Recent epidemiological studies show that short sleep duration (d5-7 h/night) correlates with overweight and obesity, such that individuals with short sleep periods tend to have a higher body mass index (BMI) than those who sleep 8-9 h/night. The mechanism for this relationship is currently unknown. However, energy balance must be disrupted to produce weight gain. Therefore, the purpose of this study is to examine the impact of short sleep duration, 4 h/night, relative to habitual sleep duration of 8-9 h/night, on energy balance. The major aims of this study are to compare energy expenditure and energy intake during the periods of habitual and short sleep duration and to examine the neural and hormonal pathways involved in eating behavior under periods of habitual and short sleep. Men and women, 30-45 y and BMI {22-25} kg/m2, will be recruited to participate in this randomized, crossover study of short and habitual sleep periods. During each period of {5} nights, subjects will be required to sleep at the laboratory under supervision. During this time, subjects will be total inpatients to ensure compliance with the protocol. Each sleep duration period will be separated by a 2-4-wk washout period. On the first day of each phase, subjects will be given a dose of doubly-labeled water to measure free-living energy expenditure over the 6-d period. {During the first 4 days, energy intake will be controlled and meals served at fixed times. The last 2 days will be ad libitum feeding of self-selected meals.} Hormones, including leptin, insulin, ghrelin, {PYY, adiponectin, and GLP-1} will be assessed daily in the fasted state {and, on day 4, over a 24- hour period, while subjects are consuming a controlled diet with fixed meal times}. Functional magnetic resonance imaging measurements of brain activity in response to food stimuli will be done on day 5 to examine brain regions associated with motivation to eat. On day 5, subjects will undergo measurements of {basal metabolic rate using indirect calorimetry}. Ad libitum energy intakes will be assessed on days 5 and 6. Polysomnographic monitoring will be performed nightly {to assess sleep duration}. Mediation analyses will allow us to determine whether hormone levels are related to and predictive of energy expenditure and energy intake data. The measurements performed in this study will allow us to determine how reduced sleep periods can impact energy balance and potentially lead to changes in body weight. As such, it will provide comprehensive information of the neural, physiological, hormonal, and behavioral networks related to energy balance and which are affected by sleep duration.

Public Health Relevance

Observational and epidemiological studies have found a link between obesity and short sleep duration with the prevalence of both increasing in the past decades. At this time, it is unknown whether short sleep is a cause of obesity and how short sleep would lead to obesity. Some studies associate short sleep with increased levels of hormone that stimulate appetite. This study will examine how food intake and energy expenditure can be modified by sleep duration as a means of understanding a potential causal pathway.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL091352-02
Application #
7649458
Study Section
Clinical and Integrative Diabetes and Obesity Study Section (CIDO)
Program Officer
Arteaga, Sonia M
Project Start
2008-07-15
Project End
2012-04-30
Budget Start
2009-05-01
Budget End
2010-04-30
Support Year
2
Fiscal Year
2009
Total Cost
$606,239
Indirect Cost
Name
St. Luke's-Roosevelt Institute for Health Sciences
Department
Type
DUNS #
623216371
City
New York
State
NY
Country
United States
Zip Code
10019
McNeil, Jessica; St-Onge, Marie-Pierre (2017) Increased energy intake following sleep restriction in men and women: A one-size-fits-all conclusion? Obesity (Silver Spring) 25:989-992
St-Onge, Marie-Pierre; Roberts, Amy; Shechter, Ari et al. (2016) Fiber and Saturated Fat Are Associated with Sleep Arousals and Slow Wave Sleep. J Clin Sleep Med 12:19-24
St-Onge, Marie-Pierre; Shechter, Ari (2014) Sleep disturbances, body fat distribution, food intake and/or energy expenditure: pathophysiological aspects. Horm Mol Biol Clin Investig 17:29-37
Shechter, A; Rising, R; Wolfe, S et al. (2014) Postprandial thermogenesis and substrate oxidation are unaffected by sleep restriction. Int J Obes (Lond) 38:1153-8
St-Onge, M-P; Wolfe, S; Sy, M et al. (2014) Sleep restriction increases the neuronal response to unhealthy food in normal-weight individuals. Int J Obes (Lond) 38:411-6
St-Onge, Marie-Pierre; Shechter, Ari; Shlisky, Julie et al. (2014) Fasting plasma adropin concentrations correlate with fat consumption in human females. Obesity (Silver Spring) 22:1056-63
Shechter, Ari; St-Onge, Marie-Pierre (2014) Delayed sleep timing is associated with low levels of free-living physical activity in normal sleeping adults. Sleep Med 15:1586-9
O'Keeffe, Majella; Roberts, Amy L; Kelleman, Michael et al. (2013) No effects of short-term sleep restriction, in a controlled feeding setting, on lipid profiles in normal-weight adults. J Sleep Res 22:717-20
St-Onge, Marie-Pierre (2013) The role of sleep duration in the regulation of energy balance: effects on energy intakes and expenditure. J Clin Sleep Med 9:73-80
Shechter, Ari; Rising, Russell; Albu, Jeanine B et al. (2013) Experimental sleep curtailment causes wake-dependent increases in 24-h energy expenditure as measured by whole-room indirect calorimetry. Am J Clin Nutr 98:1433-9

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