Maren Wolfram

• Chronic stress has since long been identified as risk factor for physical and mental health. Evidence from epidemiological research has been accumulated showing that chronic stress at work is a relevant risk factor for the development of disease. In order to design appropriate stress intervention and prevention strategies, a deeper understanding of how stress affects human physiology is essential. The biological mechanisms underlying the adverse effects of stress on health are not yet well understood. Recent studies suggest that an altered regulation of the hypothalamus-pituitary-adrenal (HPA) axis with its end-product cortisol might be a biological pathway underlying the link between stress and disease. Cortisol thus might serve as a pre-clinical marker for work stress and burnout and could be used for diagnostic and therapeutic purposes. However, the direction of HPA axis dysregulation remains unclear with reported HPA hyper- or hypoactivity. One potential source for the divergence in the literature might be of methodological origin. Differences in study design, assessment techniques of cortisol and HPA axis regulation as well as assessments of confounding variables might have contributed to the inconclusive pattern of results. Also, different levels of HPA axis functioning might be differentially affected by distinct work stress conditions. The present work thus aimed to identify factors in assessment of cortisol that could help to reduce this inconsistency. Three empirical studies were conducted. The studies contribute to our understanding of how stress can be "measured" by using cortisol as pre-clinical marker. Several methodological issues are addressed concerning the assessment of different dimensions of HPA axis functioning and recommendations for future research in the area of psychoneuroendocrinological stress research are given. Furthermore, some conclusions regarding altered HPA axis activity under conditions of chronic stress exposure are drawn as well.