The psychophysiology of burnout

Abstract

Burnout is characterized by emotional exhaustion, feelings of depersonalisation and reduced professional competence. It is an adverse health outcome to chronic work-related stress and insufficient recovery. The main aim of this thesis was to search for physiological disturbances in persons with severe burnout. HPA-axis function, salivary DHEAS, and in vitro immune function were investigated in clinically diagnosed burnout participants. Diagnosis was based on ICD-10 criteria for 'work-related neurasthenia' in combination with a semi-structured DSM-IV interview. Contrary to initial findings in a pilot-study, the cortisol awakening response (CAR), the cortisol decline during the day and cortisol suppression after a low-dose dexamethasone (DST) intake were not different in a burnout group compared to a healthy control group. The burnout related complaints; fatigue, depressive symptoms, sleep quality, and general psychopathology were significantly reduced after a treatment period, remained stable at follow-up but did not show complete recovery. There were no longitudinal changes in the CAR or DST and a small decline in the day-curve. A decrease in exhaustion and depression after treatment were related to a decrease and an increase respectively of the CAR after treatment and at follow-up, however this finding explained little variance of the changes between and within the burnout group. There were no other correlations with the complaints. The burnout group showed significantly higher DHEAS levels. Stimulated monocytes produced more of the anti-inflammatory cytokine IL-10 in burnout, but no change was observed in the pro- and anti-inflammatory cytokine (IFN-γ and IL-10 resp.) release by PHA-stimulated T-cells, nor in pro-inflammatory cytokine (TNF-α) release of LPS stimulated monocytes. No changes were observed in circulating T-cells, B-cells or NK-cells. In addition, the capacity of dexamethasone to regulate cytokine release in vitro was not different between the burnout and the control group. We conclude that there is no predictive or diagnostic value for cortisol in severe burnout. There may be a role for DHEAS. The increased IL-10 release by monocytes may be the basis of an increased sensitivity for common cold- or flu-like symptoms in burnout, however the HPA-axis does not appear to be involved.