The Link Between Sleep Loss and Obesity: Understanding the Mechanisms Responsible for Weight Gain with Sleep Deprivation

| June 11, 2008

by Cynthia K. Buffington, PhD

Introduction
Over the last several months, there have been a number of newspaper articles and television talk show discussions on the relationship between chronic sleep curtailment and obesity risk. Within our modern society, chronic sleep loss is common and due to a variety of conditions, including voluntary sleep curtailment, emotional distress, work shifts and schedules, life stressors, and health issues. Cross-sectional and prospective epidemiological studies find an inverse relationship between shortened sleep duration and body size or weight gain. The mechanisms responsible for the link between sleep debt and obesity have not been fully elucidated, but are believed to be of both behavioral and metabolic origin. The purpose of this article is to provide the bariatric professional with an understanding of the importance of sleep in long-term weight loss success and maintenance.

The Link Between Chronic Sleep Loss and Obesity
During the mid-1800s and prior to the discovery of the light bulb, Americans slept for an average of approximately 12 hours nightly.1 By the mid-1900s, Americans were sleeping between 8 and 9 hours.2 The National Sleep Foundation’s 2001 poll found that sleep duration among US adults averaged less than seven hours (6.9 hours).1 More recent data3 show that nearly one-third of US adults, ages 30 to 64, sleep for six hours or less. Today, chronic sleep loss is considered a hallmark of our society and a major contributor to a number of adverse health issues, including obesity.4–5

Epidemiological studies involving participants of varying body sizes, socioeconomic status, age, and ethnicity have demonstrated significant and independent associations between sleep duration and obesity.5–11 According to these studies, the lowest risk for obesity occurs with a sleep duration of 7 to 8 hours, and amounts of sleep that are less than seven hours are inversely correlated to body size (body weight, body mass index, or percent body fat). One large population study (NHANES 1)8 found that people who sleep four hours or less are 73 percent more likely to be obese than those who sleep for 7 to 9 hours; individuals who obtain five hours of sleep are 50 percent more likely to be obese; and people who sleep for six hours have a 23-percent greater chance of obesity. Another study7 examining changes in body fat in association with sleep duration, found a 2.8-percent increase in total body fat for each hour of sleep less than seven hours per night.

Cross-sectional studies such as those described above clearly show a link between sleep loss and larger body size, but such studies fail to provide evidence that sleep deprivation contributes to obesity. Prospective (longitudinal) studies, however, have found significant and inverse associations between shortened sleep duration and weight gain and/or future obesity, suggesting possible causation.8–12 A recent report12 involving a subpopulation (ages 21 to 64 years) of the Quebec Family Study found that individuals who sleep for only 5 to 6 hours, as compared to those who get 7 to 8 hours, are 35 percent more likely to gain at least 5kg of additional weight over the course of a six-year period. Four additional longitudinal studies8–11 have likewise found that sleeping for periods less than seven hours results, in the long-term, in weight gain and greater obesity risk.

Regretfully, chronic sleep loss is not a condition exclusive to adults. In our society, children, adolescents, and even toddlers are sleep deprived, although the extent of such deprivation is presently unknown. According to the National Sleep Foundation,1 infants up to 12 months old need 14 to 18.5 hours of sleep; toddlers 12 to 18 months old need 13 to 15 hours of sleep; children 2 to 3 years old need 12 to 14 hours; children 3 to 5 years old need 11 to 13 hours; children 5 to 12 years old need 9 to 11 hours; and adolescents need 8.5 to 9.5 hours of sleep daily.

Epidemiological studies find that shortened sleep duration among children of all ages is strongly linked to concurrent and future obesity.5,13–17 Data from three longitudinal studies have shown that sleep loss in infancy or early childhood substantially increases the risk for overweight or obesity in later childhood years.14–16 The results of these studies are quite disturbing because sleep in the early childhood years is important for brain development and plasticity. Sleep deprivation, at this time, could have an adverse impact upon the development of neuroendocrine regulators of appetite and/or energy expenditure, making body size maintenance more difficult throughout the course of life.

Mechanisms Responsible for Weight Gain with Sleep Deprivation
Behavioral as well as biological conditions contribute to the association between shortened sleep duration and obesity. Sleep loss may increase the risk for weight gain by lengthening the time an individual has available for food and beverage consumption. A person who remains awake for a longer period in the evening, particularly if they are spending time in front of the television, may be eating more snacks than would someone who goes to bed earlier. Studies find associations between sleep loss and snacking, as well as other eating irregularities, including cravings for calorie-dense carbohydrates, a reduction or absence of fruit and vegetable consumption, and inconsistent mealtimes.18–20 In addition, chronic sleep loss may reduce an individual’s desire for physical activity,17 decreasing total energy expenditure and increasing obesity risk.

Biologically, sleep restriction contributes to obesity by affecting change in neuroendocrine regulation of appetite and energy expenditure. Population and controlled laboratory studies find with sleep deprivation an increase in ghrelin and decrease in leptin.5,6,20–24 Ghrelin is a gut hormone produced primarily by the parietal cells of the gastric fundus.25 Production of the hormone is highest before meals and during periods of low-calorie intake, suggesting its importance in hunger. Ghrelin has strong orexigenic actions, stimulating appetite and food consumption and, in laboratory animals, has suppressive effects on fat oxidation and energy expenditure.25 Leptin is a product of adipose tissue and acts as an adipostat, signaling the hypothalamus as to the size of adipose depots.26 Under normal conditions, leptin has actions that are opposite those of ghrelin on appetite, fat oxidation, and energy expenditure.25–26 Conditions that increase ghrelin and/or reduce leptin, such as sleep restriction, have the potential to promote weight gain.

A recent human laboratory study of partial sleep deprivation (4-hour sleep periods) showed marked changes in ghrelin and leptin after only two nights of shortened sleep duration.20 According to the study findings, the ratio of ghrelin-to-leptin with sleep restriction increased by more than 70 percent and was strongly associated with hunger, as well as increased appetite and cravings for calorie-dense nutrients of high carbohydrate content, such as cake, candies, cookies, ice cream, pastry, bread, pasta, cereal, and chips. The study investigators estimated that the increase in appetite and food selection associated with changes in leptin and ghrelin with sleep deprivation could account for a 350 to 500cal/day increase in daily caloric consumption. Over time, such increase in energy intake could lead to substantial weight gain.

Sleep loss causes yet other hormone changes that have a metabolic link to obesity. Studies have found, for instance, that partial sleep loss raises afternoon and evening levels of cortisol.21–24 Cortisol, in turn, has the potential to promote weight gain in several ways. First, the hormone increases fat accumulation via its adipogenic actions and its stimulatory effects on adipocyte fatty acid uptake.27–28 Secondly, elevated cortisol causes neuroendocrine changes that stimulate appetite (i.e., increase in neuropeptide Y [NPY] and decreases in corticotropin-releasing hormone [CRH] and melanocortin release).27–29 Finally, cortisol reduces insulin sensitivity,27,30 and, in doing so, may increase obesity risk and impair glucose tolerance. Studies have found associations between sleep loss and elevated evening cortisol, reduced insulin sensitivity, and glucose intolerance.20–22

Adiponectin is a hormone with anti-obesity actions that may also be affected by sleep restriction. Levels of adiponectin, a product of adipose tissue, are low in association with shortened sleep duration.31 Under normal conditions, adiponectin stimulates fat oxidation, inhibits lipogenesis, improves insulin sensitivity, and has suppressive actions against proinflammatory cytokines that may adversely influence insulin sensitivity and glucose homeostasis.32 A decline in adiponectin, as may occur with sleep debt, could, thereby, increase the risk for obesity as well as diabetes.

In all of the ways discussed above, and possibly many more that remain unknown, chronic sleep loss is linked to weight gain and obesity. Fortunately, sleep loss is a modifiable variable and, in the absence of major health issues, can generally be improved or resolved with sustained effort. As discussed earlier, the lowest risk for weight gain among adults occurs with sleep durations of 7 to 8 hours. Thus, to assist in weight gain/regain prevention, we, as well as our patients, need to strive to achieve 7 to 8 hours of sleep daily. Steps to encourage patients to obtain better sleep habits may include: 1) education concerning sleep loss and obesity risk, 2) the practice of techniques for improved sleep duration and quality (see reference 1), and 3) postoperative sleep logs. Such steps may help to increase the amount of sleep our patients obtain regularly, along with improvement in long-term weight loss outcomes and overall health.

References
1. National Sleep Foundation. Available at: www.sleepfoundation.org.
2. Kripke DF, Simons RN, Garfinkel L, et al. Short and long sleep and sleeping pills. Is increased mortality associated? Arch Gen Psychiatry. 1979;36:103–16.
3. National Center for Health Statistics. Percentage of adults who reported an average of < 6 hours of sleep per 24-hour period by sex and age group—United States: 1985 and 2004. Morb Mortal Wkly Rep. 2005.
4. Trenell M, Marshall N, Rogers N. Sleep and metablic control: Waking to a problem? Clin Exp Pharmacol Physiol. 2007;34:1–9.
5. Knutson KL, Spiegel K, Penev P et al. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007;11:163–78. (review)
6. Taheri S, Lin L, Austin D, et al. Short sleep duration is associated with reduced leptin, elevated ghrelin and increased body mass index. Plos Med. 2004;1:e62.
7. Rontoyanni VG, Baic S, Cooper AR. Association between nocturnal sleep duration, body fatness, and dietary intake in Greek women. Nutrition. 2007;23:773–7.
8. Gangwisch JE, Malaspoina D, Boden-Albala B, et al. Inadequate sleep as a risk factor for obesity: Analysis of NHANES I. Sleep. 2005;28:1289–96.
9. Hasler G, Buysse DJ, Klaghofer R, et al. The association between short sleep duration and obesity in young adults: A 13-year prospective study. Sleep. 2004;27:661–6.
10. Patel SR, Malhotra A, White DP, et al. Association between reduced sleep duration and weight gain in women. Am J Epidemiol. 2006;164:947–54.
11. Lopez-Garcia E, Faubel R, Leon-Munoz L, et al. Sleep duration, general and abdominal obesity, and weight change among the older adult population of Spain. Am J Clin Nutr. 2008;87:310–16.
12. Chaput JP, Despres JP, Bouchard C, et al. The association between sleep duration and weight gain in adults: A 6-year prospective study from the Quebec Family Study. Sleep. 2008;31:517–23.
13. Taheri S. The link between short sleep duration and obesity: We should recommend more sleep to prevent obesity. Arch Dis Child. 2006;91:881–884. (review)
14. Taveras EM, Rifas-Shiman SL, Oken E, et al. Short sleep duration in infancy and the risk of childhood overweight. Arch Pediatr Adolesc Med. 2008;162:3054–11.
15. Agras WS, Hammer LD, McNicholas F, et al. Risk factors for childhood overweight: A prospective study from birth to 9.5 years. J Pediatr. 2004;145:20–5.
16. Reilly JJ, Armstrong J, Dorosty AR, et al. Early life risk factors for obesity in childhood: Cohort study. BMJ. 2005;330:1357.
17. Gupta NK, Mueller WH, Chan W, et al. Is obesity associated with poor sleep quality in adolescents? Am J Hum Biol. 2002;14:762–8.
18. Imaki M, Hatanaka Y, Ogawa Y, et al. An epidemiological study on the relationship between hours of sleep and lifestyle factors in Japanese factory workers. J Physiol Anthropol Appl Hum Sci. 2002;21:115–20.
19. Ohida T, Kamal AM, Uchiyama M, et al. The influence of lifesyle and health status factors on sleep among the Japanese general population. Sleep. 2001;24:333–8.
20. Spiegel K, Tasali E, Penev P, et al. Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels and increased hunger and appetite. Ann Intern Med. 2004;141:846–50.
21. Spiegel K, Leproult R, L’Hermite-Baterlaux M, et al. Leptin levels are dependent on sleep duration: Relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004;89:5762–71.
22. Spiegel K, Knutson K, Leproult R, et al. Sleep loss: a novel risk factor for insulin resistance and type 2 diabetes. J Appl Physiol. 2005;99:2008–19.
23. Copinschi G. Metabolic and endocrine effects of sleep deprivation. Essent Psychopharmacol. 2005;6:341–7. (review)
24. Van Cauter E, Holmback U, Knutson K, et al. Impact of sleep and sleep loss on neuroendocrine and metabolic function. Horm Res. 2007;67:2–9. (review)
25. Heiman ML, Witcher DR. Ghrelin in obesity. Metab Syndr Relat Disord. 2006;4:37–42.
26. Anubhuti AS. Leptin and its metabolic indicates—an update. Diabetes Obes Metab. 2008; Feb. 18.
27. Peeke PM, Chrousos GP. Hypercortisolism and obesity. Ann NY Acad Sci. 1995;771:665–76. (review)
28. Mattsson C, Olsson T. Estrogens and glucocorticoid hormones in adipose tissue metabolism. Curr Med Chem. 2007;14:2918–24.
29. Cavagnini F, Croci M, Putignano P, et al. Glucocorticoids and neuroendocrine function. Int J Obes Relat Metab Disord. 2000;24:S77–9.
30. Van Dijk G, de Vries K, Benthem L, et al. Neuroendocrinology of insulin resistance: Metabolic and endocrine aspects of adiposity. Eur J Pharmacol. 2003;480:31. (review)
31. Kotani K, Sakane N, Saiga K, et al. Serum adiponectin levels and lifestyle factors in Japanese men. Heart Vessels. 2007;22:21–6.
32. Matsuzawa Y. The metabolic syndrome and adipocytokines. FEBS Lett. 2006;580:2917–21.

Author Correspondence:
Cynthia Buffington, PhD, Florida Hospital Celebration Health; Phone: (407) 303-4620; E-mail:
Cynthia.buffington@flhosp.org.

Category: Past Articles, Research Perspective

Comments are closed.