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 living in low‐resource settings are at risk for failing to reach their developmental potential. While the behavioral outcomes of growing up in such settings are well‐known, the neural mechanisms underpinning poor outcomes have not been well elucidated, particularly in the context of low‐ and middle‐income countries. In this study, we measure brain metabolic responses to social and nonsocial stimuli in a cohort of 6‐ and 36‐month‐old Bangladeshi children. Study participants in both cohorts lived in an urban slum and were exposed to a broad range of adversity early in life including extreme poverty, malnutrition, recurrent infections, and low maternal education. We observed brain regions that responded selectively to social stimuli in both ages indicating that these specialized brain responses are online from an early age. We additionally show that the magnitude of the socially selective response is related to maternal education, maternal stress, and the caregiving environment. Ultimately our results suggest that a variety of psychosocial hazards have a measurable relationship with the developing social brain.

In this paper we explore the relationship between the Visual Evoked Potential (VEP), a component of the electroencephalogram elicited by visual stimuli, and cognitive functions in children growing up in an urban slum in Bangladesh. VEPs in response to pattern-reversing checkerboards were collected in 6 month-old-infants (n = 91) and 36-month-old children (n = 112). We examine variation in the amplitude and latency of the first positive component, the P1, of the VEP in relation to cognitive scores on the Mullen Scales of Early Learning and the Wechsler Preschool and Primary Scale of Intelligence. We also examine whether children’s caregiving experiences prior to the neuro-cognitive assessment explain variation in the P1 of the VEP. We find that the P1 amplitude of the VEP is related to concurrent cognitive performance in each respective cohort. We also find that the P1 amplitude at 6 months is prospectively associated with cognitive outcomes at 27 months, and the P1 amplitude at 36 months is prospectively associated with children’s IQ at 60 months. We find no associations between caregiving experiences and variation in the P1 of the VEP at 6 months, yet caregiving experience do explain variation in the P1 amplitude at 36 months. Caregiving experiences also explain variation in children’s concurrent and prospective cognitive functioning. The VEP may be used as a biomarker to index the neurobiological embedding of early adversity, which in turn may impact children’s cognitive functions.

It is well established that low resource environments early in life can predispose children to adverse health and compromised developmental outcomes. We explore possible mechanistic pathways underlying poor developmental outcomes in children growing up in a low resource setting in urban Bangladesh. We tested associations between psychosocial risks, namely maternal distress and poor caregiving experiences, and biological risks, namely poor growth (HAZ) and inflammation (C-reactive protein: CRP), and children’s developmental outcomes. Child development was measured using the Mullen Scales of Early Learning (MSEL) at 6 and 27 months in one cohort, and using the MSEL and Wechsler Preschool and Primary Scale of Intelligence (WPPSI) at 36 and 60 months respectively in another cohort. In the younger cohort, we found that more inflammation (estimated by the child’s CRP level at four months) predicted lower receptive language scores at 6 months, while more frequent caregiving interactions predicted higher receptive language scores at 6 months. In the older cohort, we found that at 27 months, a child’s growth measured by his or her current HAZ was positively associated with gross motor, visual reception, receptive language, and expressive language scores. In the oldest cohort, we found that higher HAZ and more frequent stimulating activities in the home predicted higher motor and language scores, whereas more inflammation (as estimated by CRP over the first two years of life) predicted lower motor scores at 36 months. At 60 months, we found that HAZ and caregiving experiences were positively associated with verbal IQ, whereas inflammation was negatively associated with verbal IQ. This work identifies malnutrition, inflammation, and caregiving as potential sites of intervention to improve neurodevelopment in children growing up in global poverty.