Sleep duration may be an important regulator of body weight and metabolism. An association between short habitual sleep time and increased body mass index (BMI) has been reported in large population samples. The potential role of metabolic hormones in this association is unknown. Study participants were 1,024 volunteers from the Wisconsin Sleep Cohort Study, a population-based longitudinal study of sleep disorders. Participants underwent nocturnal polysomnography and reported on their sleep habits through questionnaires and sleep diaries. Following polysomnography, morning, fasted blood samples were evaluated for serum leptin and ghrelin (two key opposing hormones in appetite regulation), adiponectin, insulin, glucose, and lipid profile. Relationships among these measures, BMI, and sleep duration (habitual and immediately prior to blood sampling) were examined using multiple variable regressions with control for confounding factors. A U-shaped curvilinear association between sleep duration and BMI was observed. In persons sleeping less than 8 h (74.4% of the sample), increased BMI was proportional to decreased sleep. Short sleep was associated with low leptin (p for slope = 0.01), with a predicted 15.5% lower leptin for habitual sleep of 5 h versus 8 h, and high ghrelin (p for slope = 0.008), with a predicted 14.9% higher ghrelin for nocturnal (polysomnographic) sleep of 5 h versus 8 h, independent of BMI. Participants with short sleep had reduced leptin and elevated ghrelin. These differences in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration. In Western societies, where chronic sleep restriction is common and food is widely available, changes in appetite regulatory hormones with sleep curtailment may contribute to obesity.

Ghrelin, a circulating growth hormone–releasing peptide derived from the stomach, stimulates food intake. The lowest systemically effective orexigenic dose of ghrelin was investigated and the resulting plasma ghrelin concentration was compared with that during fasting. The lowest dose of ghrelin that produced a significant stimulation of feeding after intraperitoneal injection was 1 nmol. The plasma ghrelin concentration after intraperitoneal injection of 1 nmol of ghrelin (2.83 ± 0.13 pmol/ml at 60 min postinjection) was not significantly different from that occurring after a 24-h fast (2.79 ± 0.32 pmol/ml). After microinjection into defined hypothalamic sites, ghrelin (30 pmol) stimulated food intake most markedly in the arcuate nucleus (Arc) (0–1 h food intake, 427 ± 43% of control; P < 0.001 vs. control, P < 0.01 vs. all other nuclei), which is potentially accessible to the circulation. After chronic systemic or intracerebroventricular (ICV) administration of ghrelin for 7 days, cumulative food intake was increased (intraperitoneal ghrelin 13.6 ± 3.4 g greater than saline-treated, P < 0.01; ICV ghrelin 19.6 ± 5.5 g greater than saline-treated, P < 0.05). This was associated with excess weight gain (intraperitoneal ghrelin 21.7 ± 1.4 g vs. saline 10.6 ± 1.9 g, P < 0.001; ICV ghrelin 15.3 ± 4.3 g vs. saline 2.2 ± 3.8 g, P < 0.05) and adiposity. These data provide evidence that ghrelin is important in long-term control of food intake and body weight and that circulating ghrelin at fasting concentrations may stimulate food intake.

Excess weight is a well-established predictor of sleep-disordered breathing (SDB). Clinical observations and population studies throughout the United States, Europe, Asia, and Australia have consistently shown a graded increase in the prevalence of SDB as body mass index, neck girth, or other measures of body habitus increases. Clinical studies of weight loss and longitudinal population studies provide strong support for a causal association. The role of excess body weight, a modifiable risk factor, with SDB raises many questions relevant to clinical practice and public health. The topic takes on added importance with the alarming rate of weight gain in children as well as adults in industrialized nations. Among adults ages 30–69 yr, averaging over the estimated United States 2003 age, sex, and BMI distributions, we estimate that ∼17% of adults have mild or worse SDB (apnea-hypopnea index ≥ 5) and that 41% of those adults have SDB “attributable” to having a body mass index of ≥25 kg/m². Similarly, we estimate that ∼5.7% of adults have moderate or worse SDB (apnea-hypopnea index ≥ 15) and that 58% of those adults have SDB attributable to excess weight. Clearly, if the expanding epidemic of obesity seen in the United States continues, the prevalence of SDB will almost certainly increase, along with the proportion of SDB attributable to obesity.

We are currently facing a major obesity pandemic. Most alarming is the accelerated increase in overweight and obesity in children, with childhood obesity tracking into adulthood. Although there is a strong genetic contribution to obesity, the current pandemic has been driven by environmental factors. Unfortunately, interventions aiming to alter food selection (eg, less fat and sugar) and calorie intake (eg, smaller portions) and to increase physical activity have not been able to result in long-term weight loss and maintenance. These approaches are confounded by the fact that only an insignificant daily energy surplus could result in obesity over time. Although changes in the basic balance between energy intake (food calories) and expenditure (physical activity) are obviously responsible for the current obesity pandemic, our understanding of the factors that alter this balance remains incomplete. Intriguingly, sleep may be a factor that alters both sides of the energy balance equation. The precise physiological functions of sleep are unknown, but the contribution of sleep to physical and psychological health, and its social and economic significance, is increasingly recognised.¹ Sleep research has mainly concentrated on the cognitive consequences of sleep loss, on the basis of the belief that sleep is for the brain alone. Recently, however, there has been a shift in interest in the consequences of sleep loss for other organs and several physiological systems. Also, more laboratory studies on sleep are now concentrating on investigating the health and performance effects of chronic partial sleep restriction, which is truer of real life, rather than acute total sleep deprivation. On …