Christian Benedict

researcher at Department of Neuroscience, Schiöth: Functional Pharmacology

Email:
Christian.Benedict[AT-sign]neuro.uu.se
Telephone:
+4618-471 4326
Visiting address:
Room B1:2 Uppsala biomedicinska centrum (BMC)
Husargatan 3
Postal address:
Institutionen för neurovetenskap
BMC, Box 593
751 24 UPPSALA

Short presentation

My Sleep Research Laboratory currently consists of three doctoral students and one postdoc. We study the effects of circadian disruption and sleep loss, as occur in night shift work, on health and performance, with a particular focus on the relationship between sleep loss and metabolism. I obtained a diploma in nutritional science in 2003 and a Ph.D. in human biology in 2008. Since 2013, I am an associate professor of neuroscience.

Citations

Pubmed

Academic merits: PhD, Associate Professor

Keywords: diabetes sleep deprivation sleep obesity alzheimer memory lifestyle experiments cohort circadian disruption circadian aging

My courses

Biography

ACADEMIC EDUCATION

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)

Podcasts

Nytta med sömn
Forskarpodden med Christian Benedict
Energirådgivning för hjärnan - Sömn med Christian Benedict
Skärmkultur och höga prestationskrav leder till sömnproblem

Research

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.

Publications

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