Epidemiological and longitudinal studies show that short sleep duration (<7h/night) is associated with obesity and weight gain. Clinical studies have provided some clues into the role of sleep in the promotion of obesity. These studies have shown that short sleep leads to increased appetite and food intake, especially for high fat, high carbohydrate snacks, during periods of short (4 h/night) relative to habitual sleep (>7.5 h/night). In our previous R01, we have shown that individuals eat more after a period of short sleep relative to habitual sleep and that neuronal signals in brain reward centers were activated to a greater extent by foods after short compared to habitual sleep. However, there has been no study to date to assess the effects of sleep restriction on energy balance and body composition when sleep restriction is less severe and maintained for a prolonged period of time, as is the case in a natural setting. We therefore propose to test the effects of milder, prolonged sleep restriction (SR: -1.5 hours/night relative to habitual sleep [HS] for 6 wk) on body composition and cardio-metabolic risk. We expect that SR will lead to a positive energy balance and increased adiposity relative to HS. Adult men and women (age 20-40 y and body mass index 25-29.9 kg/m2) will be studied under 2 different conditions: HS (regular bedtime routines, sleep ?7 h/night) and SR (delay bedtimes by 1.5 h, regular wake time, sleep HS-1.5 h/night) for 6 wk each. Sleep periods will occur in random order, at least 1 mo apart. Energy balance will be thoroughly assessed using a multi- component approach: structural MRI to assess changes in adiposity, doubly-labeled water to assess 24-h energy expenditure, actigraphy to assess physical activity level; 3-d food records to assess food intake, functional magnetic resonance imaging (fMRI) to assess neuronal responses to food stimuli. We will also assess cardio-metabolic risk factors from fasting blood samples at baseline and endpoint of each phase. Our working hypothesis is that SR will stimulate the orexin system, which will stimulate appetite and increase food intake. Physical activity level will be reduced, leading to an overall positive energy balance and weight gain (increased adiposity). Cardio-metabolic risk factors will be adversely affected by SR relative to HS, in part as a result of positive energy balance and weight gain. This study will improve our knowledge of the role of sleep, within the context of an ecologically valid model, on the control of food intake and energy expenditure. As a result, it will provide additional evidence for a causal role of short sleep duration in the etiology of obesity and cardio-metabolic risk.

Public Health Relevance

We have shown that reducing sleep by approximately 4 h leads to marked overeating in normal weight, healthy sleepers but it remains unknown whether this is maintained over time to produce weight gain. The proposed study will test whether milder sleep restriction, maintained over 6 weeks, also creates positive energy balance and weight gain. This knowledge is necessary to understand whether short sleep duration causes obesity in the general population.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
3R01HL128226-03S1
Application #
9712788
Study Section
Program Officer
Brown, Marishka
Project Start
2016-08-17
Project End
2020-05-31
Budget Start
2018-09-15
Budget End
2019-05-31
Support Year
3
Fiscal Year
2018
Total Cost
Indirect Cost
Name
Columbia University (N.Y.)
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
St-Onge, Marie-Pierre; Crawford, Allison; Aggarwal, Brooke (2018) Plant-based diets: Reducing cardiovascular risk by improving sleep quality? Curr Sleep Med Rep 4:74-78
Pizinger, Theresa M; Aggarwal, Brooke; St-Onge, Marie-Pierre (2018) Sleep Extension in Short Sleepers: An Evaluation of Feasibility and Effectiveness for Weight Management and Cardiometabolic Disease Prevention. Front Endocrinol (Lausanne) 9:392