Metabolic Consequences in Humans of Prolonged Sleep Restriction Combined with Circadian Disruption
By O. Buxton, S. Cain, Shawn P. O’Connor, J. H. Porter, Jeanne F. Duffy, Wen Wang, Charles A. Czeisler, S. Shea. Science Translational Medicine, 2012
855 citations recorded by the source corpus.
Sleep deficiency and out-of-synch circadian rhythms impair pancreatic insulin secretion, a possible precursor to metabolic syndrome and diabetes. A Reason to Go to Bed on Time Our own experience tells us that getting too little sleep or traveling across multiple time zones can impair our ability to function. And people who work on the night shift or who habitually sleep too little are more likely to be obese or have diabetes. But what is it about these stresses that translate into faulty physiology? By simulating the life-style of a shift worker or world traveler in controlled laboratory conditions, Buxton et al. now find that prolonged, simultaneous disruption of our normal sleep and circadian rhythms affects the workings of our insulin-secreting pancreatic cells, creating a prediabetic state. And even worse, under these conditions, people show a drop in their resting metabolic rate that could translate into a yearly weight gain of more than 10 pounds. Getting a firm handle on the effects of life-style changes such as sleep, activity schedule, and diet on pancreatic function is much easier in small animals than humans. But Buxton et al. successfully investigated these questions by hosting 21 human participants in a completely controlled environment for almost 6 weeks and simulating disturbances in sleep and circadian rhythms, while keeping diet constant and scheduling all activities. Because sleep and circadian rhythms are intimately related, they designed a special protocol to independently manipulate these variables. After a stabilization segment in which the participants had adequate sleep at the appropriate time within their circadian rhythms, the participants spent 3 weeks in which they got only 5.6 hours of sleep per 24-hour period, while simultaneously experiencing 28-hour circadian days—a state similar to 4 hours of jet lag accumulating each day. During this time, the participants were often trying to sleep at unusual times within their circadian cycle. A segment of 9 recovery days followed. During the 3-week disruption, the participants’ glucose control went haywire, and they were unable to mount a sufficiently high insulin response after a meal, resulting in too much glucose in their blood, in some cases at a level considered prediabetic. This magnitude of disruption, coupled with a lower resting metabolic rate that also emerged during the 3 treatment weeks, could easily set the stage for development of diabetes and obesity, although the exact process by which this happens awaits further study. These results carry a cautionary message for employers to guard against causing adverse metabolic effects in workers by their shift scheduling practices—and a reinforcement of your mother’s message to go to bed on time and get enough sleep. Epidemiological studies link short sleep duration and circadian disruption with higher risk of metabolic syndrome and diabetes. We tested the hypotheses that prolonged sleep restriction with concurrent circadian disruption, as can occur in people performing shift work, impairs glucose regulation and metabolism. Healthy adults spent >5 weeks under controlled laboratory conditions in which they experienced an initial baseline segment of optimal sleep, 3 weeks of sleep restriction (5.6 hours of sleep per 24 hours) combined with circadian disruption (recurring 28-hour “days”), followed by 9 days of recovery sleep with circadian re-entrainment. Exposure to prolonged sleep restriction with concurrent circadian disruption, with measurements taken at the same circadian phase, decreased the participants’ resting metabolic rate and increased plasma glucose concentrations after a meal, an effect resulting from inadequate pancreatic insulin secretion. These parameters normalized during the 9 days of recovery sleep and stable circadian re-entrainment. Thus, in humans, prolonged sleep restriction with concurrent circadian disruption alters metabolism and could increase the risk of obesity and diabetes.
Subfields: Endocrine and Autonomic Systems, Experimental and Cognitive Psychology
View Paper: https://www.semanticscholar.org/paper/e2193b41da78b3847275f074c6b1074c88be68ec
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In Endocrine and Autonomic Systems
In Experimental and Cognitive Psychology
Citations in the corpus
- Sleep Duration and Risk of Type 2 Diabetes: A Meta-analysis of Prospective Studies (2015, background): “ciated with hunger/appetite and caloric intake due to increases in ghrelin and decreases in leptin, short sleep may lead to greater time to eat as well as fatigue leading to lower physical activity levels, thereby increasing risk of weight gain and subsequent health risks (39,48).”
- Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis. (2014, background): “…into GF (legend on next page) 522 Cell 159, 514–529, October 23, 2014 ª2014 Elsevier Inc. cardiovascular disease, all disease states that have emerged in parallel in modern human populations (Archer et al., 2014; Buxton et al., 2012; Fonken et al., 2010; Scheer et al., 2009; Suwazono et al., 2008).”
- Short sleep duration and health outcomes: a systematic review, meta-analysis, and meta-regression. (2017, background): “Previous studies have showed that sleep deprivation reduces energy expenditure in healthy men [37], an insulin-resistant state in human adipocytes [38], and inadequate pancreatic insulin secretion and increased plasma glucose concentrations after a meal [39].”
- Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences and Countermeasures (2016, neutral): “cretion, indicating pancreatic dysfunction (244).”