Sleep and the epidemic of obesity in children and adults - PubMed (original) (raw)

Review

. 2008 Dec;159 Suppl 1(S1):S59-66.

doi: 10.1530/EJE-08-0298. Epub 2008 Aug 21.

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Review

Sleep and the epidemic of obesity in children and adults

Eve Van Cauter et al. Eur J Endocrinol. 2008 Dec.

Abstract

Sleep is an important modulator of neuroendocrine function and glucose metabolism in children as well as in adults. In recent years, sleep curtailment has become a hallmark of modern society with both children and adults having shorter bedtimes than a few decades ago. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity. There is rapidly accumulating evidence from both laboratory and epidemiological studies to indicate that chronic partial sleep loss may increase the risk of obesity and weight gain. The present article reviews laboratory evidence indicating that sleep curtailment in young adults results in a constellation of metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, elevated sympathovagal balance, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. We also review cross-sectional epidemiological studies associating short sleep with increased body mass index and prospective epidemiological studies that have shown an increased risk of weight gain and obesity in children and young adults who are short sleepers. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity.

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Figures

Figure 1

Figure 1

Prevalence of obesity (BMI>30 kg/m2) in nine European countries in 1998 and 2001 (adapted from Ref. (3)).

Figure 2

Figure 2

Prevalence of overweight (defined as above the 95th percentile for age and sex) among the US children of ages 2–5, 6–11, and 12–19 years in 1971–1972, 1976–1980, 1988–1994, 1999–2000, 2001–2002, and 2003–2004 (adapted from Ref. (4)).

Figure 3

Figure 3

Self-reported sleep duration (hours) by age for the US children aged 11–18 years .

Figure 4

Figure 4

Mean (±

s.e.m.

) 24-h leptin, cortisol, and HOMA profiles with 4-, 8-, and 12-h bedtimes. Note that the relative synchronization of the leptin and cortisol profiles in the study with 8-h bedtimes was intermediate between that observed with 4-h bedtimes and that observed with 12-h bedtimes. Similarly, the HOMA response to breakfast gradually increased from the 12-h bedtime condition to the 4-h bedtime condition, with an intermediate response during the 8-h bedtime condition. Black bars, Sleep periods. (Copied with permission from Ref. (22)).

Figure 5

Figure 5

Percent difference in levels of leptin and ghrelin comparing short sleep to longer sleep conditions from three different studies (25–27).

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