Socioeconomic and psychological correlates of postpartum depression at 6 months in Dhaka, Bangladesh.

To current study aimed to estimate the point prevalence and identify correlates of postpartum depression (PPD) in a sample of mothers in Dhaka. A total of 235 participants from low- and middle-SES neighbourhoods in Dhaka completed the Edinburgh Postnatal Depression Scale (EPDS) and other assessments of socioeconomic and psychological factors at 24 weeks postpartum. Regression models were fit to explore potential correlates of PPD. The estimated prevalence of high PPD risk in the current sample is 24.3%. In multivariable linear regression models, recent life events, perceived stress and household resources (e.g., access to cooking gas, telephone, furniture, electricity, television, etc.) were significantly associated with PPD. The association of social support with PPD when controlling for other variables was sensitive to the choice of social support measure, highlighting an important methodological issue. The point prevalence of PPD among poor, urban mothers in Bangladesh ranges from 12.3 to 28.5%, with psychological risk factors and household resources as strong correlates.

Cumulative psychosocial risk and early child development: validation and use of the Childhood Psychosocial Adversity Scale in global health research.

BACKGROUND: Evidence suggests that cumulative early psychosocial adversity can influence early child development (ECD). The Childhood Psychosocial Adversity Scale (CPAS) is a novel measure of cumulative risk designed for use in global ECD research. We describe its development and assess validity from its first application in Bangladesh, where it predicts cognitive development scores among young children. METHODS: Items were generated from literature review and qualitatively assessed for local relevance. Two-hundred and eighty-five mother-child dyads from an urban slum of Dhaka completed the CPAS at child ages 18, 24, 48, and/or 60 months. The CPAS was assessed for internal consistency, retest reliability, and convergent, incremental, and predictive validity. RESULTS: The CPAS includes subscales assessing child maltreatment, caregiver mental health, family conflict, domestic violence, and household/community psychosocial risks. In Bangladesh, subscales had good internal consistency (Cronbach's α > 0.70). Full-scale score had good 2-week test-retest reliability (intra-class correlation coefficient = 0.89; F(38,38) = 8.45, p < 0.001). Using multivariate regression, 48-month CPAS score significantly predicted 60-month intelligence quotient, accounting for more variance than socioeconomic status or malnutrition. CONCLUSIONS: The CPAS is a novel tool assessing cumulative childhood psychosocial risk. Evidence supports validity of its use in ECD research in Bangladesh, and ongoing work is applying it in additional countries.

Biological embedding of childhood adversity: from physiological mechanisms to clinical implications.

BACKGROUND: 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. OBSERVATIONS: 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. CONCLUSIONS: 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.

The science of early adversity: is there a role for large institutions in the care of vulnerable children?

It has been more than 80 years since researchers in child psychiatry first documented developmental delays among children separated from family environments and placed in orphanages or other institutions. Informed by such findings, global conventions, including the 1989 UN Convention on the Rights of the Child, assert a child's right to care within a family-like environment that offers individualised support. Nevertheless, an estimated 8 million children are presently growing up in congregate care institutions. Common reasons for institutionalisation include orphaning, abandonment due to poverty, abuse in families of origin, disability, and mental illness. Although the practice remains widespread, a robust body of scientific work suggests that institutionalisation in early childhood can incur developmental damage across diverse domains. Specific deficits have been documented in areas including physical growth, cognitive function, neurodevelopment, and social-psychological health. Effects seem most pronounced when children have least access to individualised caregiving, and when deprivation coincides with early developmental sensitive periods. Offering hope, early interventions that place institutionalised children into families have afforded substantial recovery. The strength of scientific evidence imparts urgency to efforts to achieve deinstitutionalisation in global child protection sectors, and to intervene early for individual children experiencing deprivation.

Effects of poverty on interacting biological systems underlying child development.

The developmental sequelae of childhood poverty are well documented. However, it is not poverty per se, but a multitude of risk factors associated with poverty that have a deleterious effect on children's development. Key risks factors that are likely to contribute to the adverse developmental effects of poverty include, for instance, food insecurity, infectious disease, and psychological stress related to the child's rearing environment. In this Review, we highlight synergistic biological pathways through which co-occurring risks related to poverty interact to shape children's neurocognitive development. We focus on pathways related to neural growth, energy metabolism, inflammation, and neuroendocrine responses to stress as key biological axes through which poverty becomes biologically embedded and might have long-term effects on children's neurocognitive development. We also discuss how biomarkers targeting these axes can be used to advance research on the biological processes through which poverty affects children's cognitive outcomes. Although the discussion has global relevance, we focus on low-resource settings where rates of poverty are highest and access to treatment might be limited.