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The results of this book are associated with precedent hypotheses and suggest that chronic stress exposure can cause long-term alterations in the HPA axis activation, with the consequence of long-term changes in the amount of available cortisol. Burnout, representing a pre-clinical syndrome caused by chronic work overload, was associated with increased cortisol levels. Importantly, a dose-response effect was indicated by the fact that associations were restricted to severe burnout symptomatology. In contrast, stress exposure due to SLE was not associated with HCC, neither in the cross-sectional nor in the longitudinal design. It can therefore be concluded that characteristics of a stressor such as timing, duration, and/or severity contribute to the endocrine stress response and determine whether long-term alterations at the level of the HPA axis are detectable or not.