Chronic Sleep Restriction is a Risk Factor for Obesity
Len Kravitz, Ph.D.
Article Reviewed: Magee, C. A., Huang, X-F, Iverson, D. C., Caputi, P. (2010). Examining the pathways linking chronic sleep restriction to obesity. Journal of Obesity, Volume 2010, dol:10:1155/2010/821710
Introduction:
Obesity is a pervasive and soaring health problem that has become a decisive medical, psychosocial and economic obstacle for developing and developed countries of the world. It is associated with coronary heart disease, diabetes, osteoarthritis, gout, hypertension, stroke, certain types of cancer (colon, endometrial, breast, kidney, and esophagus), gallbladder disease, abnormal cholesterol levels and some pulmonary diseases (Hainer, Toplak, and Mitrakou, 2008; Haslam and James 2005). The two major reasons for the epidemic rise in overweight/obesity are progressively increasing sedentary lifestyles combined with high calorie (and fat) diets (Magee et al., 2010). One factor that is emerging as a consequential contributing factor to weight gain is chronic sleep restriction. However, the sequence through which continual sleep restriction contributes to obesity, and the magnitude of these effects has not been fully explained. This research column will highlight findings from a recent scientific review article examining the linkage between chronic sleep restriction and obesity.
Sleep, Sleep Restriction and Obesity: Research Directions and Constraints
Scientists suggest that sleep provides the following 3 major functions: 1) it serves as the energy restoration (recharging) period from the daytime activities, 2) it affords bodily protection at night when sensory capacities are down-regulated, and 3) sleep affords the brain needed time to consolidate important experiences and memories for learning (Gerber et al., 2010). Investigating the sleep restriction/obesity connection is quite expansive. As Magee and colleagues (2010) suggest, the causes of chronic sleep debt are multifaceted and consist of numerous factors, not all of which are fully understood. The authors note that obesity may also negatively impact sleep quality and duration. Acknowledging these constraints, the review article by Magee and colleagues integrates the most contemporary research findings on chronic sleep restriction with three potential pathways to obesity.
Determinants of Chronic Sleep Duration/Restriction
Sleep duration is affected by a cluster of behavioral, environmental, sociological, demographic, health and genetic factors, all of which may also contribute to chronic sleep restriction (Magee et al., 2010). Most men and women need 7-8 hours of sleep a night and Magee et al. (2010) note that chronic sleep debt is commonly defined as sleeping between 4 to 7 hours of sleep a night. Contrariwise, acute sleep deficit refers to an uncommon (and not chronic) loss of sleep during a 24-hour period. Krueger and Friedman (2008) summarize some notable predictors of sleep duration. For instance, supportive marriages foster healthy behaviors and satisfactory sleep. Parenting and pregnancy also promote healthier lifestyles and suitable sleep, although caring for young children may disrupt sleep duration. Low economic status may limit a person's financial resources and thus affect the person's health, resulting in impaired sleep duration. Krueger and Friedman point out that smoking and alcohol consumption often lead to persistent sleep reduction. Also, men and women aged 40 to 55 years of age tend to have less sleep than younger (<40 years) and older (>55 years) adults. Lastly, Krueger and Friedman acknowledge that some individuals voluntarily limit the amount of sleep they get in order to meet family, work or social responsibilities.
Processes Linking Chronic Sleep Restriction to Obesity
The three major processes linking chronic sleep restriction to obesity discussed below are 1) metabolic and neuroendocrine function, 2) glucose regulation and 3) waking behavior (Magee et al., 2010).
Sleep Restriction and Obesity: Metabolic and Neuroendrocine Function
Spiegel, Leproult, and Van Cauter (1999) specify that consecutive sleep restriction (4 hours per night) elevates the sympathetic nervous system (the autonomic nervous system that speeds up physiological processes) and increases evening cortisol production, which has been shown to increase food intake and the accumulation of abdominal fat. Copinschi (2005) adds that sleep debt is associated with lower levels of leptin secretion. Leptin is secreted from fat cells and transmits energy (fat energy) balance messages to the hypothalamus (brain center for hunger). As leptin levels decrease, the hypothalamus interprets the message that the fat cells need more food, and directs the body to eat more. Magee and colleagues (2010) underscore that sleep restriction also leads to a significant increase in ghrelin, a hunger hormone produced and secreted from the stomach. Higher (then normal) circulating ghrelin levels stimulate hunger and food intake (once again by the hypothalamus). Lastly, peptide tyrosine tyrosine (often referred to as PYY) is a protein secreted from the gastrointestinal tract in response to ingested foodstuffs. Magee and colleagues note that PYY levels lower with sleep debt, triggering the hypothalamus to have the body to eat more.
Sleep Restriction and Obesity: Glucose Regulation Processes
Another meaningful link of chronic sleep restriction and obesity is the interference of glucose metabolism, thus also establishing a high association of sleep debt with diabetes (Magee et al., 2010). Magee and colleagues state that glucose regulation impairment is often coupled with weight gain, because glucose plays an important role in the regulation of appetite. Essentially, chronic sleep restriction induces impaired glucose utilization in parts of the brain, which promotes the hunger response and increased food intake. Magee et al. hypothesize that the increase in the sympathetic nervous system, from chronic sleep debt, may inhibit insulin secretion levels (from the pancreas) and thus impair optimal glucose utilization.
Sleep Restriction and Obesity: Waking Behavior Correlation
Magee et al. (2010) suggest that a third feasible association of sleep restriction and obesity is that the increased waking time during the day has been shown to be associated with watching television and other sedentary behaviors, such as snacking and eating. Thus, less daily sleeping gives persons more time and opportunities to eat. In addition, the authors note that a lack of sleep is also associated with sleepiness during the day. Many people will then begin to consume more high-energy (super-caffeinated) drinks and foods to oppose the consequence of this weariness. The feelings of fatigue during the day also inhibit individuals from doing more physical activity, thus promoting more sedentary behavior--and the unhealthful cycle continues.
Action Plan for Exercise Professionals
Chronic sleep restriction is a consequential risk factor to weight gain and obesity, and thus imperative for exercise professionals to discuss with clients seeking weight loss goals. The following are sleep hygiene tips to share with clients reporting chronic sleep restriction and/or sleep disorder problems (i.e., insomnia) from the University of California Wellness Letter (2008).
1) Cut down on caffeine consumption in the late afternoon and evening.
2) Do not smoke or use any other products with nicotine before bed, as the nicotine keeps many people awake. Encourage clients who smoke to quit.
3) Create a 'noise-free' sleeping environment.
4) Create a sleep-friendly bedroom by doing the following: use comfortable linens and pillows, put up darker shades, replace a worn-out mattress, and keep the bedroom cool during sleep.
5) Drink fewer fluids after dinner so the need to get up to go to the restroom is minimized.
6) Attempt to deal with stressful issues during the day and put them away at night (seek professional consultation if necessary to better deal with the stress).
7) Set a regular time to go to bed and a consistent time to awaken, and keep to this schedule.
8) Avoid bringing paperwork and work projects to bed.
9) Avoid bringing food to bed.
10) Limit naps to a maximum of 30 minutes and try to do earlier in the day.
Summary Point
Short sleep and short sleepers are very likely to become obese. Helping clients target and/or improve the amount of sleep they get is therefore a most consequential health intervention exercise professionals can provide.
Side Bar 1: Ten Facts About Sleep Restriction
It is well established in the scientific literature that long-term sleep deprivation and disturbances negatively influence a person's health and well being (Gerber et al. 2010). Below are some dispiriting facts about sleep restriction.
1) Since 1960, chronic sleep restriction has more than doubled in the U.S.
2) One-third of U.S. adults report chronic sleep restriction.
3) Chronic sleep restriction is particularly connected to motor vehicle accidents.
4) Sleeping more on the weekends to make-up for a loss of sleep during the workweek is not good sleep hygiene as it disturbs normal sleep-wake cycles.
5) Constant sleep restriction is highly associated to industrial and workplace accidents.
6) Women of all age groups suffer more insomnia than their male counterparts. As well, menopause may often intensify insomnia.
7) Continual sleep restriction is linked to diabetes, depression, hypertension and cardiovascular disease.
8) Although alcohol may help commence sleep for some people, it may disrupt sleep in the latter part of the night, thus offsetting the body's normal sleep cycle.
9) Persistent sleep restriction is related to elevated rates of mortality.
10) Ever-present sleep restriction is associated with learning and memory loss
Sources: Magee et al. (2010), Krueger and Friedman (2008), and the American Academic of Sleep Medicine
Side Bar 2. How Much Sleep Should Children Get?
Below are the sleep recommendations from the American Academy of Sleep Medicine (http://www.sleepeducation.com/Topic.aspx?id=8)
Infants (3 to 11 months): 14 to 15 hours
Toddlers: 12 to 14 hours
Preschoolers: 11 to 13 hours
School-age children: 10 to 11 hours
Additional References:
American Academy of Sleep Medicine http://www.sleepeducation.com
Retrieved May 25, 2010.
Copinschi, G. (2005). Metabolic and endocrine effects of sleep deprivation. Essential Psychopharmacology, 6(6), 341-347.
Gerber, M., Brand, S., Holsboer-Trachsler, and Puhse, U. (2010). Fitness and exercise as correlates of sleep complaints: Is it all in our minds? Medicine & Science in Sports & Exercise, 42(5), 893-901.
Haslam, D.W. and James, W.P.T. (2005). Obesity. Lancet, 366, 1197-1209.
Hainer, V., Toplak, H, and Mitrakou, A. (2008). Treatment modalities of obesity: what fits whom? Diabetes Care, 31(Supplement 2), S269-S277.
Krueger, P.M and Friedman, E.M. (2008). Sleep duration in the United States: A cross-sectional population-based study. American Journal of Epidemiology, 169(9), 1052-1063.
Perchance to sleep. (2008). University of California, Berkeley Wellness Letter. 24(6), 4-5.
Spiegel, K., Leproult, R. and Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. Lancet, 9188, 1435-1439.
@Bio:Len Kravitz, PhD, is the program coordinator of exercise science and a researcher at the University of New Mexico, Albuquerque, where he won the Outstanding Teacher of the Year award. Len was recently honored with the 2009 Canadian Fitness Professional Specialty Presenter of the Year award and chosen as the American Council on Exercise 2006 Fitness Educator of the Year. He has also received the prestigious Can-Fit-Pro Lifetime Achievement Award and the Aquatic Exercise Association Global Award.
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