Childhood Maltreatment History and Cortisol Concentration Across Pregnancy
1 Institute of Medical Psychology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Berlin, Germany. 2 Einstein Center for Neurosciences Berlin
2 Institute of Medical Psychology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Berlin, Germany.
3 Department of Experimental Obstetrics, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Berlin, Germany
4 Department of Obstetrics, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Berlin, Germany
5 Development, Health and Disease Research Program, University of California, Irvine, California, USA
Exposure to childhood maltreatment (CM) and early adversity is considered one of the most important preventable contributors to poor health outcomes later in life. These health consequences can be the result of immediate injuries, but they can also increase the risk of developing a range of health problems later in life, including depression, post-traumatic stress disorder, heart disease, diabetes and obesity. Such maltreatment has been associated with significant and persistent alterations in the hypothalamic-pituitary-adrenal (HPA) axis. Case reports and studies from the past few decades have revealed that such trauma-induced sequelae are not restricted to the individual having experienced the maltreatment, but that they may extend to that individual’s offspring as well. Given the inherently synergistic nature of the placental-fetal environment, persistent changes in HPA axis functioning induced by maternal trauma-exposure in early life likely play a significant role in the intergenerational transmission of childhood maltreatment (CM) sequelae. To better understand the effects of CM on cortisol secretion during pregnancy, hierarchal mixed-effects linear models were constructed to predict diurnal salivary cortisol secretion over the course of a day in early and late gestation. CM was not found to be a significant main predictor of total day cortisol secretion, but timing in gestation significantly modified the effects of CM on cortisol output across all models. These findings contradict the idea that fetal programming of CM sequelae occur through CM-induced hyperactive HPA functioning during pregnancy.