Exposure to traumatic stress is associated with increased risk for posttraumatic stress disorder (PTSD) and alterations of hypothalamic-pituitary-adrenocortical (HPA) function. Research linking traumatic stress with HPA function in PTSD has been inconsistent, however, in part due to (a) the inclusion of trauma-exposed individuals without PTSD (TE) in control groups and (b) a failure to consider comorbid major depressive disorder (MDD) and moderating variables. This meta-analysis of 47 studies (123 effect sizes, N=6,008 individuals) revealed that daily cortisol output was lower for PTSD (d=−.36, SE=.15, p=.008) and PTSD+MDD (d=−.65, SE=.25, p=.008) groups relative to no trauma controls (NTC); TE and NTC groups did not differ significantly from each other. Afternoon/evening cortisol was lower in TE (d=−.25, SE=.09, p=.007) and PTSD (d=−.27, SE=.12, p=.021) groups and higher in PTSD+MDD groups (d=.49, SE=.24, p=.041) relative to NTC. Post-DST cortisol levels were lower in PTSD (d=−.40, SE=.12, p<.001), PTSD+MDD (d=−.65, SE=.14, p<.001), and TE groups (d=−.53, SE=.14, p<.001) relative to NTC. HPA effect sizes were moderated by age, sex, time since index event, and developmental timing of trauma exposure. These findings suggest that enhanced HPA feedback function may be a marker of trauma-exposure rather than a specific mechanism of vulnerability for PTSD, whereas lower daily cortisol output may be associated with PTSD in particular.

This longitudinal study investigated the stress autonomy, stress sensitization, and depression vulnerability hypotheses in adolescents across six years (i.e., grades 6 through 12). Participants were 240 children (Time 1 mean age = 11.86, SD = 0.57) who varied in risk for depression based on their mother's history of mood disorders. All analyses were conducted as multilevel models to account for nesting in the data. Results were consistent with the stress sensitization hypothesis. The withinsubject relation of stress levels to depressive symptoms strengthened with increasing numbers of prior depressive episodes. In addition, evidence consistent with the vulnerability hypothesis was found. The relation of stress levels to depressive symptoms was stronger for adolescents who were at risk for depression based on maternal depression history and for those who had experienced more depressive episodes through grade 12. These findings suggest that onsets of depression in adolescents may be predicted by both relatively stable and dynamic transactions between stressful life events and vulnerabilities such as maternal depression and youths' own history of depressive episodes. A Prospective Study of Stress Autonomy versus Stress Sensitization in Adolescents at Varied Risk for DepressionThe link between the experience of stressful life events (SLEs) and the onset of major depressive disorder (MDD) has received strong empirical support in both children and adults (Grant, Compas, Thurm, McMahon, & Gipson, 2004;Kendler, Karkowski, & Prescott, 1999), although considerable variability exists in individuals' responses to similar stressors. Diathesis-stress theories (e.g., Abramson, Metalsky, & Alloy, 1989;Abramson, Seligman, & Teasdale, 1978;Beck, 1967Beck, , 1976Monroe & Simons, 1991) have attempted to account for this variability by proposing relatively stable individual vulnerability factors that moderate the relation between stress and depression. Current evidence suggests that the risk of having a major depressive episode (MDE) increases as a function of the number of prior episodes (American Psychiatric Association, 2000;Solomon et al., 2000). Moreover, first lifetime Corresponding Author: Matthew C. Morris, M.S., Address: Psychology & Human Development, Vanderbilt University, Peabody MSC 512, 230 Appleton Place, Nashville, TN 37203, Phone: (615) 427-2688, Fax: (615) 343-9494, matthew.c.morris@vanderbilt.edu . Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at www.apa.org/pubs/journals/abn. NIH Public AccessAuthor Manuscript J Abnorm Psychol. ...

Research on the psychobiological sequelae of trauma has typically focused on long-term alterations in individuals with chronic posttraumatic stress disorder (PTSD). Far less is known about the nature and course of psychobiological risk factors for PTSD during the acute aftermath of trauma. In this review, we summarize data from prospective studies focusing on the relationships among sympathetic nervous system activity, hypothalamic-pituitary-adrenal function, coping strategies and PTSD symptoms during the early recovery (or non-recovery) phase. Findings from pertinent studies are integrated to inform psychobiological profiles of PTSD-risk in children and adults in the context of existing models of PTSD-onset and maintenance. Data regarding bidirectional relations between coping strategies and stress hormones is reviewed. Limitations of existing literature and recommendations for future research are discussed.

Background Alterations of hypothalamic-pituitary-adrenal (HPA) function are well-established in adults with current depression. HPA alterations may persist into remission and confer increased risk for recurrence. Methods A modified version of the Trier Social Stress Test (TSST) was administered at baseline to 32 young adults with remitted major depressive disorder and 36 never-depressed controls. Participants were randomly assigned to either a ‘high–stress’ condition involving social evaluation or a ‘low-stress’ control condition. Cortisol concentrations were measured in saliva samples throughout the TSST. Participants were assessed again after 6 months for the occurrence of stressful life events and depressive symptoms/disorders during the follow-up period. Results Participants who exhibited enhanced cortisol reactivity in the low-stress condition showed increases in depressive symptoms over follow-up, after controlling for stressful life events during the follow-up period. Anticipatory stress cortisol and cortisol reactivity each interacted with history of depressive episodes to predict depression trajectories. Limitations The single TSST administration limits conclusions about whether alterations of cortisol reactivity represent trait-like vulnerability factors or consequences (“scars’) of past depression. Conclusions These results extend previous findings on stress sensitivity in depression and suggest that altered HPA function during remission could reflect an endophenotype for vulnerability to depression recurrence. Findings support interactive models of risk for depression recurrence implicating HPA function, depression history, and sensitivity to minor stressors. Results may have implications for interventions that match treatment approaches to profiles of HPA function.

These results suggest that clinically referred preschoolers with BPD share with school-age children with BPD high rates of comorbid psychopathology and impaired functioning. Follow-up of these clinically referred preschoolers with BPD evaluating the stability of their diagnoses, treatment response, and their long-term outcome is necessary.