European Journal of Psychotraumatology | |
Understanding the role of early life trauma in the neuroendocrine dysregulation of youth depression | |
关键词: abuse; acute stress; adolescent; depression; salivary cortisol; trauma; | |
DOI : 10.3402/ejpt.v3i0.19436 | |
来源: DOAJ |
【 摘 要 】
Background : To date there are inconsistent empirical findings regarding the nature of hypothalamic–pituitary–adrenal (HPA)-axis dysregulation in depressed youth. Some of these inconsistencies may be explained in part by exposure to different types of trauma. The purpose of this study is to clarify the interplay between trauma exposure and neuroendocrine reactivity in depressed youth. We hypothesized that exposure to specific subtypes of trauma will moderate the effect of depression on dysregulation of the stress response system. Methods : Participants were 51 depressed and non-depressed youth (22 males; mean age = 12.9, SD = 2.8). Participants completed a semi-structured clinical interview, an Early Trauma Inventory (ETI), and a 90-minute stress task which included saliva samples upon arrival, after a 30 minute baseline, 25, 35, 45, 55, and 65 minutes following the SE-Current Procedural Terminology (CPT). Results : There were no differences between depressed and non-depressed participants in reported exposure to trauma of any type. However, depressed participants had higher cortisol levels during the regulation phase, 45 [F(15,35) = 2.65, p < 0.05], 55 [F(15,35) = 2.64, p < 0.05], and 65 [F(15,35) = 3.11, p < 0.01] minutes after the stressor. We also found that there was a main effect of depression symptoms [F(11,35) = 296.18, p<0.05] on cortisol reactivity (AUCi). In addition, we found that there was a significant interaction of depression and trauma history [F(2,30) = 523.29, p<0.05], in that exposure to abuse, but not general trauma, increased AUCi in the depressed sample only. Conclusions : Depressed youth with a history of abuse are more likely to have a specific dysregulation of the HPA-axis related to an inability to “shut down” the stress response as evidenced by later peak times. This suggests that abuse may have an impact specifically on HPA regulatory capacity. We did not find this effect for general trauma highlighting the potential differential role of various types of trauma on HPA functioning.