Arlet V. Nedeltcheva, MD; Jennifer M. Kilkus, MS; Jacqueline Imperial, RN; Dale A. Schoeller, PhD; Plamen D. Penev, MD, PhD
Acknowledgment: This study involved more than 250 inpatient days in the University of Chicago Sleep Research Laboratory, which is directed by Eve Van Cauter. The authors thank Theodore Karrison for advice on the selection of an appropriate approach for statistical analysis; Eve Van Cauter for advice during the planning of this study; and the staff of the University of Chicago Clinical Resource Center, Sleep Research Laboratory, Endocrinology Clinic, and Diabetes Research and Training Center for their skilled technical assistance.
Grant Support: By the National Institutes of Health (grants P01-AG11412, R01-HL089637, CTSA-RR 04999, and P60-DK020595).
Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M10-0838.
Reproducible Research Statement:Study protocol, statistical code, and data set: Available from Dr. Penev (e-mail, firstname.lastname@example.org).
Requests for Single Reprints: Plamen D. Penev, MD, PhD, Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Chicago, 5841 South Maryland Avenue, MC-1027, Chicago, IL 60637; e-mail, email@example.com.
Current Author Addresses: Dr. Nedeltcheva: U.S. Food and Drug Administration, Center for Drug Evaluation and Research, 10903 New Hampshire Avenue, White Oak 22, Silver Spring, MD 20993.
Ms. Kilkus and Ms. Imperial: General Clinical Resource Center, University of Chicago, 5841 South Maryland Avenue, MC-7100, Chicago, IL 60637.
Dr. Schoeller: Nutritional Sciences, University of Wisconsin, 1415 Linden Drive, Madison, WI 53706.
Dr. Penev: Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Chicago, 5841 South Maryland Avenue, MC-1027, Chicago, IL 60637.
Author Contributions: Conception and design: D.A. Schoeller, P.D. Penev.
Analysis and interpretation of the data: A.V. Nedeltcheva, J.M. Kilkus, J. Imperial, D.A. Schoeller, P.D. Penev.
Drafting of the article: P.D. Penev.
Critical revision of the article for important intellectual content: A.V. Nedeltcheva, J.M. Kilkus, J. Imperial, D.A. Schoeller, P.D. Penev.
Final approval of the article: A.V. Nedeltcheva, J.M. Kilkus, J. Imperial, D.A. Schoeller, P.D. Penev.
Provision of study materials or patients: A.V. Nedeltcheva, J.M. Kilkus, J. Imperial.
Statistical expertise: A.V. Nedeltcheva, P.D. Penev.
Obtaining of funding: D.A. Schoeller, P.D. Penev.
Administrative, technical, or logistic support: A.V. Nedeltcheva, J.M. Kilkus, J. Imperial, D.A. Schoeller, P.D. Penev.
Collection and assembly of data: A.V. Nedeltcheva, J.M. Kilkus, J. Imperial, D.A. Schoeller, P.D. Penev.
Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD. Insufficient Sleep Undermines Dietary Efforts to Reduce Adiposity. Ann Intern Med. 2010;153:435-441. doi: 10.7326/0003-4819-153-7-201010050-00006
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Published: Ann Intern Med. 2010;153(7):435-441.
Sleep loss can modify energy intake and expenditure.
To determine whether sleep restriction attenuates the effect of a reduced-calorie diet on excess adiposity.
Randomized, 2-period, 2-condition crossover study.
University clinical research center and sleep laboratory.
10 overweight nonsmoking adults (3 women and 7 men) with a mean age of 41 years (SD, 5) and a mean body mass index of 27.4 kg/m2 (SD, 2.0).
14 days of moderate caloric restriction with 8.5 or 5.5 hours of nighttime sleep opportunity.
The primary measure was loss of fat and fat-free body mass. Secondary measures were changes in substrate utilization, energy expenditure, hunger, and 24-hour metabolic hormone concentrations.
Sleep curtailment decreased the proportion of weight lost as fat by 55% (1.4 vs. 0.6 kg with 8.5 vs. 5.5 hours of sleep opportunity, respectively; P = 0.043) and increased the loss of fat-free body mass by 60% (1.5 vs. 2.4 kg; P = 0.002). This was accompanied by markers of enhanced neuroendocrine adaptation to caloric restriction, increased hunger, and a shift in relative substrate utilization toward oxidation of less fat.
The nature of the study limited its duration and sample size.
The amount of human sleep contributes to the maintenance of fat-free body mass at times of decreased energy intake. Lack of sufficient sleep may compromise the efficacy of typical dietary interventions for weight loss and related metabolic risk reduction.
National Institutes of Health.
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Pulmonary/Critical Care, Obesity, Sleep Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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