Hypothalamic–Pituitary–Adrenal Axis Activity and Sleep in Posttraumatic Stress Disorder

Abstract

Alterations of the hypothalamic-pituitary-adrenal (HPA) axis and sleep disturbances have been described separately in post-traumatic stress disorder (PTSD). It is not known if HPA alterations and sleep disturbances are associated in PTSD. This study examined sleep and HPA activity in 20 male medication-free subjects with PTSD and 16 matched healthy controls. Two nights of polysomnography were obtained and 24-h urinary cortisol was collected during day 2. Subjects self-administered a low-dose (0.5 mg) salivary dexamethasone test at home. Compared with controls, PTSD subjects had higher 24-h urinary mg cortisol/g creatinine (mean7SD 40717 vs 28712, p ¼ 0.03) but not significantly higher 24-h urinary cortisol (mean7SD 52715 mg/day vs 43723, p ¼ 0.19). PTSD subjects showed a trend towards less cortisol suppression after dexamethasone (73%718 vs 83%710, p ¼ 0.06). In the combined sample, delta sleep was significantly and negatively correlated with 24-h urinary cortisol (r ¼ À0.36, p ¼ 0.04), and with 24-h urinary cortisol/g creatinine on a trend level (r ¼ À0.34, p ¼ 0.06). Our results suggest that increased cortisol is negatively associated with delta sleep. This may contribute to sleep abnormalities in conditions associated with elevated cortisol, possibly including PTSD. Future studies should explore the temporal relationship between HPA activity, sleep disturbances, and psychopathology after a traumatic event.

Stability of the dexamethasone suppression test in borderline personality disorder with and without comorbid PTSD: A one‐year follow‐up study

“…In accordance with these results a negative relationship between the severity of PTSD symptoms and cortisol levels was reported by Yehuda and coworkers and an enhanced cortisol suppression was repeatedly found in PTSD patients (for review, see Yehuda, 2002). However, it must be mentioned that there are also diverging findings in this field (Kellner, Baker, et al, 2002;Maes et al, 1998;Otte et al, 2005).…”

Transcriptional Control of Monocyte Gene Expression in Post-Traumatic Stress Disorder

“…As an index of lower glucocorticoid signaling to the monocyte transcriptome in PTSD, this finding is in line with a substantial body of research showing lower circulating levels of cortisol in PTSD [37,60,63,67]. However, an almost equally large body of previous research supported the hypothesis of enhanced negative feedback or enhanced GR sensitivity in PTSD [42,61,66,68]. While it is difficult to draw firm conclusions about such GR sensitivity without knowing the level of circulating cortisol in our participants, our data are not supportive of greater GR sensitivity on monocytes in PTSD.…”

Innovative Approaches for the Treatment of Depression: Targeting the HPA Axis

“…However, experience shows that using endocrinological tests to identify individuals with HPA axis dysfunction is unlikely to aid selection of a subset of patients for clinical studies. Variability in neuroendocrine responsiveness due to age, gender, characteristics of the disease such as subtype and severity, hospitalization status and co-morbidity with other disorders (e.g., PTSD) are all complicating factors [179][180][181][182][183]. In summary, tantalising clinical and preclinical data do exist that suggest that drugs which intervene with the dysfunctional HPA axis could be useful in the treatment of depressive disorders.…”