported in some traits across different models on the same strain background. One source of variation across studies may be the impact of Chd8 haploinsufficiency on maternal-offspring interactions. While differences in maternal care as a function of Chd8 genotype have not been studied directly, a previous study showed that pup survival was reduced when reared by Chd8 heterozygous dams compared with wild-type (WT) dams, suggesting altered maternal care as a function of Chd8 genotype. Through systematic observation of the C57BL/6 strain, we first determined the impact of Chd8 haploinsufficiency in the offspring on WT maternal care frequencies across preweaning development. We next determined the impact of maternal Chd8 haploinsufficiency on pup care. Compared with litters with all WT offspring, WT dams exhibited less frequent maternal behaviors toward litters consisting of offspring with mixed Chd8 genotypes, particularly during postnatal week 1. Dam Chd8 haploinsufficiency decreased litter survival and increased active maternal care also during postnatal week 1. Determining the impact of Chd8 haploinsufficiency on early life experiences provides an important foundation for interpreting offspring outcomes and determining mechanisms that underlie heterogeneous phenotypes.