One in five children in the US grows up in poverty. These children face high risk for psychopathology, which often lasts a lifetime and perpetuates low socioeconomic status. Poor children often experience greater chronic stress, which may allow poverty to become biologically embedded by altering gene-brain links via epigenetic patterns which influence later brain structure and function, and broader physiological functioning. Despite a growing appreciation of the link between poverty and psychopathology, little is known about how poverty impacts underlying biological mechanisms and gives rise to anxiety and depression. This lack of knowledge hinders efforts to develop interventions targeting mechanisms linking poverty and psychopathology. By adding epigenetic data to the already existing NIMH funded grant ?Effects of poverty on affective development: A multi-level, longitudinal study? (1-R01MH103761-01) this study will add a significant novel measurement resource to an already rich study. Our objective is to improve the primary grant?s goal of understanding how poverty affects biology during development and leads to psychopathology. Like the primary grant, our central hypothesis is that living in poverty increases the occurrence of stressors (i.e. exposure to danger, family conflict, residential instability, and neglect), which leads to several biological changes. More specifically, epigenetic modifications (i.e. DNA methylation) represent an additional RDoC level through which poverty is biologically embedded and affects later brain structure and function and psychopathology. We examine teens from The Fragile Families and Child Wellbeing Study (FFCWS), an ongoing study of children born to predominantly low-income families. There are four key attributes of the FFCWS that make this an ideal sample to test our central hypothesis: 1) children were assessed at birth, 1, 3, 5 and 9 years, are being assessed at age 15; 2) although approximately 60% of the sample lives in poverty, a full range of incomes are represented allowing for comparisons; 3) saliva DNA was collected and stored at ages 9 and 15?thereby allowing for rare large-sample longitudinal DNA methylation analyses; and 4) all children will have several additional measures as part of the year 15 parent grant study, including: a) brain (with fMRI to assess activation and functional connectivity in response to emotional faces and with diffusion tensor imaging to measure structural connectivity); b) HPA axis function (cortisol in response to a stressor and DHEA); c) behavior (using an attention bias measure); and d) psychiatric interview, self- and parent-report measures of negative affect, and psychiatric symptoms. By leveraging the FFCWS, containing a wealth of longitudinal measures of exposures to poverty-related stressors, we are well positioned to conduct research that integrates experience across childhood with neurobiological and psychological data to better elucidate pathways to psychopathology.
Health and Human Services, Department of-National Institutes of Health
06/06/2014 to 05/31/2020