The low and single dose of DEX may also explain why we do not observe a significant blood pressure difference between the groups, as Brotman et. al. observed an elevated blood pressure after a 5 day, 3 mg twice a day regiment of dexamethasone. Nonetheless, despite the lack of group difference, both variables did show a typical pattern of stress reactivity. Taken together, the combination of Dexamethasone with the TSST paradigm allowed us to investigate the interaction between the various stress LDN-193189 ALK inhibitor systems by suppressing the HPA. This task may be used to further examine and disentangle the contribution of each of these systems in disorders involving a dysregulation of either of these systems, such as chronic stress, or the metabolic syndrome. In conditions where one of the available physiological stress systems is chronically changed, it would be very informative to investigate what effect such a change has on the complimentary stress response systems. We suggest that the DEX/TSST paradigm will allow you to that. In addition, other known effects of stress like memory, cognition, attention and decision making. Future studies could also expand this line of research by performing the reverse test, i.e. by suppressing the SNS to investigate the effect on the HPA axis by using an appropriate SNS inhibitor like propranolol; this study is currently being conducted in our laboratory. In conclusion, this study demonstrated that the SNS clearly responded differentially to a standardized stress paradigm in the presence or absence of an HPA axis response. When the HPA was suppressed, a significantly higher heart rate response to the TSST occurred, indicating an inverse relationship between the two systems, where SNS activity may be elevated in the presence of a blunted HPA axis response. An overactive SNS has previously been linked to hypertension, atherosclerosis, increased cardiovascular risk and events. Knowing that several psychopathologies, such as depression and burnout, are linked with the dysregulation of the HPA, this finding may further have critical health implications. It is unclear whether the interaction between the HPA and the SNS is continuous, i.e. whether a more subtle blunting of the HPA would similarly result in a more slightly elevated heart rate response. However, given the high prevalence of cardiovascular diseases in the developed world, this clearly deserves further investigation. The incidence of obesity continues to grow, bringing with it an increased prevalence of non-alcoholic fatty liver disease. While the cause of hepatic steatosis is unknown, obesityassociated hyperinsulinemia is a logical candidate. Nonetheless, the link between insulin and the liver’s handling of lipids is not completely understood and likely is more complex than a simple linear relationship. For instance, NAFLD is also increased in states of low insulin such as poorly controlled type-1 diabetes and prolonged fasting.