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Background: Adolescent mothers have disproportionally high rates of childhood maltreatment or trauma (Noll & Shenk, 2013). Existing research suggests such early adversity may disrupt the hypothalamic-pituitary-adrenal (HPA) axis and psychobiological stress systems (Jones et al., 2013; Tarullo & Gunnar, 2006). Separately, children of adolescent parents often exhibit subpar neurocognitive development (Sommer et al., 2000). Potential mechanisms of this process may be increased prenatal psychological or physiological stress, which have both been negatively associated with fetal and infant neurodevelopment (e.g., Davis & Sandman, 2010). This longitudinal study explored associations between maternal childhood maltreatment (CM), prenatal cortisol and psychological stress, and infant cognition in pregnant adolescents and their toddlers.
Methods: Pregnant adolescents (N = 79) were assessed at three time points during pregnancy, approximately corresponding to once per trimester, and their infants were assessed at 14 months of age. CM was assessed using the sum score of the Childhood Trauma Questionnaire (Bernstein & Fink, 1997) at the first visit, while cortisol and stress were assessed at each timepoint. Cortisol was assessed with six saliva samples over a 24-hour period, which together were used to calculate the area under the curve (AUC), a commonly-used metric of cortisol excretion over a day (Pruessner et al., 2003). Psychological stress was assessed with the Perceived Stress Scale (Cohen et al., 1983). Values at each timepoint were combined to calculate mean cortisol and stress levels across gestation. Commonly-used perinatal (birthweight, gestational age) and demographic variables (maternal age, education, race/ethnicity, household income) were tested as covariates.
Results: Two distinct mediation models using the PROCESS macro (Hayes, 2013) in SPSS 24 separately assessed for the mediating role of prenatal cortisol and psychological stress across gestation between maternal CM and infant cognition. Results indicated that maternal CM exposure predicts both increased prenatal psychological stress (b = 7.52, t(72) = 4.22, p < .001) and worse infant cognitive outcomes (b = -11.20, t(71) = -2.32, p < .05) in adolescent mother-infant dyads. However, findings did not reveal a mediation effect of prenatal cortisol or psychological stress.
Discussion: Overall, the results of this study suggest that maternal childhood maltreatment is an underlying risk factor for non-optimal infant cognitive development in an already high-risk population. Assessing young mothers for a history of childhood trauma as part of routine prenatal care may better identify mothers who could be experiencing high stress and infants who are at risk for poorer cognitive development. Findings from this study add to the complexity of our understanding of how early adversity alters developmental trajectories throughout adolescence and what prenatal and familial factors may influence infant development. Future work should continue to examine the associations between maternal adversity, prenatal stress, and infant developmental outcomes to examine how the nature or directionality of the relationship changes depending on different populations and the magnitude, timing, and severity of adversity exposure.
Sophie Foss, Columbia University Medical Center
Presenting Author
Sara C. Haden, Long Island University
Non-Presenting Author
Nicholas Papouchis, Long Island University
Non-Presenting Author
Nicole M. Cain, Long Island University
Non-Presenting Author
Catherine Monk, Columbia University
Non-Presenting Author