Presenter: Jason David
Mentors: Jeffrey Measelle and Jennifer Ablow, Psychology
Oral Presentation
Major: Psychology
Early life adversity is associated with adult elevations of inflammatory markers like circulating levels of C-reactive protein (CRP). Few studies have examined whether exposure to adversity prenatally is associated with inflammation during childhood. Exposure to adversity before birth may engender disease vulnerability via alterations in inflammatory biomarkers (i.e. fetal programming of disease hypothesis). This study examines the association between exposure to prenatal vs. postnatal adversity and CRP concentrations when infants were 18 months old. We followed 105 low-SES (socio-economic stress) infant-mother dyads across the perinatal transition. Our measures of psychosocial and contextual measured prenatally and at 5- and 18-months postnatally. When infants were 18 months old, resting state saliva samples were collected to assess CRP (mg/L) levels via enzyme immunoassay. Hierarchical regression analyses reveals a composite measure of prenatal maternal adversity, that uniquely predicts variability in infants’ log transformed CRP levels, B = 1.15 (SE = .05), p < .05. Maternal adversity at 5 months is not predictive of infant CRP, but maternal adversity at 18 months is marginally associated. These results raise questions about timing of exposure to adverse events as well as the potentially lasting effects on inflammatory processes when such exposure occurs very early in development.