Xenia Hengesch

• Early life adversity (ELA) poses a high risk for developing major health problems in adulthood including cardiovascular and infectious diseases and mental illness. However, the fact that ELA-associated disorders first become manifest many years after exposure raises questions about the mechanisms underlying their etiology. This thesis focuses on the impact of ELA on startle reflexivity, physiological stress reactivity and immunology in adulthood. The first experiment investigated the impact of parental divorce on affective processing. A special block design of the affective startle modulation paradigm revealed blunted startle responsiveness during presentation of aversive stimuli in participants with experience of parental divorce. Nurture context potentiated startle in these participants suggesting that visual cues of childhood-related content activates protective behavioral responses. The findings provide evidence for the view that parental divorce leads to altered processing of affective context information in early adulthood. A second investigation was conducted to examine the link between aging of the immune system and long-term consequences of ELA. In a cohort of healthy young adults, who were institutionalized early in life and subsequently adopted, higher levels of T cell senescence were observed compared to parent-reared controls. Furthermore, the results suggest that ELA increases the risk of cytomegalovirus infection in early childhood, thereby mediating the effect of ELA on T cell-specific immunosenescence. The third study addresses the effect of ELA on stress reactivity. An extended version of the Cold Pressor Test combined with a cognitive challenging task revealed blunted endocrine response in adults with a history of adoption while cardiovascular stress reactivity was similar to control participants. This pattern of response separation may best be explained by selective enhancement of central feedback-sensitivity to glucocorticoids resulting from ELA, in spite of preserved cardiovascular/autonomic stress reactivity.