Background:
Total sleep deprivation in rodents and in humans has been associated with hyperphagia. Over the past 40 years, self-reported sleep duration in the United States has decreased by almost 2 hours.
Objective:
To determine whether partial sleep curtailment, an increasingly prevalent behavior, alters appetite regulation.
Design:
Randomized, 2-period, 2-condition crossover clinical study.
Setting:
Clinical Research Center, University of Chicago, Chicago, Illinois.
Patients:
12 healthy men (mean age [±SD], 22 ± 2 years; mean body mass index [±SD], 23.6 ± 2.0 kg/m2).
Measurements:
Daytime profiles of plasma leptin and ghrelin levels and subjective ratings of hunger and appetite.
Intervention:
2 days of sleep restriction and 2 days of sleep extension under controlled conditions of caloric intake and physical activity.
Results:
Sleep restriction was associated with average reductions in the anorexigenic hormone leptin (decrease, 18%; P = 0.04), elevations in the orexigenic factor ghrelin (increase, 28%; P < 0.04), and increased hunger (increase, 24%; P < 0.01) and appetite (increase, 23%; P = 0.01), especially for calorie-dense foods with high carbohydrate content (increase, 33% to 45%; P = 0.02).
Limitations:
The study included only 12 young men and did not measure energy expenditure.
Conclusions:
Short sleep duration in young, healthy men is associated with decreased leptin levels, increased ghrelin levels, and increased hunger and appetite.
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Author, Article and Disclosure Information
Acknowledgment: The authors thank Paul Rue for performing the leptin assays, Miho Yoshida for performing the ghrelin assays, and Kristen Knutson for providing statistical assistance. The authors also thank the volunteers for their participation in this demanding study and the nursing staff of the University of Chicago General Clinical Research Center for their expert assistance.
Grant Support: In part by grants from the National Institutes of Health (DK-41814, AG-11412, and HL-72694), from the European Sleep Research Society, from the Belgian Fonds de la Recherche Scientifique Médicale (FRSM-3.4583.02), from the University of Chicago Diabetes Research and Training Grant (NIH DK-20595), and from The University of Chicago General Clinical Research Center (NIH MO1-RR-00055).
Disclosures: None disclosed.
Corresponding Author: Eve Van Cauter, PhD, Department of Medicine, MC 1027, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637.
Current Author Addresses: Dr. Spiegel: Laboratoire de Physiologie, Centre d'Etude des Rythmes Biologiques (CERB), Université Libre de Bruxelles, Campus Hôpital Erasme–CPI 604, 808, Route de Lennik, B-1070 Brussels, Belgium.
Drs. Tasali, Penev, and Van Cauter: Department of Medicine, MC 1027, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637.
Author Contributions: Conception and design: K. Spiegel, E. Van Cauter.
Analysis and interpretation of the data: K. Spiegel, E. Tasali, P. Penev, E. Van Cauter.
Drafting of the article: K. Spiegel, E. Tasali, E. Van Cauter.
Critical revision of the article for important intellectual content: E. Tasali, P. Penev, E. Van Cauter.
Final approval of the article: K. Spiegel, E. Tasali, P. Penev, E. Van Cauter.
Provision of study materials or patients: E. Van Cauter.
Statistical expertise: E. Van Cauter.
Obtaining of funding: K. Spiegel, E. Van Cauter.
Administrative, technical, or logistic support: E. Van Cauter.
Collection and assembly of data: K. Spiegel, E. Tasali, E. Van Cauter.

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