The Benedict lab currently consists of one doctoral student and one postdoc + several term medical and biomedical students. We study the effects of circadian disruption and sleep loss on health and performance, with a particular focus on the relationship between sleep loss and metabolism. Benedict obtained a diploma in nutritional science in 2003 and a Ph.D. in human biology in 2008. Since 2013, Benedict is an associate professor in neuroscience.
Academic merits: PhD, Associate Professor
Keywords: diabetes sleep deprivation sleep obesity alzheimer memory lifestyle experiments cohort circadian disruption circadian aging
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2013 State doctorate in neuroscience (Uppsala University, Sweden)
2008 Doctor in human biology, summa cum laude (University of Lübeck, Germany)
2003 Master in nutritional science, final grading: excellent (University of Kiel, Germany)
My research has provided insight into why chronic sleep and circadian disruption increase the risk of weight gain and type 2 diabetes. Specifically, I was the first to demonstrate that acute sleep loss increases the brain reward response to food in young men (J Clin Endocrinol Metab. 2012). This, together with an impaired cognitive ability to suppress salient brain responses to food (Obesity. 2014) may explain why sleep-deprived subjects increase food purchases and select larger portions of energy-dense meal and snack items (Obesity. 2014 & PNEC 2013). Further increasing the risk of weight gain, I found that acute sleep loss reduces postprandial thermogenesis and lowers physical activity energy expenditure (AJCN 2009/11). A shift from satiety hormones toward hunger-promoting hormones was also noted (reviewed in Diabetes 2015). I also observed that recurrent partial sleep loss alters the balance of gut bacteria in humans, which was paralleled by reduced systemic insulin sensitivity (Mol Met 2016). A recent study from my sleep research lab demonstrated that the activity of circulating DPP-4 increased by about 14% in women (Diabetes Care 2018). This enzyme catalyzes a variety of important physiological processes in humans and has been implicated in the development of obesity, non-alcoholic fatty liver, and type 2 diabetes. I also investigated the genomic and physiological impact of acute sleep loss in peripheral tissues. We observed a molecular signature suggestive of muscle breakdown that contrast with an anabolic adipose tissue signature (Sci Advances 2018). These experimental findings could explain the paradoxical observation that chronic short sleep duration promotes weight gain and sarcopenia (as demonstrated in JCSM 2019). Collectively, these studies explain why metabolic disorders, such as obesity and type 2 diabetes, are on the rise since perturbed sleep is such a common feature of modern life.
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