Sleep and obesity.
Obesity (Demographic aspects)
Sleep deprivation (Health aspects)
Sleep deprivation (Reports)
|Publication:||Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2011 National Herbalists Association of Australia ISSN: 1033-8330|
|Issue:||Date: Winter, 2011 Source Volume: 23 Source Issue: 4|
Beccuti G, Pannain S. 2011. Sleep and obesity. Curr Opin Clin Nutr
Metab Care 14;402-12.
The prevalence of obesity worldwide has doubled since 1980. Growing evidence from both laboratory and epidemiological studies points to short sleep duration as a new risk factor for the development of obesity and its sequelae. Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result in metabolic and endocrine alterations; this includes decreased glucose tolerance and alteration of appetite regulating hormone. This article summarises the most recent literature examining the link between sleep loss and obesity.
The review examined current literature on sleep, obesity and metabolic dysfunction including a number of large scale studies. Approximately 50 epidemiological studies done in different geographical regions have examined the association between sleep and obesity in adults and children. The majority found a significant association between short sleep (generally <6 h per night) and increased obesity risk.
A meta-analysis of 18 studies in 604 509 adults demonstrated a pooled obesity odds ratio (OR) of 1.55 (1.43-1.68; P<0.0001) for less than 5 h of sleep and a dose effect of sleep duration such that for each additional hour of sleep BMI decreased by 0.35 kg/[m.sup.2]
The largest prospective study followed 35 247 Japanese workers (90% males) over 1 year. Short sleep duration (6 h or less) was associated with an increased risk of obesity in men only with an AOR 1.91 for the shortest sleep duration (<5 h; CI 1.36-2.67) and AOR 1.5 for 5-6 h of sleep (CI 1.24-1.8).
An American study showed a 6% increase in the probability of obesity in 56 507 US adults with a wide age range (18-85 years) for self reported sleep duration of less than 7 h per night. An analysis of the data in 45 325 adults from the 45 and UP Australian study confirmed an increased risk of obesity for short sleep duration in the 55-64 age group [adjusted OR (AOR) 1.52 for sleep <6 h, confidence interval (CI) 1.21-1.89, and 1.42 for sleep = 6 h, CI 1.26-1.61] but not in the elderly (>65 years). A six year Italian study demonstrated in 1597 male and female adults that every additional hour of sleep decreased the incidence of obesity by 30%.
The relationship between sleep and obesity is likely mediated by multiple pathways. An upregulation of the activity of orexin neurons and changes in appetite regulating hormones may affect food intake. It has been previously shown that ghrelin, a hormone promoting hunger, increases with sleep restriction whereas leptin, a hormone contributing to satiety perception, decreases.
Sleep loss could affect energy balance by decreasing both exercise and non exercise energy expenditure. Leptin by itself increases energy expenditure therefore changes in leptin after sleep deprivation would affect both caloric intake and energy expenditure. The Wisconsin Sleep Cohort study, consisting of 1024 volunteers, found that 5 hr of habitual sleep time, as assessed by polysomnography, was associated with a 15% decrease in morning leptin levels and a similar increase in morning ghrelin levels.
Eating behaviour after sleep deprivation was examined in two small scale studies showing significant increase in caloric intake. These suggest that excessive food intake associated with insufficient sleep may be a mechanism for increased obesity risk.
Sleep loss occurs not only as a result of habitual behaviour but also in the presence of pathological conditions associated with disturbed sleep such as obstructive sleep apnea (OSA). The increase in both the prevalence and the severity of obesity has translated into an increase in the prevalence of obesity related comorbidities including OSA. Although compelling evidence shows that obesity predisposes to OSA and that losing weight results in OSA improvement, recent studies suggest that OSA itself may cause weight gain.
Severe obesity appears to be associated with marked sleep disturbances even in individuals who do not have OSA. Such sleep disturbances may equally predispose severely obese individuals to accumulate a sleep debt and may contribute to the dysregulation of appetite, limit the drive for physical activity and further compromise weight maintenance.
The authors conclude that the current evidence supports recommending sufficient amounts of habitual sleep and good sleep hygiene, particularly in patients at risk of obesity.
Kathleen Murphy MNHAA
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