Associations between Sleep Loss and Increased Risk of Obesity and Diabetes

Annals of the New York Academy of Sciences
Volume 1129 Issue Molecular and Biophysical Mechanisms of Arousal, Alertness, and Attention, Pages 287 - 304

Published Online: 28 Jun 2008

© 2009 New York Academy of Sciences

Associations between Sleep Loss and Increased Risk of Obesity and Diabetes

Kristen L. Knutson a and Eve Van Cauter b
a Department of Health Studies, University of Chicago, Chicago, Illinois, USA b Department of Medicine, University of Chicago, Chicago, Illinois, USA
Address for correspondence: Eve Van Cauter, Ph.D., Department of Health Studies, 5841 S. Maryland Ave, MC 1027, Chicago, IL 60637. Voice: +773-702-0169; fax: +773-702-7686.
evcauter@medicine.bsd.uchicago.edu
Copyright © 2008 New York Academy of Sciences

KEYWORDS
sleep deprivation • diabetes • obesity • glucose tolerance • energy expenditure • epidemiology • leptin • ghrelin • appetite • orexins

ABSTRACT
During the past few decades, sleep curtailment has become a very common in industrialized countries. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. Evidence is rapidly accumulating to indicate that chronic partial sleep loss may increase the risk of obesity and diabetes. Laboratory studies in healthy volunteers have shown that experimental sleep restriction is associated with an adverse impact on glucose homeostasis. Insulin sensitivity decreases rapidly and markedly without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Prospective epidemiologic studies in both children and adults are consistent with a causative role of short sleep in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite, with a reduction of the satiety factor, leptin, and an increase in the hunger-promoting hormone, ghrelin. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need, acting in concert to produce an internal misperception of insufficient energy availability. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins that promote both waking and feeding. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher body mass index after controlling for a variety of possible confounders.

DIGITAL OBJECT IDENTIFIER (DOI)
10.1196/annals.1417.033 About DOI