Preliminary observations on the effects of sleep time in a sleep restriction paradigm

Guilleminault, Christian; Powell, Nelson B.; Martínez, Sandra Elena; Kushida, Clete A.; Raffray, Tifenn; Palombini, Luciana; Philip, Pierre

doi:10.1016/s1389-9457(03)00061-3

Cited by 81 publications

(56 citation statements)

References 12 publications

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“…Evening cortisol and sympathetic nervous system activation were increased; both are risk factors for the development of insulin resistance and obesity. The 24-h profile of blood constituents revealed that leptin levels are particularly sensitive to sleep duration (45), confirming an early report (69). Mean leptin levels were 19% lower in the sleep-debt vs. sleep-extension condition and intermediate with 8-h bedtimes (Fig.…”

Section: Methodology and Findings Of Previous Laboratory Studiessupporting

confidence: 85%

Quantification of sleep behavior and of its impact on the cross-talk between the brain and peripheral metabolism

Hanlon

Cauter

2011

Proc. Natl. Acad. Sci. U.S.A.

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Rates of obesity have been steadily increasing, along with disorders commonly associated with obesity, such as cardiovascular disease and type II diabetes. Simultaneously, average sleep times have progressively decreased. Recently, evidence from both laboratory and epidemiologic studies has suggested that insufficient sleep may stimulate overeating and thus play a role in the current epidemic of obesity and diabetes. In the human sleep laboratory it is now possible to carefully control sleep behavior and study the link between sleep duration and alterations in circulating hormones involved in feeding behavior, glucose metabolism, hunger, and appetite. This article focuses on the methodologies used in experimental protocols that have examined modifications produced by sleep restriction (or extension) compared with normal sleep. The findings provide evidence that sleep restriction does indeed impair glucose metabolism and alters the cross-talk between the periphery and the brain, favoring excessive food intake. A better understanding of the adverse effects of sleep restriction on the CNS control of hunger and appetite may have important implications for public health.

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Section: Methodology and Findings Of Previous Laboratory Studiessupporting

confidence: 85%

Quantification of sleep behavior and of its impact on the cross-talk between the brain and peripheral metabolism

Hanlon

Cauter

2011

Proc. Natl. Acad. Sci. U.S.A.

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“…It could be speculated that the lower prevalence in Japan may be a function of under-reporting because of the possible cultural reticence among Japanese people to associate sleep problems and psychiatric disorders 27 . Indeed, the relatively short mean time spent in bed (6.5 h) reported previously in the Japanese adult population 13 might lead to reduced difficulty maintaining sleep, as bedtime restriction has been shown to improve sleep efficiency 28 . The prevalence of insomnia we found in the Japanese is consistent with that found by Doi and colleagues in a nationwide sample of 2800 subjects: 17.3% in males and 21.5% in females 29 .…”

Section: Discussionmentioning

confidence: 95%

An international survey of sleeping problems in the general population

Léger

Poursain²,

Neubauer

et al. 2007

Current Medical Research and Opinion

310

159

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“…Studies that assess 24-h leptin profiles exclusively in men consistently report that sleep restriction reduces diurnal leptin amplitude (87,90,92) and mean leptin levels (87), which should increase appetite, although appetite was not directly measured (Table 4). Two other 24-h sampling studies, which have not separated analyses according to gender, report no change in leptin (88,107).…”

Section: Appetite Regulation-leptinmentioning

confidence: 99%