Acute partial sleep deprivation increases food intake in healthy men.

Acute partial sleep deprivation increases plasma concentrations of ghrelin and decreases those of leptin.



The objective was to observe modifications in energy intake and physical activity after acute partial sleep deprivation in healthy men.



Twelve men [age: 22 +/- 3 y; body mass index (in kg/m(2)): 22.30 +/- 1.83] completed a randomized 2-condition crossover study. During the first night of each 48-h session, subjects had either approximately 8 h (from midnight to 0800) or approximately 4 h (from 0200 to 0600) of sleep. All foods consumed subsequently (jam on buttered toast for breakfast, buffet for lunch, and a free menu for dinner) were eaten ad libitum. Physical activity was recorded by an actimeter. Feelings of hunger, perceived pleasantness of the foods, desire to eat some foods, and sensation of sleepiness were also evaluated.



In comparison with the 8-h sleep session, subjects consumed 559 +/- 617 kcal (ie, 22%) more energy on the day after sleep restriction (P < 0.01), and preprandial hunger was higher before breakfast (P < 0.001) and dinner (P < 0.05). No change in the perceived pleasantness of the foods or in the desire to eat the foods was observed. Physical activity from 1215 to 2015 was higher after sleep restriction than after 8 h of sleep (P < 0.01), even though the sensation of sleepiness was more marked (P < 0.01).



One night of reduced sleep subsequently increased food intake and, to a lesser extent, estimated physical activity-related energy expenditure in healthy men. These experimental results, if confirmed by long-term energy balance measurements, suggest that sleep restriction could be a factor that promotes obesity.

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title: Short and long sleep and sleeping pills. Is increased mortality associated?
abstract: Prospective epidemiologic data of the American Cancer Society disclosed that reported usual sleep durations among groups who complained of insomnia and sleeping pill use "often" overlapped with those of groups who had no complaints. Reports of insomnia were not consistently associated with increased mortality when several factors were controlled; however, men who reported usually sleeping less than four hours were 2.80 times as likely to have died within six years as men who reported 7.0 to 7.9 hours of sleep. The ratio for women was 1.48. Men and women who reported sleeping ten hours or more had about 1.8 times the mortality of those who reported 7.0 to 7.9 hours of sleep. Those who reported using sleeping pills "often" had 1.5 times the mortality of those who "never" used sleeping pills. These results do not prove that mortality could be reduced by altering sleep durations or by reducing hypnotic prescribing. Rather, studies are needed to determine the causes of these mortality risk factors.

title: An epidemiological study on relationship between the hours of sleep and life style factors in Japanese factory workers.
abstract: To prevent "life style-related diseases", it is necessary to evaluate not only the factors directly related to sleep but also the relationship between sleep and other life style-related factors (such as smoking, alcohol drinking, food habits, and exercise routines). There have been no extensive studies conducted on these relationships. A survey was conducted on 2,000 employees of a large plant over a 6-year period to provide data that would allow one to analyze correlation between hours of sleep and other life style factors, such as smoking, alcohol drinking, dietary habit, and exercise. It focused on a serial evaluation, with special reference to the correlation between sleep and smoking and drinking habits, exercise, and food habits. In relation to smoking or an alcohol drinking habit, no significant correlation was found between those who did not get enough sleep and those who got adequate sleep. For the dietary habits, the group with insufficient hours of sleep was related to a less than satisfactory frequency of meal taking, irregularity of eating, snacking habits, excessive seasoning of food, and consumption of insufficient quantities of vegetables. Conversely, it was recognized that those who have satisfactory food habits are more likely to enjoy an appropriate amount of sleep. Those who fail to get sufficient sleep engage in food habits that are more likely to cause life style-related diseases.

title: Is sleep duration related to obesity? A critical review of the epidemiological evidence.
abstract: 1. Observational studies have implicated habitual sleep duration as a risk factor for mortality and morbidity. Part of this association might be mediated by obesity, which has also been associated with habitual sleep duration. These studies generate wide media attention because of the public's health concerns surrounding increasing obesity and the temporal association with the other modern "epidemic" of sleep loss. Some commentators have recommended public health interventions to control obesity via habitual sleep duration modification. We conducted a critical review of the available literature describing the relationship between habitual sleep duration and obesity in community-based studies in both adults and children, with particular emphasis on longitudinal studies and on studies with objective measures of habitual sleep duration. 2. Existing data have variable consistency. Only one study objectively measured sleep duration for more than one 24-h period. Cross-sectional and longitudinal studies in adults often demonstrated an association of short sleep duration with BMI. However, some of these studies also showed that long sleep duration was also associated with obesity. In contrast, other studies showed that neither long nor short sleep was associated with obesity. In paediatric populations there appeared to be a clear pattern where shorter sleep durations were associated with obesity. We did not locate any interventional studies where sleep duration had been manipulated in order to prevent or treat obesity. 3. We contend that the evidence base is not yet strong enough to give public health advice to the general population or specific groups about sleep duration being a modifiable risk factor for obesity. We need to experimentally clarify whether sleep duration variability is a risk factor for obesity, in what manner, and in which populations. If a reliable aetiological model could be found, we would ideally then need community-based randomised controlled trials that show that sleep duration can be changed and that sleep duration manipulation produces actual weight loss and/or prevents the development of obesity without undue side-effects.

title: Short Sleep Duration and Weight Gain: A Systematic Review
abstract: The recent obesity epidemic has been accompanied by a parallel growth in chronic sleep deprivation. Physiologic studies suggest sleep deprivation may influence weight through effects on appetite, physical activity, and/or thermoregulation. This work reviews the literature regarding short sleep duration as an independent risk factor for obesity and weight gain.

title: The metabolic consequences of sleep deprivation.
abstract: The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.

title: Time spent watching television, sleep duration and obesity in adults living in Valencia, Spain
abstract: To analyse the association of time watching television (TV) and physical activity with obesity in the Mediterranean area of Spain with the highest prevalence of obesity. Valencia Region in Spain. A representative sample of 814 men and 958 women, aged 15 y and older, participating in a Health and Nutrition Survey conducted in 1994.MEASUREMENTS: Height and weight were directly measured during home interviews. The outcome measure was obesity, defined as a body mass index ≥30 kg/m2. Covariates were self-reported hours of TV viewing, physical activity habits, sleeping duration, age, gender, educational level, smoking and marital status. Prevalence odds ratios (POR) estimated by logistic regression were used as effect measures. Obese people reported to spend more time watching TV (mean±s.d.: 3.6±1.5 h/day) than non-obese ones (3.0±1.4 h/day), and less sleeping time. In multivariate analysis, obesity was associated with TV viewing, sleeping time and physical activity at work. People watching TV ≥4 h/day showed a higher adjusted prevalence odds ratio of obesity, POR=2.38 (95% confidence interval, 1.54–3. 69), compared with those watching TV ≤1 h/day. People who reported to sleep ≥9 h/day presented a lower POR of obesity than those sleeping ≤6 h/day, POR=0.43 (0.27–0.67). Statistically significant dose–responses were observed for both associations, so that the prevalence odds ratio of obesity was 30% higher for each hour of increased TV viewing and 24% lower for each additional hour of sleeping time. In addition, the prevalence of obesity was lowest among single people, those more physically active at work, and those with a high educational level. Time spent watching television and a low physical activity at work were related to obesity in adults. The inverse association between obesity and sleep duration deserves further research.

title: Environmental factors associated with body mass index in a population of Southern France
abstract: Study objective Environmental-factor changes may largely be accountable for the dramatic increase of obesity prevalence in industrialized countries. This study investigated the relationships between body mass index (BMI) and various socioeconomic, clinical, behavioural and reproductive factors in a population from Southern France.  Using a cross-sectional study, a sample of 3127 current and former salaried workers (1658 men and 1469 women) completed a questionnaire on personal and medical histories, and had a clinical examination including height and weight measurements. Age-adjusted and multiple linear regression analyses were performed.  The overall prevalence of obesity (BMI ≤ 30kg/m2) was 9.8% and was higher in men than in women (11.1 versus 8.3%). Multivariate analyses showed that in both sexes, low educational level, television watching, low physical activity and ex-smoking habits, were independently associated with a higher BMI. Furthermore, in women, we found independent and positive associations between BMI and the number of naps per week, short sleep duration, daily alcohol consumption, the number of pregnancies, early age at menarche or the non-use of oral contraceptives.  Our results reveal the complexity that exists between BMI and environmental factors and stress the need to analyse and to handle these factors simultaneously.

title: Lifestyle, obesity, and insulin resistance.
abstract: The prevention of diabetes is an urgent worldwide public health concern. The period preceding onset of type 2 diabetes is typically characterized by obesity and insulin resistance induced by overeating and physical inactivity. In the 1970s, Belloc and Breslow (1) presented evidence that physical health is associated with the following seven favorable habits: sleeping 7–8 h, eating breakfast almost every day, avoiding eating between meals, maintaining a desirable weight with respect to height, participating in active sports, limiting alcohol intake, and avoiding smoking cigarettes. We studied the relationships between unhealthy habits and the presence of obesity and insulin resistance.

Subjects consulting the …

title: Overweight and obese patients in a primary care population report less sleep than patients with a normal body mass index.
abstract: Insufficient sleep and obesity are common in the United States. Restricted sleep causes important neurocognitive changes, including excessive daytime sleepiness and altered mood. This may result in work-related injuries and automotive crashes. Evidence links sleep loss to hormonal changes that could result in obesity. This article examines the association between restricted sleep and obesity in a heterogeneous adult primary care population.



A total of 1001 patients from 4 primary care practices participated in this prospective study. Patients completed a questionnaire administered by a nurse or study coordinator concerning demographics, medical problems, sleep habits, and sleep disorders. Professional staff measured height and weight in the office. The relationship between body mass index (BMI) and reported total sleep time per 24 hours was analyzed after categorizing patients according to their BMI (calculated as weight in kilograms divided by the square of height in meters) as being of normal weight (<25), overweight (25-29.9), obese (30-39.9), or extremely obese (> or =40).



Analyzable forms from 924 patients aged between 18 and 91 years indicated that (1) the mean BMI was 30; (2) women slept more than men; (3) overweight and obese patients slept less than patients with a normal BMI (patients reported less sleep in a nearly linear relationship from the normal through the obese group); and (4) this trend of decreasing sleep time was reversed in the extremely obese patients.



This study found that reduced amounts of sleep are associated with overweight and obese status. Interventions manipulating total sleep time could elucidate a cause-and-effect relationship between insufficient sleep and obesity.

title: The association between obesity and short sleep duration: a population-based study.
abstract: To assess the association between nightly total sleep time (TST) and obesity in an epidemiologic sample of metropolitan Detroit, Michigan.



Data were collected through telephone interviews completed using a population-based sample of 3158. The self-reported average nightly TST during the 2 weeks before the interview was used to divide the sample into 6 groups (hours per night of sleep; < or = 5, > 5 < or = 6, > 6 < or = 7, > 7 < or = 8, > 8 < or = 9, > 9). Obesity was defined as a body mass index > or = 30. Health and demographic variables were also assessed.



The overall prevalence of obesity was 24.8% and was significantly higher in individuals with lower amounts of TST. Compared with those with 7 to 8 hours of TST, individuals obtaining 5 hours or less and more than 5 but 6 hours or less of TST had significantly increased odds of being obese, after controlling for age, sex, loud snoring, hypertension, diabetes, arthritis, and alcohol intake (odds ratio = 1.7, 95% confidence interval = 1.3-2.3 and odds ratio = 1.4, 95% confidence interval = 1.1-1.8, respectively). A low TST was a significant predictor of a high body mass index. Furthermore, a low TST was also a significant predictor of diabetes, prior to controlling for body mass index. Interestingly, the prevalence of reduced habitual TST (< or = 5 hours) was higher in African Americans, in comparison with Caucasians (18.7% vs 7.4%; p < .001).



Our population-based data suggest that short sleep duration is associated with elevated prevalence of obesity and adds to the growing body of evidence supporting this relationship.

title: Inadequate sleep as a risk factor for obesity: analyses of the NHANES I.
abstract: Sleep deprivation has been hypothesized to contribute toward obesity by decreasing leptin, increasing ghrelin, and compromising insulin sensitivity. This study examines cross-sectional and longitudinal data from a large United States sample to determine whether sleep duration is associated with obesity and weight gain.



Longitudinal analyses of the 1982-1984, 1987, and 1992 NHANES I Followup Studies and cross-sectional analysis of the 1982-1984 study.



Probability sample of the civilian noninstitutionalized population of the United States.



Sample sizes of 9,588 for the cross-sectional analyses, 8,073 for the 1987, and 6,981 for the 1992 longitudinal analyses.



Measured weight in 1982-1984 and self-reported weights in 1987 and 1992. Subjects between the ages of 32 and 49 years with self-reported sleep durations at baseline less than 7 hours had higher average body mass indexes and were more likely to be obese than subjects with sleep durations of 7 hours. Sleep durations over 7 hours were not consistently associated with either an increased or decreased likelihood of obesity in the cross-sectional and longitudinal results. Each additional hour of sleep at baseline was negatively associated with change in body mass index over the follow-up period, but this association was small and statistically insignificant.



These findings support the hypothesis that sleep duration is associated with obesity in a large longitudinally monitored United States sample. These observations support earlier experimental sleep studies and provide a basis for future studies on weight control interventions that increase the quantity and quality of sleep.

title: Sleeping more as a way to lose weight
abstract: Caloric consumption in a society with readily available food is likely to be approximately proportional to the number of hours of being awake. Thus, replacing 1 h of inactive wakefulness (e.g. watching TV), with sleeping is likely to result in a substantial reduction in caloric intake. Calculations are presented to illustrate the possible benefits of such a switch on weight reduction.

title: Sleep Duration and Eating Behaviors of College Students
abstract: 31 short-sleeping college students tended to eat more small meals or snacks than 37 long sleepers, all of whom were satisfied with their sleep. This disrupted pattern of larger meals was predicted from work of Elomaa and Johansson with rats who were partially REM-sleep deprived.

title: Brief Communication: Sleep Curtailment in Healthy Young Men Is Associated with Decreased Leptin Levels, Elevated Ghrelin Levels, and Increased Hunger and Appetite
abstract: Studies in animals and humans suggest that sleep duration is an important regulator of metabolism.  In this study, 12 young, healthy, normal-weight men exhibited reductions in the satiety hormone leptin, increases in the hunger hormone ghrelin, and increases in hunger after 2 nights of only 4 hours of sleep compared with after 2 nights of 10 hours of sleep.  Inadequate sleep seems to influence the hormones that regulate satiety and hunger in a way that could promote excess eating. The Editors Sleep plays an important role in energy balance. In rodents, food shortage or starvation results in decreased sleep (1), and, conversely, total sleep deprivation leads to marked hyperphagia (2). Leptin and ghrelin are peripheral signals that contribute to the central regulation of food intake. Leptin, a hormone released by the adipocytes, provides information about energy status to hypothalamic regulatory centers (3). In humans, circulating leptin levels rapidly decrease or increase in response to acute caloric shortage or surplus, respectively (4). These changes in leptin levels have been associated with reciprocal changes in hunger (4). Ghrelin, a peptide produced predominantly by the stomach, is also involved in energy balance regulation, but, in contrast to the anorexigenic effects of leptin, ghrelin stimulates appetite (5). It has been proposed that leptin and ghrelin represent the yinyang of one regulatory system that has developed to inform the brain about the current energy balance state (6). Over the past 40 years, sleep duration in the U.S. population has decreased by 1 to 2 hours (7-10). The proportion of young adults sleeping fewer than 7 hours per night has more than doubled between 1960 and 20012002 (from 15.6% to 37.1%) (7-10). The effect of sleep curtailment on the control of appetite and food intake is not known. Because of the well-documented associations between sleep and food intake (1, 2), we sought to determine whether sleep duration influences the daytime profiles of leptin and ghrelin.  Twelve healthy men(mean age [SD], 22 2 years]; mean body mass index [SD], 23.6 2.0 kg/m2) who did not smoke or take any medications participated in the study. All of the men were within 10% of ideal body weight and had regular nocturnal time in bed of 7 to 9 hours. We excluded persons who had traveled across time zones less than 4 weeks before the study.  During the week preceding each study, we asked participants not to deviate from a fixed time in bed (11:00 p.m. to 7:00 a.m.) by more than 30 minutes. Naps were not allowed. The men participated in 2 studies that were conducted in a randomized order, were spaced at least 6 weeks apart, and were performed in the Clinical Research Center at the University of Chicago, Chicago, Illinois. Six of the 12 men first performed the study with restricted time in bed, and the remaining 6 men first performed the study with extended time in bed. Average weight did not change over the time period separating the 2 study conditions (75.2 kg in the sleep restriction condition vs. 75.4 kg in the sleep extension condition; P> 0.2). We obtained blood samples at 20-minute intervals from 8:00 a.m. to 9:00 p.m. after 2 consecutive nights of 10 hours in bed (10:00 p.m. to 8:00 a.m.; sleep extension) and after 2 consecutive nights of 4 hours in bed (1:00 a.m. to 5:00 a.m.; sleep restriction). Sleep was recorded every night. For both extension and restriction conditions, each overnight stay began at 7:00 p.m. with a standard hospital dinner, and the first overnight stay ended after breakfast, which was served at 8:00 a.m. We instructed the participants not to deviate from their usual eating habits between breakfast and dinner, but caloric intake was not otherwise monitored. Participants were readmitted in the early evening and, after receiving a standard hospital dinner at 7:00 p.m., remained at bed rest. At 8:00 a.m. after the second night, the participants' caloric intake was kept constant to avoid meal-related fluctuations of hunger and satiety and consisted of an intravenous glucose infusion at a constant rate of 5 g/kg of body weight every 24 hours. There was no other source of calories. Every hour from 9:00 a.m. to 9:00 p.m., the men completed validated visual analogue scales (0 to 10 cm) for hunger (11) and appetite for various food categories (12). To assess hunger, we asked participants to mark their response to the question How hungry do you feel right now? on a 10-cm scale (with not at all hungry on the left and extremely hungry on the right). To assess appetite, we asked participants to mark their response to how much they would enjoy eating foods from 7 different food categories on a 10-cm scale (with not at all on the left and very much on the right). They were asked to provide a score based only on their appetite at the moment, without concern for calories, fat, or a healthy diet. The food categories were sweets (such as cake, candy, cookies, ice cream, and pastry); salty foods (such as chips, salted nuts, pickles, and olives); starchy foods (such as bread, pasta, cereal, and potatoes); fruits and fruit juices; vegetables; meat, poultry, fish, and eggs; and dairy products (such as milk, cheese, and yogurt). Assays We measured serum leptin levels in all samples by using a human leptin radioimmunoassay kit (Linco Research, St. Charles, Missouri) with a sensitivity of 0.5 ng/mL and an intra-assay coefficient of variation of 8.3%. In 9 of the 12 participants, we also measured total ghrelin levels at hourly intervals by radioimmunoassay (Linco Research) with a sensitivity of 0.5 ng/mL and an intra-assay coefficient of variation of 7.9%. Statistical Analysis We performed paired comparisons by using the Wilcoxon matched-pairs signed-rank test. We calculated correlations by using the Spearman coefficient. The mean relative changes in leptin, ghrelin, hunger, and appetite between extended sleep (the reference category) and restricted sleep were calculated by using the ratios of the corresponding individual data and then deriving the mean across all individuals. Role of the Funding Sources This work was partially supported by grants from the National Institutes of Health, the European Sleep Research Society, the Belgian Fonds de la Recherche Scientifique Mdicale, the University of Chicago Diabetes Research and Training Grant, and The University of Chicago General Clinical Research Center. The funding sources had no role in the design, conduct, and reporting of the study or in the decision to submit the manuscript for publication.  Leptin levels were stable across the daytime period under both sleep conditions, which was consistent with the fact that calories were exclusively delivered in the form of a constant glucose infusion. Average total sleep time was 9 hours and 8 minutes when the men spent 10 hours in bed and 3 hours and 53 minutes when the men spent 4 hours in bed (P< 0.01). When spending 4 hours in bed, the participants had mean leptin levels that were 18% lower (2.1 ng/mL vs. 2.6 ng/mL; P= 0.04)  and mean ghrelin levels that were 28% higher (3.3 ng/mL vs. 2.6 ng/mL; P= 0.04)  than when the participants spent 10 hours in bed. The ratio of the concentrations of orexigenic ghrelin to anorexigenic leptin increased by 71% (CI, 7% to 135%) with 4 hours in bed compared with 10 hours in bed. Sleep restriction relative to sleep extension was associated with a 24% increase in hunger ratings on the 10-cm visual analogue scale (P< 0.01) and a 23% increase in appetite ratings for all food categories combined (P= 0.01) . The increase in appetite tended to be greatest for calorie-dense foods with high carbohydrate content (sweets, salty foods, and starchy foods: increase, 33% to 45%; P= 0.06) (Table 1). The increase in appetite for fruits and vegetables was less consistent and of lesser magnitude (increase, 17% to 21%) (Table 1). Appetite for protein-rich nutrients (meat, poultry, fish, eggs, and dairy foods) was not significantly affected by sleep duration (Table 1). When we considered the changes in ghrelin and leptin in an integrated fashion by calculating the ghrelin-to-leptin ratio, the increase in hunger was proportional to the increase in ghrelin-to-leptin ratio (r= 0.87) . Almost 70% of the variance in increased hunger could be accounted for by the increase in the ghrelin-to-leptin ratio.  Effect of sleep duration on daytime leptin levels, ghrelin levels, hunger, and appetite. A. B. C D C D Table. Average Ratings of Appetite after 2 Days of Sleep Restriction or Sleep  Association between the change in hunger ratings and the change in ghrelin-to-leptin ratio during the 12:00 noon to 9:00 p.m. time period when sleep is restricted as compared with extended.  We observed that sleep duration may affect the circulating levels of neuroendocrine factors that regulate hunger and appetite. Two days with 4 hours of time in bed each night were associated with an 18% decrease in the levels of the anorexigenic hormone leptin. By comparison, 3 days of underfeeding by approximately 900 calories per day in healthy lean volunteers has been reported to result in a decrease of leptin levels averaging 22% (4). Sleep curtailment was also associated with an almost 28% increase in daytime levels of the orexigenic factor ghrelin. The reciprocal changes in leptin and ghrelin that we observed in response to sleep restriction were associated with a 24% increase in hunger and a 23% increase in appetite. Appetite for calorie-dense nutrients with high carbohydrate content, including sweets, salty snacks, and starchy foods, increased by 33% to 45%. In contrast, appetite

title: A single night of sleep deprivation increases ghrelin levels and feelings of hunger in normal‐weight healthy men
abstract: Sleep loss is currently proposed to disturb endocrine regulation of energy homeostasis leading to weight gain and obesity. Supporting this view, a reduction of sleep duration to 4 h for two consecutive nights has recently been shown to decrease circulating leptin levels and to increase ghrelin levels, as well as self‐reported hunger. We hypothesized that similar endocrine alterations occur even after a single night of sleep restriction. In a balanced order, nine healthy normal‐weight men spent three nights in our sleep laboratory separated by at least 2 weeks: one night with a total sleep time of 7 h, one night with a total sleep time of 4.5 h and one night with total sleep deprivation (SD). On a standard symptom‐rating scale, subjects rated markedly stronger feelings of hunger after total SD than after 7 h sleep (3.9 ± 0.7 versus 1.7 ± 0.3; P = 0.020) or 4.5 h sleep (2.2 ± 0.5; P = 0.041). Plasma ghrelin levels were 22 ± 10% higher after total SD than after 7 h sleep (0.85 ± 0.06 versus 0.72 ± 0.04 ng mL−1; P = 0.048) with intermediate levels of the hormone after 4.5 h sleep (0.77 ± 0.04 ng mL−1). Serum leptin levels did not differ between conditions. Feelings of hunger as well as plasma ghrelin levels are already elevated after one night of SD, whereas morning serum leptin concentrations remain unaffected. Thus, our results provide further evidence for a disturbing influence of sleep loss on endocrine regulation of energy homeostasis, which on the long run may result in weight gain and obesity.

title: Short Sleep Duration Is Associated with Reduced Leptin, Elevated Ghrelin, and Increased Body Mass Index
abstract: 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.

title: Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin.
abstract: Sleep plays an important role in energy homeostasis. The present study tests the hypothesis that circulating levels of leptin, a hormone that signals energy balance to the brain, are influenced by sleep duration. We also analyzed associations between leptin and sympathovagal balance, cortisol, TSH, glucose, and insulin under different bedtime conditions. Twenty-four-hour hormonal and glucose profiles were sampled at frequent intervals, and sympathovagal balance was estimated from heart rate variability in 11 subjects studied after 6 d of 4-h bedtimes (mean +/- sem of sleep duration during last 2 d: 3 h and 49 +/- 2 min) and after 6 d of 12-h bedtimes (sleep: 9 h and 03 +/- 15 min). A study with 8-h bedtimes was performed 1 yr later (sleep: 6 h and 52 +/- 10 min). Caloric intake and activity levels were carefully controlled in all studies. Mean levels, maximal levels, and rhythm amplitude of leptin were decreased (-19%, -26%, and -20%, respectively) during sleep restriction compared with sleep extension. The decrease in leptin levels was concomitant with an elevation of sympathovagal balance. The effects of sleep duration on leptin were quantitatively associated with alterations of the cortisol and TSH profiles and were accompanied by an elevation of postbreakfast homeostasis model assessment values. Measures of perceived stress were not increased during sleep restriction. During the study with 8-h bedtimes, hormonal and metabolic parameters were intermediate between those observed with 4-h and 12-h bedtimes. In conclusion, sleep modulates a major component of the neuroendocrine control of appetite.

title: Sleep Loss Reduces Diurnal Rhythm Amplitude of Leptin in Healthy Men
abstract: The aim of the current study was to investigate the effects of sleep loss on the diurnal rhythm of circulating leptin levels. An indwelling forearm catheter was used to sample blood at 90‐min intervals for a total of 120 h, which included 88 h of sustained sleeplessness, in 10 healthy men. The diurnal amplitude of leptin was reduced during total sleep deprivation and returned toward normal during the period of recovery sleep. This finding provides evidence that sleep influences the nocturnal leptin profile, and may have implications for the understanding of the role of sleep in metabolic regulation and the aetiologies of obesity and the night eating syndrome.

title: Short Sleep Duration is Associated with Reduced Leptin Levels and Increased Adiposity: Results from the Québec Family Study
abstract: To explore cross‐sectional associations between short sleep duration and variations in body fat indices and leptin levels during adulthood in a sample of men and women involved in the Québec Family Study.

title: Impact of sleep debt on metabolic and endocrine function
abstract: Chronic sleep debt is becoming increasingly common and affects millions of people in more-developed countries. Sleep debt is currently believed to have no adverse effect on health. We investigated the effect of sleep debt on metabolic and endocrine functions.



We assessed carbohydrate metabolism, thyrotropic function, activity of the hypothalamo-pituitary-adrenal axis, and sympathovagal balance in 11 young men after time in bed had been restricted to 4 h per night for 6 nights. We compared the sleep-debt condition with measurements taken at the end of a sleep-recovery period when participants were allowed 12 h in bed per night for 6 nights.



Glucose tolerance was lower in the sleep-debt condition than in the fully rested condition (p<0.02), as were thyrotropin concentrations (p<0.01). Evening cortisol concentrations were raised (p=0.0001) and activity of the sympathetic nervous system was increased in the sleep-debt condition (p<0.02).



Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.

title: The influence of lifestyle and health status factors on sleep loss among the Japanese general population.
abstract: To examine the relationship between lifestyle, health status factors and sleep loss.



A cross-sectional questionnaire survey conducted by the Ministry of Health and Welfare, Japan.



N/A.



Approximately 30,000 subjects selected from the general population in Japan.



N/A.



This study indicated that approximately 28% of the general population sleep less than 6 hours nightly and approximately 65% sleep less than 7 hours. However, approximately 80% of the population reported getting sufficient sleep. Multiple logistic regression analysis showed that being females, being of younger age, living in an urban environment, being unemployed, and having an unhealthy lifestyle (i.e., lack of exercise, poor health status, and irregular eating habits) were associated with sleep loss.



In this study, sleep loss was found to be associated with having an unhealthy lifestyle and being in poor general health. These findings suggest that health education and promotion of a healthy lifestyle should be advocated.

title: Cumulative sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per night.
abstract: To determine whether a cumulative sleep debt (in a range commonly experienced) would result in cumulative changes in measures of waking neurobehavioral alertness, 16 healthy young adults had their sleep restricted 33% below habitual sleep duration, to an average 4.98 hours per night [standard deviation (SD) = 0.57] for seven consecutive nights. Subjects slept in the laboratory, and sleep and waking were monitored by staff and actigraphy. Three times each day (1000, 1600, and 2200 hours) subjects were assessed for subjective sleepiness (SSS) and mood (POMS) and were evaluated on a brief performance battery that included psychomotor vigilance (PVT), probed memory (PRM), and serial-addition testing, Once each day they completed a series of visual analog scales (VAS) and reported sleepiness and somatic and cognitive/emotional problems. Sleep restriction resulted in statistically robust cumulative effects on waking functions. SSS ratings, subscale scores for fatigue, confusion, tension, and total mood disturbance from the POMS and VAS ratings of mental exhaustion and stress were evaluated across days of restricted sleep (p = 0.009 to p = 0.0001). PVT performance parameters, including the frequency and duration of lapses, were also significantly increased by restriction (p = 0.018 to p = 0.0001). Significant time-of-day effects were evident in SSS and PVT data, but time-of-day did not interact with the effects of sleep restriction across days. The temporal profiles of cumulative changes in neurobehavioral measures of alertness as a function of sleep restriction were generally consistent. Subjective changes tended to precede performance changes by 1 day, but overall changes in both classes of measure were greatest during the first 2 days (P1, P2) and last 2 days (P6, P7) of sleep restriction. Data from subsets of subjects also showed: 1) that significant decreases in the MSLT occurred during sleep restriction, 2) that the elevated sleepiness and performance deficits continued beyond day 7 of restriction, and 3) that recovery from these deficits appeared to require two full nights of sleep. The cumulative increase in performance lapses across days of sleep restriction correlated closely with MSLT results (r = -0.95) from an earlier comparable experiment by Carskadon and Dement (1). These findings suggest that cumulative nocturnal sleep debt had a dynamic and escalating analog in cumulative daytime sleepiness and that asymptotic or steady-state sleepiness was not achieved in response to sleep restriction.

title: Operant control of ambient temperature during sleep deprivation.
abstract: Rats subjected to total sleep deprivation (TSD) by the disk-over-water method were provided with a continuously available operant by which they could increase ambient temperature (T(amb)). TSD rats progressively increased operant responses for heat to 700% of baseline levels. During the last quarter of sleep deprivation, they maintained mean T(amb) at 9 degrees C above baseline and held T(amb) over 40 degrees C for 35% of the day. In contrast, yoked control rats (TSC) did not change mean T(amb). Although both TSD and TSC rats showed a progressive decline in intraperitoneal temperature (T(ip)), TSD rats maintained an elevated T(amb) even during periods when T(ip) and brain temperatures (T(br)) were above baseline levels. Thus these results confirm and extend earlier findings that rats subjected to TSD show an increase in temperature set point (T(set)). The earlier studies, which utilized short daily trials in a thermal gradient, demonstrated an increase in T(set) early in the deprivation period. The present study, which obtained more extensive data on thermal preference at a range of body temperatures demonstrated an increasing T(amb) for almost all T(ip) and T(br) values, suggesting a progressive increase in T(set) over the course of sleep deprivation. Surprisingly, survival time was shorter than in previous TSD studies. Reduced survival could not be attributed to differences in T(br), T(ip), energy expenditure, or sleep loss from previous studies.

title: Sleep curtailment is accompanied by increased intake of calories from snacks.
abstract: Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite.



We tested the hypothesis that the curtailment of human sleep could promote excessive energy intake.



Eleven healthy volunteers [5 women, 6 men; mean +/- SD age: 39 +/- 5 y; mean +/- SD body mass index (in kg/m(2)): 26.5 +/- 1.5] completed in random order two 14-d stays in a sleep laboratory with ad libitum access to palatable food and 5.5-h or 8.5-h bedtimes. The primary endpoints were calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-h profiles of serum leptin and ghrelin.



Sleep was reduced by 122 +/- 25 min per night during the 5.5-h bedtime condition. Although meal intake remained similar (P = 0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 +/- 541 compared with 866 +/- 365 kcal/d; P = 0.026), with higher carbohydrate content (65% compared with 61%; P = 0.04), particularly during the period from 1900 to 0700. These changes were not associated with a significant increase in energy expenditure (2526 +/- 537 and 2390 +/- 369 kcal/d during the 5.5-h and 8.5-h bedtime periods, respectively; P = 0.58), and we found no significant differences in serum leptin and ghrelin between the 2 sleep conditions.



Recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks but not meals.

title: Short-term sleep loss decreases physical activity under free-living conditions but does not increase food intake under time-deprived laboratory conditions in healthy men.
abstract: Short sleep duration is correlated with an increased risk of developing obesity and cardiovascular disease, but the mechanisms behind this relation are largely unknown.



We aimed to test the hypothesis that acute sleep loss decreases physical activity while increasing food intake, thereby shifting 2 crucial behavioral components of energy homeostasis toward weight gain.



In 15 healthy, normal-weight men, spontaneous physical activity was registered by accelerometry during the entire experiment, and food intake as well as relevant hormones were assessed during a 15-h daytime period after 2 nights of regular sleep (bed time: 2245-0700) and after 2 nights of restricted sleep (bed time: 0245-0700). Experiments were performed in a crossover design.



Sleep restriction significantly decreased physical activity during the daytime spent under free-living conditions after the first night of sleep manipulation (P = 0.008). Also, intensities of physical activity were shifted toward lower levels, with less time spent with intense activities (P = 0.046). Total energy intake, feelings of hunger, and appetite as well as ghrelin and leptin concentrations during day 2 remained unaffected by acute sleep restriction.



In contrast to our expectation, short-term sleep loss neither increased food intake nor affected concentrations of the hunger-regulating hormones leptin and ghrelin. However, the observed decrease in daytime physical activity may point to another potentially important behavioral mechanism for the health-impairing influence of sleep loss.

title: The association between sleep duration and weight gain in adults: a 6-year prospective study from the Quebec Family Study.
abstract: To investigate the relationship between sleep duration and subsequent body weight and fat gain.



Six-year longitudinal study.



Community setting.



Two hundred seventy-six adults aged 21 to 64 years from the Quebec Family Study. More than half of the sample is drawn from families with at least 1 parent and 1 offspring with a body mass index of 32 kg/m2 or higher.



Body composition measurements and self-reported sleep duration were determined. Changes in adiposity indices were compared between short- (5-6 hours), average- (7-8 hours), and long- (9-10 hours) duration sleeper groups. After adjustment for age, sex, and baseline body mass index, short-duration sleepers gained 1.98 kg (95% confidence interval: 1.16-2.82) more and long-duration sleepers gained 1.58 kg (95% CI: 1.02-2.56) more than did average-duration sleepers over 6 years. Short- and long-duration sleepers were 35% and 25% more likely to experience a 5-kg weight gain, respectively, as compared with average-duration sleepers over 6 years. The risk of developing obesity was elevated for short- and long-duration sleepers as compared with average-duration sleepers, with 27% and 21% increases in risk, respectively. These associations remained significant after inclusion of important covariates and were not affected by adjustment for energy intake and physical activity participation.



This study provides evidence that both short and long sleeping times predict an increased risk of future body weight and fat gain in adults. Hence, these results emphasize the need to add sleep duration to the panel of determinants that contribute to weight gain and obesity.

title: Early life risk factors for obesity in childhood: cohort study
abstract: To identify risk factors in early life (up to 3 years of age) for obesity in children in the United Kingdom.  Prospective cohort study.  Avon longitudinal study of parents and children, United Kingdom. Participants 8234 children in cohort aged 7 years and a subsample of 909 children (children in focus) with data on additional early growth related risk factors for obesity. Main outcome measures Obesity at age 7 years, defined as a body mass index 3 95th centile relative to reference data for the UK population in 1990.  Eight of 25 putative risk factors were associated with a risk of obesity in the final models: parental obesity (both parents: adjusted odds ratio, 10.44, 95% confidence interval 5.11 to 21.32), very early (by 43 months) body mass index or adiposity rebound (15.00, 5.32 to 42.30), more than eight hours spent watching television per week at age 3 years (1.55, 1.13 to 2.12), catch-up growth (2.60, 1.09 to 6.16), standard deviation score for weight at age 8 months (3.13, 1.43 to 6.85) and 18 months (2.65, 1.25 to 5.59); weight gain in first year (1.06, 1.02 to 1.10 per 100 g increase); birth weight, per 100 g (1.05, 1.03 to 1.07); and short (< 10.5 hours) sleep duration at age 3 years (1.45, 1.10 to 1.89).  Eight factors in early life are associated with an increased risk of obesity in childhood.

title: Risk factors for childhood overweight: a prospective study from birth to 9.5 years.
abstract: To ascertain risk factors for the development of overweight in children at 9.5 years of age.



This was a prospective study of 150 children from birth to 9.5 years of age, with assessment of multiple hypothesized risk factors drawn from research reports.



Five independent risk factors for childhood overweight were found. The strongest was parent overweight, which was mediated by child temperament. The remaining risk factors were low parent concerns about their child's thinness, persistent child tantrums over food, and less sleep time in childhood. Possible mechanisms by which each of these factors influence weight gain are outlined. Two different pathways to childhood overweight/obesity were found, depending on degree of parental overweight.



There is evidence of considerable interaction between parent and child characteristics in the development of overweight. Several of the identified risk factors are amenable to intervention possibly leading to the development of early prevention programs.

title: Reduced risk for overweight and obesity in 5- and 6-y-old children by duration of sleep—a cross-sectional study
abstract: To assess the relationship between sleep duration and adiposity in 5- and 6-y-old Bavarian children. A total of 6862 German children aged 5–6 y participating in the obligatory health examination in Bavaria, southern Germany. Routine data were collected on the height and weight of children at the time of school entry in six public health offices in 1999 and in another two in 2000. Body fat mass was estimated by BIA performed in three of those offices. An extensive questionnaire was given to all children's parents in order to assess risk factors for overweight and obesity. The main outcome measures were overweight, defined by a body mass index (BMI) above the 90th centile and obesity, defined by a BMI above the 97th centile for the German children in Bavaria. Excessive body fat was defined as fat mass above the 90th centile for all German children seen in this survey. The main exposure was usual sleeping hours on week days. The prevalence of obesity decreased by duration of sleep: ≤10 h, 5.4% (95% CI 4.1–7.0), 10.5–11.0 h, 2.8% (95% CI 2.3–3.3), and ≥11.5 h, 2.1% (95% CI 1.5–2.9). Similar relations were found with the prevalence of overweight and excessive body fat. These effects could not be explained by confounding due to a wide range of constitutional, sociodemographic and lifestyle factors. The adjusted odds ratio for obesity were: for sleeping 10.5–11.0 h, 0.52 (95% CI 0.34–0.78) and 0.46 (95% CI 0.28–0.75) for sleeping 11.5 h. The effect of sleep duration on obesity in children reflects a higher body fat composition and appears to be independent of other risk factors for childhood obesity.

title: The three-factor eating questionnaire to measure dietary restraint, disinhibition and hunger.
abstract: This report describes the construction of a questionnaire to measure three dimensions of human eating behavior. The first step was a collation of items from two existing questionnaires that measure the related concepts of 'restrained eating' and 'latent obesity', to which were added items newly written to elucidate these concepts. This version was administered to several populations selected to include persons who exhibited the spectrum from extreme dietary restraint to extreme lack of restraint. The resulting responses were factor analyzed and the resulting factor structure was used to revise the questionnaire. This process was then repeated: administration of the revised questionnaire to groups representing extremes of dietary restraint, factor analysis of the results and questionnaire revision. Three stable factors emerged: (1) 'cognitive restraint of eating', (2) 'disinhibition' and (3) 'hunger'. The new 51-item questionnaire measuring these factors is presented.

title: Food reward: Brain substrates of wanting and liking
abstract: What are the neural substrates of food reward? Are reward and pleasure identical? Can taste pleasure be assessed in animals? Is reward necessarily conscious? These questions have re-emerged in recent years, and there is now sufficient evidence to prompt re-examination of many preconceptions concerning reward and its relation to brain systems. This paper reviews evidence from many sources regarding both the psychological structure of food reward and the neural systems that mediate it. Special attention is paid to recent evidence from "tasty reactivity" studies of affective reactions to food. I argue that this evidence suggests the following surprising possibilities regarding the functional components and brain substrates of food reward. (1) Reward contains distinguishable psychological or functional components--"liking" (pleasure/palatability) and "wanting" (appetite/incentive motivation). These can be manipulated and measured separately. (2) Liking and wanting have separable neural substrates. Mediation of liking related to food reward involves neurotransmitter systems such as opioid and GABA/benzodiazepine systems, and anatomical structures such as ventral pallidum and brainstem primary gustatory relays. Mediation of wanting related to food reward involves mesotelencephalic dopamine systems, and divisions of nucleus accumbens and amygdala. Both liking and wanting arise from vastly distributed neural systems, but the two systems are separable. (3) Neural processing of food reward is not confined to the limbic forebrain. Aspects of food reward begin to be processed in the brainstem. A neural manipulation can enhance reward or produce aversion but no single lesion or transection is likely abolish all properties of food reward. (4) Both wanting and liking can exist without subjective awareness. Conscious experience can distort or blur the underlying reward process that gave rise to it. Subjective reports may contain false assessments of underlying processes, or even fail at all to register important reward processes. The core processes of liking and wanting that constitute reward are distinct from the subjective report or conscious awareness of those processes.

title: Sleep and circadian rhythms: Key components in the regulation of energy metabolism
abstract: In this review, we present evidence from human and animal studies to evaluate the hypothesis that sleep and circadian rhythms have direct impacts on energy metabolism, and represent important mechanisms underlying the major health epidemics of obesity and diabetes. The first part of this review will focus on studies that support the idea that sleep loss and obesity are “interacting epidemics.” The second part will discuss recent evidence that the circadian clock system plays a fundamental role in energy metabolism at both the behavioral and molecular levels. These lines of research must be seen as in their infancy, but nevertheless, have provided a conceptual and experimental framework that potentially has great importance for understanding metabolic health and disease.

title: Feeding and circadian clocks.
abstract: The mammalian genome encodes at least a dozen of genes directly involved in the regulation of the feedback loops constituting the circadian clock. The circadian system is built up on a multitude of oscillators organized according to a hierarchical model in which neurons of the suprachiasmatic nuclei of the hypothalamus may drive the central circadian clock and all the other somatic cells may possess the molecular components allowing tissues and organs to constitute peripheral clocks. Suprachiasmatic neurons are driving the central circadian clock which is reset by lighting cues captured and integrated by the melanopsin cells of the retina and define the daily rhythms of locomotor activity and associated physiological regulatory pathways like feeding and metabolism. This central clock entrains peripheral clocks which can be synchronized by non-photic environmental cues and uncoupled from the central one depending on the nature and the strength of the circadian signal. The human circadian clock and its functioning in central or peripheral tissues are currently being explored to increase the therapeutic efficacy of timed administration of drugs or radiation, and to offer better advice on lighting and meal timing useful for frequent travelers suffering from jet lag and for night workers' comfort. However, the molecular mechanism driving and coordinating the central and peripheral clocks through a wide range of synchronizers (lighting, feeding, physical or social activities) remains a mystery.

title: Staying awake for dinner: hypothalamic integration of sleep, feeding, and circadian rhythms.
abstract: Daily patterns of sleep and wakefulness are inextricably linked to the regulation of feeding and energy metabolism. Both are affected by homeostatic as well as circadian drives, and both are tightly linked to thermoregulation. In this chapter, we review the basic drain circuitry that regulates sleep and wakefulness, including the flip-flop switch relationship of the arousal system and the ventrolateral preoptic sleep-promoting neurons. We then examine the role of the orexin/hypocretin neurons, which stabilize the switch while driving both wakefulness and foraging for food. We also review the role of the subparaventricular nucleus and the dorsomedial nucleus of the hypothalamus in circadian integration and modulation of both feeding and wake-sleep patterns.

title: Correlates of long sleep duration.
abstract: Sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality. Whether this association is causal and what pathways explain this association are unknown. We sought to identify factors that could potentially explain the association between long sleep and mortality.



Cross-sectional epidemiologic survey.



Middle-aged women (n = 60,028) participating in the Nurses Health Study II who reported a habitual sleep duration of 7 hours or more.



Multiple sclerosis (odds ratio [OR] = 3.7, 95% confidence interval [3.0-4.5]), antidepressant use (OR = 3.1, [2.9-3.3]), benzodiazepine use (OR = 3.0 [2.6-3.3]), and systemic lupus erythematosus (OR = 2.9, [2.3-3.6]) were the factors most strongly associated with prolonged sleep. Combining these data with prevalence information and a range of plausible associations with mortality, the confounding rate ratio was estimated. This parameter is the ratio of the unadjusted long sleep-mortality rate ratio to the rate ratio adjusted for the factor and measures the extent that the factor can alter the long sleep-mortality association, either through confounding or as a causal intermediate. Based on this parameter, psychiatric and socioeconomic factors have the greatest potential to influence the long sleep-mortality relationship. Assuming each factor doubles mortality risk, the confounding rate ratios for depression, antidepressant use, and unemployment were 1.10, 1.18, and 1.12. Lesser influential factors were benzodiazepine use, poverty, low societal status, sedentary lifestyle, and obesity.



Depression and low socioeconomic status are strong candidates for producing the statistical association between long sleep and mortality, either as confounders or as causal intermediates. Future causal research on the effects of long sleep should include a detailed assessment of psychiatric disease and socioeconomic status.

title: Dietary fat and sleep duration in Chinese men and women
abstract: Many recent studies have highlighted the complex interaction between sleep duration, food intake and metabolic balance. Although a causal link is yet to be established, emerging evidence suggests that short sleep duration may alter the balance between energy intake and energy expenditure. Thus far, most research has focussed on the link between sleep duration and carbohydrate metabolism. The role of sleep duration in fat intake and vice versa remains relatively unknown.The aim of this analysis was to determine whether there exists a significant association between sleep duration and fat intake.Data from 2828 adults living in Jiangsu province, China, collected during a national survey of nutrition and health conducted in 2002.Results:The analysis showed a statistically significant association between sleep duration and fat and carbohydrate intake but not protein or fasting blood glucose. Those who slept for less than 7 h a day had significantly higher (P=0.005) percentage of energy from fat intake than those who slept for 7–9 h per day. Analysis of the influence of high fat intake upon sleep demonstrated a trend to reduced sleep duration between the highest and lowest quartiles of fat intake (P=0.056).Conclusions:To our knowledge, this is the first data from a large cross-sectional study to show an association between decreased sleep duration and increased fat intake in humans. Given the trend towards decreased sleep duration in modern societies and the parallel obesity epidemic, the significance of this association warrants more research.

title: Risk factors of obesity in a five year old population. Parental versus environmental factors.
abstract: To be more effective, the prevention of obesity in childhood should be focused on the population at risk. The purpose of the present study is firstly to find correlations between certain environmental factors and obesity in childhood, and secondly to measure the influence of the environmental factors after taking the parental history of obesity into account. This case controlled study includes 704 controls vs. 327 cases selected in a population of five year old school children. The anthropometric assessment was completed at school. Obesity was defined as a weight for height > or = 2 s.d. using the French weight charts for French children based on sex and height. Interviews of the parents recorded parental overweight and child birth overweight as 'constitutional' factors and family structure, socio-economic level and daily lifestyle (sleep, TV viewing, after school care, etc.) as 'environmental' factors. The results show that parental overweight and birth overweight are closely related to the child's obesity at five years of age (estimated relative risks 3.1 and 2.4 respectively). The environmental factors which contribute to child obesity are: southern European origin of the mother, snacks, excessive television viewing and, more importantly, short sleep duration (estimated relative risks = 1.9, 1.3, 2.1 and 4.9 respectively). A logistic regression model, after taking parental overweight into account, shows that the relationship between obesity and short sleep duration persists independently of television viewing. The hypotheses raised by these findings are discussed.

title: Is obesity associated with poor sleep quality in adolescents?
abstract: Obesity has reached epidemic proportions in the U.S. and more developed countries, particularly so among adolescents. A substantial impact on public health could be achieved if other factors causing obesity besides the conventional ones of diet and physical activity could be identified and acted upon. The present study investigates whether there is a link between low sleep quality and obesity in a tri‐ethnic, cross‐sectional sample (n = 383) of male and female adolescents ages 11–16 years old (Heartfelt Study). Sleep quality was expressed as two variables, total sleep time and sleep disturbance time obtained by 24‐hour wrist actigraphy. Percent body fat and body mass index (BMI) were used together to define obesity. The potential influence of demographic and behavioral confounders were considered in models that described the relation of sleep to obesity occurrence. Obese adolescents experienced less sleep than nonobese adolescents (P < 0.01). For each hour of lost sleep, the odds of obesity increased by 80%. Sleep disturbance was not directly related to obesity in the sample, but influenced physical activity level (P < 0.01). Daytime physical activity diminished by 3% for every hour increase in sleep disturbance. The above observations were independent of potential confounding variables. Inadequate and poor sleep quality in adolescents may be important factors to consider in the prevention of childhood obesity.  2002.

title: Nutritional status, growth and sleep habits among Senegalese adolescent girls
abstract: To study the relation between sleep habits, nutritional status, growth and maturation in a group of African adolescent girls. The main hypothesis to be tested was that sleep length could be an effective way to spare energy, and thus malnourished girls sleep longer than normal girls. Three repeated yearly surveys (1997–1999) on a subsample of girls drawn from a larger study cohort on growth at adolescence. The Niakhar district in the central part of Senegal. In total, 40 girls were initially drawn. Missing girls were replaced at each round by girls having the same characteristics and belonging to the same cohort. At each round, data on pubertal development (breast stages and occurrence of menarche), growth and nutritional status were collected. Adolescents wore an accelerometer for three or four consecutive nights and days at each round. At the beginning of the survey, girls were 13.3±0.5 y old. They were under international reference values in weight and height. Their mean sleep duration was 8.5±0.9 h. Their puberty status did not influence their sleep habits; however, they slept more in March than in June, which was related to the seasonal change in daylight. There was a significant relation between body mass index and sleep habits: thinner girls slept a longer time and more quietly than the more corpulent girls. The nutritional status of these girls influenced their sleep habits: this may have been either a direct causal relation or a consequence of a protective attitude on the part of the mothers towards the frailer girls. The R024 ‘Epidémiologie et Prévention’ of the IRD (France) and the Nestlé Foundation.

title: The association between short sleep duration and obesity in young adults: a 13-year prospective study.
abstract: Obesity has become a major health problem with increasing prevalence. Given the limited availability of effective treatment of weight problems, the identification of potentially modifiable risk factors may lead to preventive approaches to obesity. The objective of this study was to test the hypothesis that short sleep duration is associated with obesity and weight gain during young adulthood.



Prospective single-age cohort study of young adults. Information was derived from 4 interviews when participants were ages 27, 29, 34, and 40 years.



Community setting.



496 young adults.



Trained health professionals administered a semistructured interview for psychiatric and medical conditions and health habits. This study showed an association between short sleep duration and obesity (at age 27 years, odds ratio: 7.4, 95% confidence interval: 1.3-43.1) and a negative association between sleep duration and body mass index in young adults. These associations persisted after controlling for a variety of potentially confounding variables, including family history of weight problems, levels of physical activity, and demographic variables. Associations between sleep duration and obesity diminished after age 34 years. There was a trend (P = .08) for average change rate of weight gain to be negatively associated with average change rate of sleep duration.



Because sleep duration is a potentially modifiable risk factor, these findings might have important clinical implications for the prevention and treatment of obesity.

title: The Association between Sleep Duration and Obesity in Older Adults
abstract: Reduced sleep has been reported to predict obesity in children and young adults. However, studies based on self-report have been unable to identify an association in older populations. In this study, the cross-sectional associations between sleep duration measured objectively and measures of weight and body composition were assessed in two cohorts of older adults.Wrist actigraphy was performed for a mean (s.d.) of 5.2 (0.9) nights in 3055 men (age: 67–96 years) participating in the Osteoporotic Fractures in Men Study (MrOS) and 4.1 (0.8) nights in 3052 women (age: 70–99 years) participating in the Study of Osteoporotic Fractures (SOF). A subgroup of 2862 men and 455 women also underwent polysomnography to measure sleep apnea severity.Compared to those sleeping an average of 7–8 h per night, and after adjusting for multiple risk factors and medical conditions, a sleep duration of less than 5 h was associated with a body mass index (BMI) that was on average 2.5 kg/m2 (95% confidence interval (CI): 2.0–2.9) greater in men and 1.8 kg/m2 (95% CI: 1.1–2.4) greater in women. The odds of obesity (BMI ⩾30 kg/m2) was 3.7-fold greater (95% CI: 2.7–5.0) in men and 2.3-fold greater in women (95% CI: 1.6–3.1) who slept less than 5 h. Short sleep was also associated with central body fat distribution and increased percent body fat. These associations persisted after adjusting for sleep apnea, insomnia and daytime sleepiness.In older men and women, actigraphy-ascertained reduced sleep durations are strongly associated with greater adiposity.

title: Effect of sleep and circadian cycle on sleep period energy expenditure.
abstract: Energy expenditure is lower during sleep than relaxed wakefulness. However, there is disagreement as to the particular metabolic changes that produce the difference. The present study assessed the contribution of sleep, circadian cycle, and the specific dynamic action effect of the evening meal to the sleep period fall in metabolic rate. Five subjects were tested for a total of nine nights under three conditions in a repeated-measures design. Subjects were confined to bed throughout their usual sleep period but were instructed to go to sleep 0, 3, or 6 h after their usual time for lights out. O2 consumption was measured in all conditions for the 0.5 h before and after each of the times for lights out and then throughout the sleep period after lights out. The results demonstrated that changes in energy expenditure during the sleep period are a function of both sleep and circadian cycle. In this study, the contribution of the two components was approximately equal. However, the effect of sleep was rapid asymptoting within 15 min of sleep onset, whereas that of circadian cycle was constant over the assessment period.

title: Metabolism during normal, fragmented, and recovery sleep.
abstract: Average metabolic data (O2 uptake and CO2 output) were obtained for each 3-min period during consecutive nights of normal, experimentally fragmented, and recovery sleep in a group of 12 normal young adult males. Naturally occurring arousals and awakenings resulted in a characteristic increase in metabolism on the baseline night. The placement of brief frequent experimental arousals on the following night resulted in significantly increased metabolism throughout the night and significantly decreased sleep restoration as measured by morning performance, mood, and alertness tests, even though total sleep time was minimally reduced. Metabolic variables were significantly decreased compared with baseline on the nondisturbed recovery night that followed the sleep fragmentation night. The data cannot be used to infer that increased metabolism during sleep causes nonrestorative sleep, but the direction and time course of metabolic change accompanying arousal are consistent with that hypothesis.

title: Relationship between sleep stages and metabolic rate in humans.
abstract: Differences in sleeping metabolic rate (SMR) among subjects may be related to different levels of energy expenditure associated with sleep stages. The relationship between energy expenditure and sleep stages was investigated overnight in 29 subjects (14 Caucasians and 15 Pima Indians, 18 males and 11 females; mean +/- SD, 31 +/- 7 yr, 83 +/- 26 kg, 27 +/- 11% fat). Sleep stages were determined by electroencephalogram recording, whereas energy expenditure was measured in a 1,000-liter Plexiglas sleep box constructed around a bed as a fast-response open-circuit indirect calorimeter. Eighty-five percent of the interindividual variability in SMR was explained by differences in fat-free mass, fat mass, age, sex, and race (r2 = 0.85). The intra-individual variance in SMR over time was related to sleep stages and to clock time. Within subjects, SMR in stage 3 was significantly lower than in stage 2 (-39 +/- 18 kcal/day; P < 0.05) and rapid eye movement sleep (-51 +/- 23 kcal/day; P < 0.05). Also, sleep stages were associated with different respiratory quotients. Because sleep stages are associated with only small differences in energy metabolism, our results suggest that sleep stages play a minor role in the variance of SMR among subjects. However, the duration of sleep may contribute to the variability of 24-h energy expenditure.

title: Daily activity energy expenditure and mortality among older adults.
abstract: Exercise is associated with mortality benefits but simply expending energy through any activity in an individual's free-living environment may confer survival advantages.



To determine whether free-living activity energy expenditure is associated with all-cause mortality among older adults.



Free-living activity energy expenditure was assessed in 302 high-functioning, community-dwelling older adults (aged 70-82 years). Total energy expenditure was assessed over 2 weeks using doubly labeled water. Resting metabolic rate was measured using indirect calorimetry and the thermic effect of meals was estimated at 10% of total energy expenditure. Free-living activity energy expenditure was calculated as: (total energy expenditure x 0.90) - resting metabolic rate. Participants were followed up over a mean of 6.15 years (1998-2006).



Free-living activity energy expenditure (3 tertiles: low, <521 kcal/d; middle, 521-770 kcal/d; high, >770 kcal/d) and all-cause mortality.



Fifty-five participants (18.2%) died during follow-up. As a continuous risk factor, an SD increase in free-living activity energy expenditure (287 kcal/d) was associated with a 32% lower risk of mortality after adjusting for age, sex, race, study site, weight, height, percentage of body fat, and sleep duration (hazard ratio, 0.68; 95% confidence interval, 0.48-0.96). Using the same adjustments, individuals in the highest tertile of free-living activity energy expenditure were at a significantly lower mortality risk compared with the lowest tertile (hazard ratio, 0.31; 95% confidence interval, 0.14-0.69). Absolute risk of death was 12.1% in the highest tertile of activity energy expenditure vs 24.7% in the lowest tertile; absolute risks were similar to these for tertiles of physical activity level. The effect of free-living activity energy expenditure changed little after further adjustment for self-rated health, education, prevalent health conditions, and smoking behavior. According to self-reports, individuals expending higher levels of free-living activity energy were more likely to work for pay (P = .004) and climb stairs (P = .01) but self-reported high-intensity exercise, walking for exercise, walking other than for exercise, volunteering, and caregiving did not differ significantly across the activity energy expenditure tertiles.



Objectively measured free-living activity energy expenditure was strongly associated with lower risk of mortality in healthy older adults. Simply expending energy through any activity may influence survival in older adults.

title: Sleep restriction and appetite control: waking to a problem?
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