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Andrew D. Calvin, MD, MPH; Virend K. Somers, MD, PhD, FCCP
Author and Funding Information

From the Division of Cardiovascular Diseases, Mayo Clinic.

Correspondence to: Virend K. Somers, MD, PhD, FCCP, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905; e-mail: somers.virend@mayo.edu


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Somers is supported by NIH [Grant HL65176, UL1 RR024150, HL96071, HL114024, and HL114676] and the Mayo Foundation. Dr Somers has served as a consultant for ResMed; Respicardia; NeuPro; Apnex Medical, Inc; Medtronic; Deshum Medical; and Sova Pharmaceuticals. He has served as a PI or coinvestigator on grants from Philips Respironics Foundation and the NIH and works with Mayo Health Solutions on intellectual property related to sleep and to obesity. The Mayo Foundation has received a gift from the Philips Respironics Foundation for the study of sleep apnea and cardiovascular disease. Dr Calvin has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(2):711-712. doi:10.1378/chest.13-0618
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To the Editor:

We thank Dr Benedict for his interest and thoughtful comments regarding our study1 and the potential role of age in the modification of the response to sleep deprivation. Dr Benedict points out that in contrast to the work of others,2,3 we found no change in energy expenditure or in the level of hormones leptin and ghrelin and suggests that confounding by age be considered as a potential explanation.

We indeed found no change in activity energy expenditure or circulating levels of leptin and ghrelin after 8 nights of restricted sleep. These findings are consistent with the work of Nedeltcheva et al,4 who also found no changes in total energy expenditure and its components or in leptin or ghrelin levels over a 14-day period of restricted sleep. Their findings and ours are in contrast to other studies that used 24 h of continuous wakefulness2 or 2 nights of restricted sleep.3 On the other hand, Buxton et al5 found that sleep restriction and circadian misalignment over a 3-week period decreased leptin and increased ghrelin levels when food intake was fixed. We suggest that one simple synthesis of these apparently conflicting data may be that acute sleep restriction promotes caloric intake, lowering ghrelin levels, and that subclinical fat gain secondary to positive energy balance attenuates the initial decrease in leptin level.

We agree with Dr Benedict that age-related changes in sleep parameters may be clinically important, although we are not aware of data specifically pertaining to the role of age in modifying the relationship between sleep duration and energy balance. The present study inclusion criteria were age 18 to 40 years, and the study actually included individuals between the ages of 18 and 33 years, which would seem to make confounding by age less likely. Furthermore, we note that the average age in our study (24 years in the sleep-deprived group, 25 years in the control group) seems reasonably close to the average age in the study by Benedict et al2 (23 years) and Spiegel et al3 (22 years). We hope that future studies will carefully consider age and aging when examining the metabolic effects of sleep restriction.

References

Calvin AD, Carter RE, Adachi T, et al. Effects of experimental sleep restriction on caloric intake and activity energy expenditure. Chest. 2013;144(1):79-86. [CrossRef]
 
Benedict C, Hallschmid M, Lassen A, et al. Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr. 2011;93(6):1229-1236. [CrossRef]
 
Spiegel K, Leproult R, L’hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004;89(11):5762-5771. [CrossRef]
 
Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller DA, Penev PD. Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr. 2009;89(1):126-133. [CrossRef]
 
Buxton OM, Cain SW, O’Connor SP, et al. Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption. Sci Transl Med. 2012;4(129): 129ra143.
 

Figures

Tables

References

Calvin AD, Carter RE, Adachi T, et al. Effects of experimental sleep restriction on caloric intake and activity energy expenditure. Chest. 2013;144(1):79-86. [CrossRef]
 
Benedict C, Hallschmid M, Lassen A, et al. Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr. 2011;93(6):1229-1236. [CrossRef]
 
Spiegel K, Leproult R, L’hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004;89(11):5762-5771. [CrossRef]
 
Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller DA, Penev PD. Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr. 2009;89(1):126-133. [CrossRef]
 
Buxton OM, Cain SW, O’Connor SP, et al. Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption. Sci Transl Med. 2012;4(129): 129ra143.
 
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