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Sleep curtailment is accompanied by increased intake of calories from snacks^1,2,3

¹ From the Department of Medicine (AVN and PDP), the General Clinical Research Center (JMK and JI), and the Department of Health Studies (KK), The University of Chicago, Chicago, IL, and Nutritional Sciences, University of Wisconsin, Madison, WI (DAS).

² Supported by a program project grant PO1-AG11412 from the National Institute on Aging, a General Clinical Research Center grant MO1-RR00055 from the National Institutes of Health, and a Diabetes Research and Training Center grant P60-DK020595 from the National Institute of Diabetes and Digestive and Kidney Diseases.

³ Address correspondence and reprint requests to P Penev, Section of Adult and Pediatric Endocrinology, Diabetes, and Metabolism, Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, MC-1027, Chicago, IL 60637. E-mail: ppenev{at}medicine.bsd.uchicago.edu.

Background: Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite.

Objective: We tested the hypothesis that the curtailment of human sleep could promote excessive energy intake.

Design: Eleven healthy volunteers [5 women, 6 men; mean ± SD age: 39 ± 5 y; mean ± SD body mass index (in kg/m²): 26.5 ± 1.5] completed in random order two 14-d stays in a sleep laboratory with ad libitum access to palatable food and 5.5-h or 8.5-h bedtimes. The primary endpoints were calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-h profiles of serum leptin and ghrelin.

Results: Sleep was reduced by 122 ± 25 min per night during the 5.5-h bedtime condition. Although meal intake remained similar (P = 0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 ± 541 compared with 866 ± 365 kcal/d; P = 0.026), with higher carbohydrate content (65% compared with 61%; P = 0.04), particularly during the period from 1900 to 0700. These changes were not associated with a significant increase in energy expenditure (2526 ± 537 and 2390 ± 369 kcal/d during the 5.5-h and 8.5-h bedtime periods, respectively; P = 0.58), and we found no significant differences in serum leptin and ghrelin between the 2 sleep conditions.

Conclusions: Recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks but not meals.