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=6008 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.