Early life events can exert a powerful influence on both the pattern of brain architecture and behavioral development. In this study a conceptual framework is provided for considering how the ...structure of early experience gets "under the skin," The study begins with a description of the genetic framework that lays the foundation for brain development, and then proceeds to the ways experience interacts with and modifies the structures and functions of the developing brain. Much of the attention is focused on early experience and sensitive periods, although it is made clear that later experience also plays an important role in maintaining and elaborating this early wiring diagram, which is critical to establishing a solid footing for development beyond the early years.
It is now widely recognized that children exposed to adverse life events in the first years of life are at increased risk for a variety of neural, behavioral, and psychological sequelae. As we ...discuss in this paper, adverse events represent a violation of the expectable environment. If such violations occur during a critical period of brain development, the detrimental effects of early adversity are likely to be long lasting. Here we discuss the various ways adversity becomes neurobiologically embedded, and how the timing of such adversity plays an important role in determining outcomes. We conclude our paper by offering recommendations for how to elucidate the neural mechanisms responsible for the behavioral sequelae and how best to model the effects of early adversity.
Adversity might best be thought of as a violation of the expectable environment.Adversity can take many forms, including exposure to biological and psychosocial hazards, which often coexist as complex exposures.Many forms of early adversity are not time limited, making it difficult to tease apart the cumulative effects of adversity from the effects of early life adversity.Exposure to various forms of adversity early in life is associated with alterations in brain development, which in turn is associated with psychological, behavioral, and physical health consequences.Exposure to adversity during critical periods of development is more likely to lead to permanent rather than transient effects on the brain.Parallel studies across humans and animal models of early adversity will prove essential to understanding how adversity becomes neurobiologically embedded.
In a randomized controlled trial, we compared abandoned children reared in institutions to abandoned children placed in institutions but then moved to foster care. Young children living in ...institutions were randomly assigned to continued institutional care or to placement in foster care, and their cognitive development was tracked through 54 months of age. The cognitive outcome of children who remained in the institution was markedly below that of never-institutionalized children and children taken out of the institution and placed into foster care. The improved cognitive outcomes we observed at 42 and 54 months were most marked for the youngest children placed in foster care. These results point to the negative sequelae of early institutionalization, suggest a possible sensitive period in cognitive development, and underscore the advantages of family placements for young abandoned children.
Significance Disruptions in stress response system functioning are thought to be a central mechanism by which exposure to adverse early-life environments influences human development. Although rodent ...models support this possibility, results from human studies have been decidedly mixed. Using data from an experimental study examining whether random assignment to a caregiving environment alters development of the autonomic nervous system and hypothalamic–pituitary–adrenal axis in humans, we provide causal evidence for persistent effects of the early caregiving environment on stress response system functioning in humans with effects that differ markedly from those observed in rodent models. We also provide evidence of a sensitive period in human development during which the environment is particularly likely to alter stress response system development.
Disruptions in stress response system functioning are thought to be a central mechanism by which exposure to adverse early-life environments influences human development. Although early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis in rodents, evidence from human studies is inconsistent. We present results from the Bucharest Early Intervention Project examining whether randomized placement into a family caregiving environment alters development of the autonomic nervous system and HPA axis in children exposed to early-life deprivation associated with institutional rearing. Electrocardiogram, impedance cardiograph, and neuroendocrine data were collected during laboratory-based challenge tasks from children (mean age = 12.9 y) raised in deprived institutional settings in Romania randomized to a high-quality foster care intervention ( n = 48) or to remain in care as usual ( n = 43) and a sample of typically developing Romanian children ( n = 47). Children who remained in institutional care exhibited significantly blunted SNS and HPA axis responses to psychosocial stress compared with children randomized to foster care, whose stress responses approximated those of typically developing children. Intervention effects were evident for cortisol and parasympathetic nervous system reactivity only among children placed in foster care before age 24 and 18 months, respectively, providing experimental evidence of a sensitive period in humans during which the environment is particularly likely to alter stress response system development. We provide evidence for a causal link between the early caregiving environment and stress response system reactivity in humans with effects that differ markedly from those observed in rodent models.
Adverse psychosocial exposures in early life, namely experiences such as child maltreatment, caregiver stress or depression, and domestic or community violence, have been associated in ...epidemiological studies with increased lifetime risk of adverse outcomes, including diabetes, heart disease, cancers, and psychiatric illnesses. Additional work has shed light on the potential molecular mechanisms by which early adversity becomes "biologically embedded" in altered physiology across body systems. This review surveys evidence on such mechanisms and calls on researchers, clinicians, policymakers, and other practitioners to act upon evidence.
Childhood psychosocial adversity has wide-ranging effects on neural, endocrine, immune, and metabolic physiology. Molecular mechanisms broadly implicate disruption of central neural networks, neuroendocrine stress dysregulation, and chronic inflammation, among other changes. Physiological disruption predisposes individuals to common diseases across the life course.
Reviewed evidence has important implications for clinical practice, biomedical research, and work across other sectors relevant to public health and child wellbeing. Warranted changes include increased clinical screening for exposures among children and adults, scale-up of effective interventions, policy advocacy, and ongoing research to develop new evidence-based response strategies.
Children exposed to various forms of adversity early in life are at increased risk for a broad range of developmental difficulties, affecting both cognitive and emotional adjustment. We review a ...growing body of evidence suggesting that exposure to adverse circumstances affects the developing brain in ways that increase risk for a myriad of problems. We focus on two forms of adversity, one in which children are exposed to childhood maltreatment in family environments, and another in which children are exposed to extreme psychosocial deprivation in contexts of institutional rearing. We discuss ways in which each of these experiences represent violations of species-expected caregiving conditions, thereby imposing challenges to the developing brain. We also review emerging data pointing to the effectiveness of early intervention in remediating neurodevelopmental consequences associated with maltreatment or institutional rearing. We conclude by discussing implications of this work for public health efforts and highlight important directions for the field.
Abstract The human brain requires a wide variety of experiences and environmental inputs in order to develop normally. Children who are neglected by caregivers or raised in institutional environments ...are deprived of numerous types of species-expectant environmental experiences. In this review, we articulate a model of how the absence of cognitive stimulation and sensory, motor, linguistic, and social experiences common among children raised in deprived early environments constrains early forms of learning, producing long term deficits in complex cognitive function and associative learning. Building on evidence from animal models, we propose that deprivation accelerates the neurodevelopmental process of synaptic pruning and constrains myelination, resulting in age-specific reductions in cortical thickness and white matter integrity among children raised in deprived early environments. We review evidence linking early experiences of psychosocial deprivation to reductions in cognitive ability, associative and implicit learning, language skills, and executive functions as well as atypical patterns of cortical and white matter development—domains that should be profoundly influenced by deprivation through the learning and neural mechanisms we propose. These patterns of atypical development are difficult to explain with existing models that emphasize stress pathways and accelerated limbic system development. A learning account of how deprived early environments influence cognitive and neural development provides a complementary perspective to stress models and highlights novel pathways through which deprivation might confer risk for internalizing and externalizing psychopathology. We end by reviewing evidence for plasticity in cognitive and neural development among children raised in deprived environments following interventions that improve caregiving quality.
The COVID-19 pandemic priorities have focused on prevention, detection, and response. Beyond morbidity and mortality, pandemics carry secondary impacts, such as children orphaned or bereft of their ...caregivers. Such children often face adverse consequences, including poverty, abuse, and institutionalisation. We provide estimates for the magnitude of this problem resulting from COVID-19 and describe the need for resource allocation.
We used mortality and fertility data to model minimum estimates and rates of COVID-19-associated deaths of primary or secondary caregivers for children younger than 18 years in 21 countries. We considered parents and custodial grandparents as primary caregivers, and co-residing grandparents or older kin (aged 60–84 years) as secondary caregivers. To avoid overcounting, we adjusted for possible clustering of deaths using an estimated secondary attack rate and age-specific infection–fatality ratios for SARS-CoV-2. We used these estimates to model global extrapolations for the number of children who have experienced COVID-19-associated deaths of primary and secondary caregivers.
Globally, from March 1, 2020, to April 30, 2021, we estimate 1 134 000 children (95% credible interval 884 000–1 185 000) experienced the death of primary caregivers, including at least one parent or custodial grandparent. 1 562 000 children (1 299 000–1 683 000) experienced the death of at least one primary or secondary caregiver. Countries in our study set with primary caregiver death rates of at least one per 1000 children included Peru (10·2 per 1000 children), South Africa (5·1), Mexico (3·5), Brazil (2·4), Colombia (2·3), Iran (1·7), the USA (1·5), Argentina (1·1), and Russia (1·0). Numbers of children orphaned exceeded numbers of deaths among those aged 15–50 years. Between two and five times more children had deceased fathers than deceased mothers.
Orphanhood and caregiver deaths are a hidden pandemic resulting from COVID-19-associated deaths. Accelerating equitable vaccine delivery is key to prevention. Psychosocial and economic support can help families to nurture children bereft of caregivers and help to ensure that institutionalisation is avoided. These data show the need for an additional pillar of our response: prevent, detect, respond, and care for children.
UK Research and Innovation (Global Challenges Research Fund, Engineering and Physical Sciences Research Council, Medical Research Council), UK National Institute for Health Research, US National Institutes of Health, and Imperial College London.
We used structural MRI and EEG to examine brain structure and function in typically developing children in Romania (n = 20), children exposed to institutional rearing (n = 29), and children ...previously exposed to institutional rearing but then randomized to a high-quality foster care intervention (n = 25). In so doing, we provide a unique evaluation of whether placement in an improved environment mitigates the effects of institutional rearing on neural structure, using data from the only existing randomized controlled trial of foster care for institutionalized children. Children enrolled in the Bucharest Early Intervention Project underwent a T1-eighted MRI protocol. Children with histories of institutional rearing had significantly smaller cortical gray matter volume than never-institutionalized children. Cortical white matter was no different for children placed in foster care than never-institutionalized children but was significantly smaller for children not randomized to foster care. We were also able to explain previously reported reductions in EEG α-power among institutionally reared children compared with children raised in families using these MRI data. As hypothesized, the association between institutionalization and EEG α-power was partially mediated by cortical white matter volume for children not randomized to foster care. The increase in white matter among children randomized to an improved rearing environment relative to children who remained in institutional care suggests the potential for developmental "catch up" in white matter growth, even following extreme environmental deprivation.
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