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Background Heightened amygdala response to threatening cues has been repeatedly observed in borderline personality disorder (BPD). A previous report linked hyperactivation to deficient amygdala habituation to repeated stimuli, but the biological underpinnings are incompletely understood. Methods We examined a sample of 120 patients with BPD and 115 healthy control subjects with a well-established functional magnetic resonance imaging emotional face processing task to replicate the previously reported amygdala habituation deficit in BPD and probed this neural phenotype for associations with symptom severity and early social risk exposure. Results Our results confirm a significant reduction in amygdala habituation to repeated negative stimuli in BPD (pFWE = .015, peak-level familywise error [FWE] corrected for region of interest). Post hoc comparison and regression analysis did not suggest a role for BPD clinical state (pFWE > .56) or symptom severity (pFWE > .45) for this phenotype. Furthermore, deficient amygdala habituation was significantly related to increased exposure to adverse childhood experiences (pFWE = .013, region of interest corrected). Conclusions Our data replicate a prior report on deficient amygdala habituation in BPD and link this neural phenotype to early adversity, a well-established social environmental risk factor for emotion dysregulation and psychiatric illness.

The hypothalamus-pituitary-adrenal axis (HPAA) and its end product, the glucocorticoid cortisol, has been shown to be associated with psychopathology. Determining cortisol concentrations in hair (HCC) allows the investigation of long-term HPAA-activity. There is a significant scarcity of studies investigating the link between HCC and psychopathology and quality of life in child and adolescent samples. In addition, as the HPAA constitutes a feedback system enabling adaption to environmental demands, it is important to consider the socio-environmental context that the children grow up in. We therefore investigated the associations between child HCC and psychopathology/quality of life and compared these links in two groups of five to 12-year-olds: children living with mothers who report experiences of early life maltreatment (ELM) (high-risk group) and children whose mothers did not report any ELM (low-risk group). We expected that, under conditions of a high-risk environment, elevated HPAA-functioning would be associated with low levels of psychopathology and high levels of quality of life in children. Under low-risk conditions, elevated HPAA-functioning would be associated with high levels of psychopathology and low levels of quality of life in children. For the complete sample of N = 130 children, three-months HCC did not significantly predict child psychopathology or quality of life. However, there was a significant moderating effect of group membership: In the high-risk group, high levels of HCC were significantly associated with high levels of self-reported quality of life. In the low-risk group, there was no association between HCC and self-reported quality of life. For child psychopathology, in the low-risk group, high levels of HCC were significantly associated with high levels of teacher reported behavior problems, whereas in the high-risk group, the association did not reach significance. Our results underline the importance of accounting for the social environment children grow up in when investigating the link between HCC and child psychopathology and quality of life.