No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Acute sleep deprivation increases portion size and affects food choice in young men
Abstract
Acute sleep loss increases food intake in adults. However, little is known about the influence of acute sleep loss on portion size choice, and whether this depends on both hunger state and the type of food (snack or meal item) offered to an individual. The aim of the current study was to compare portion size choice after a night of sleep and a period of nocturnal wakefulness (a condition experienced by night-shift workers, e.g. physicians and nurses). Sixteen men (age: 23 ± 0.9 y, BMI: 23.6 ± 0.6 kg/m2) participated in a randomized within-subject design with two conditions, 8-h of sleep and total sleep deprivation (TSD). In the morning following sleep interventions, portion size, comprising meal and snack items, was measured using a computer-based task, in both fasted and sated state. In addition, hunger as well as plasma levels of ghrelin were measured. In the morning after TSD, subjects had increased plasma ghrelin levels (13%, p=0.04), and chose larger portions (14%, p=0.02), irrespective of the type of food, as compared to the sleep condition. Self-reported hunger was also enhanced (p<0.01). Following breakfast, sleep-deprived subjects chose larger portions of snacks (16%, p=0.02), whereas the selection of meal items did not differ between the sleep interventions (6%, p=0.13). Our results suggest that overeating in the morning after sleep loss is driven by both homeostatic and hedonic factors. Further, they show that portion size choice after sleep loss depend on both an individual’s hunger status, and the type of food offered.
... Studies have observed that sleep deprivation might be one of the modifiable factors that promote inadequate nutritional intake and contribute to unhealthy food consumption behavior and excess weight gain [4][5][6]. In the last decade, the increased prevalence of obesity has been associated with sleep curtailment [7]. ...
... When food environment is carefully controlled, sleep deprivation is associated with a lower secretion of the satiety hormone leptin and a higher secretion of hunger-stimulating hormone ghrelin, which may induce hunger feelings, and therefore, increase food intake and contribute to increased obesity [46]. Disrupted sleep increase susceptibility of brain regions associated with motivation, reward, and decision making in response to pleasurable stimuli like palatable calorie-dense and carbohydrate-rich food or snacks [5,20,65]. Furthermore, some neuroimaging studies evidenced that sleep curtailment induces an increased activity in brain reward centers in response to palatable food [54,65]. Moreover, sleep deprivation has been related to lower inhibitory impulse control, leading to increased hedonistic eating conduct [66]. ...
... Since children are still developing behavioral controls, the effect of irregular sleep pattern on emotional and impulsive eating of highly palatable food could be greater. Moreover, sleep induces daytime fatigue and stress and other emotional symptoms [67], resulting in a sensation of less energy that can increase food intake to compensate for the energy deficit caused by increased waking time [5]. For example, caffeinated drinks reduce sleep duration; however, people who are sleep deprived may consume more caffeinated drinks to feel more alert. ...
The objective of this study was to examine the relationship between different sleep parameters and energy and macronutrient intake in school-aged children. A total of 203 children 6 to 9 years of age participated in this cross-sectional study. Anthropometric measurements were taken first. Diet was assessed with 3-day food logs and sleep was measured with a questionnaire on sleep quality and a wrist actigraph worn for at least 7 days. A decrease of 165.45 kcal was observed per each additional hour of sleep during the week (β (95% CI) = −165.45 (−274.01, −56.88); p = 0.003). This relationship was also observed for fat (β (95% CI) = −11.14 (−18.44, −3.84); p = 0.003) and protein (β (95% CI) = −13.27 (−22.52, −4.02); p = 0.005). An increase in weekend sleep efficiencies for those under the recommended threshold of 85% also had a similar association with energy (β (95% CI) = −847.43 (−1566.77, 128.09); p = 0.021) and carbohydrate (β (95% CI) = −83.96 (−161.76, −6.15); p = 0.035)) intake. An increase in habitual sleep variability was related with a slight increase in protein intake (β (95% CI) = 0.32 (0.031, 0.62); p = 0.031). Children who slept less had a higher energy intake, especially from fat and protein and those who presented inefficient sleep had a higher carbohydrate intake. Strategies to enhance sleep quality and quantity combined with dietary recommendations could help to improve energy and macronutrient intake levels in children.
... Insufficient sleep is an independent risk factor for overweight and obesity [1], and interventional studies demonstrate greater food intake after a night of curtailed sleep [2] or total sleep deprivation (TSD) [3]. Insufficient sleep, like obesity [4], is a global problem. ...
... Insufficient sleep is associated with an increased energy intake [2] and an increased risk of obesity [1]. This study evaluated the effect of modest sleep curtailment on hunger, food cravings, food reward, and portion size, all of which have been shown to contribute to excess intake and possible weight gain, but previous interventional studies have used more extreme curtailments [2] or even total deprivation [3,12,33]. The modest curtailment in this study resulted in significantly reduced TIB, TST, SWS, and REM sleep durations as well as reduced subjective sleep quality. ...
... Despite the fact that participants consumed the same amount of food at the same time each day, hunger at lunchtime was increased, as was the portion size of selected foods and the energy content of meal-associated foods after sleep curtailment. These findings are consistent with other research that reported that TSD led to higher hunger ratings after TSD compared to after a normal night's sleep in men [3,9]. These studies also observed that concentrations of the hunger hormone ghrelin increased, which could contribute to feelings of increased hunger. ...
This study examined the effects of one night of sleep curtailment on hunger, food cravings, food reward, and portion size selection. Women who reported habitually sleeping 7–9 h per night, were aged 18–55, were not obese, and had no sleep disorders were recruited. Sleep conditions in this randomized crossover study consisted of a normal night (NN) and a curtailed night (CN) where time in bed was reduced by 33%. Hunger, tiredness, sleep quality, sleepiness, and food cravings were measured. A progressive ratio task using chocolates assessed the food reward. Participants selected portions of various foods that reflected how much they wanted to eat at that time. The sleep duration was measured using a single-channel electroencephalograph. Twenty-four participants completed the study. The total sleep time was shorter during the CN (p < 0.001). Participants reported increased hunger (p = 0.013), tiredness (p < 0.001), sleepiness (p < 0.001), and food cravings (p = 0.002) after the CN. More chocolate was consumed after the CN (p = 0.004). Larger portion sizes selected after the CN resulted in increased energy plated for lunch (p = 0.034). In conclusion, the present study observed increased hunger, food cravings, food reward, and portion sizes of food after a night of modest sleep curtailment. These maladaptive responses could lead to higher energy intake and, ultimately, weight gain.
... Suboptimal sleep (i.e., reduced sleep time, poor sleep quality, and continuity) alters the physiologic and hedonic signals controlling eating behavior and contributes to overeating, weight gain, and obesity (1,2,8). Daily hunger (9)(10)(11)(12)(13); circulating ghrelin, which is associated with hunger and meal initiation (9,13,14); food cravings (14,15); and the desire to overeat (9,13) are increased in adults with poor sleep compared with those with healthy sleep patterns and good sleep quality. In contrast, fullness and circulating peptide YY (PYY), a potent satiety signal, are blunted with poor sleep (16). ...
... Suboptimal sleep (i.e., reduced sleep time, poor sleep quality, and continuity) alters the physiologic and hedonic signals controlling eating behavior and contributes to overeating, weight gain, and obesity (1,2,8). Daily hunger (9)(10)(11)(12)(13); circulating ghrelin, which is associated with hunger and meal initiation (9,13,14); food cravings (14,15); and the desire to overeat (9,13) are increased in adults with poor sleep compared with those with healthy sleep patterns and good sleep quality. In contrast, fullness and circulating peptide YY (PYY), a potent satiety signal, are blunted with poor sleep (16). ...
... Suboptimal sleep (i.e., reduced sleep time, poor sleep quality, and continuity) alters the physiologic and hedonic signals controlling eating behavior and contributes to overeating, weight gain, and obesity (1,2,8). Daily hunger (9)(10)(11)(12)(13); circulating ghrelin, which is associated with hunger and meal initiation (9,13,14); food cravings (14,15); and the desire to overeat (9,13) are increased in adults with poor sleep compared with those with healthy sleep patterns and good sleep quality. In contrast, fullness and circulating peptide YY (PYY), a potent satiety signal, are blunted with poor sleep (16). ...
Background
Observational studies show associations between breakfast skipping, reduced satiety, and poor sleep quality; however, intervention studies are lacking.
Objective
The purpose of this study was to examine the effects of consuming breakfast compared with breakfast skipping on appetitive, hormonal, and neural markers of appetite and satiety; ad libitum food intake; and exploratory measures of sleep health in young adults.
Methods
Thirteen adults [aged 23.5 ± 0.9 y (mean ± SEMs); body mass index (kg/m²): 23.6 ± 0.6] completed the following randomized crossover-design study. Participants consumed a high-protein breakfast (“Breakfast”; 340 kcal, 30 g protein, 36 g carbohydrate, 9 g fat) or skipped breakfast (“Skip”) for 7 d/treatment. On day 7, an 8-h clinical testing day was completed including assessments of hunger, fullness, desire to eat, prospective food consumption (PFC), related hormones, food cue–stimulated functional magnetic resonance imaging brain scans, and ad libitum evening food intake. Sleep quantity and quality were assessed with 7-d actigraphy, 7-d sleep diaries, and sleep-related hormones.
Results
Morning and daily hunger, desire to eat, PFC, and ghrelin decreased, whereas fullness increased after the Breakfast pattern compared with after the Skip pattern (all, P < 0.05). No difference in peptide YY (PYY) concentrations were detected. Hippocampal, parahippocampal, and middle frontal gyrus activations were reduced after the Breakfast pattern compared with the Skip pattern (all, P < 0.01). Although no differences in daily food intake were observed, the Breakfast pattern reduced evening intake of high-carbohydrate and high-fat foods (P < 0.05), whereas evening sugar intake tended to be reduced compared with the Skip pattern (P = 0.085). Although Breakfast led to shorter total sleep time (TST) compared with Skip (P < 0.05), no difference in sleep efficiency (TST/sleep period) was detected. Perceived sleep quality and sleep onset tended to improve after Breakfast compared with after Skip (P = 0.060 and P = 0.07, respectively).
Conclusion
Breakfast consumption improved appetite, satiety, and diet quality and may support some aspects of sleep health in healthy young adults. This trial was registered at clinicaltrials.gov as NCT03031132.
... Elle a également été confirmée dans plusieurs études récentes [66][67][68][69][70][71][72][73]. La plupart des études portant sur les effets de la privation de sommeil ont également rapporté une augmentation de la faim et de l'appétit [74][75][76][77][78][79][80][81]même si certaines ne font état d'aucun effet [48,61,65,82,83] . Dans plusieurs études, la privation de sommeil a engendré une modification des choix alimentaires : les sujets ingéraient plus d'aliments énergétiques riches en lipides [48,61,62,69,72,84,85] ou en sucres [64,70,72], ou alors en avaient davantage envie, notamment pour les desserts [60,86]. ...
... Dans plusieurs études, la privation de sommeil a engendré une modification des choix alimentaires : les sujets ingéraient plus d'aliments énergétiques riches en lipides [48,61,62,69,72,84,85] ou en sucres [64,70,72], ou alors en avaient davantage envie, notamment pour les desserts [60,86]. Parfois, ils augmentaient le nombre de collations [64] ou la taille des portions au cours du petit déjeuner [81]. Une étude a même observé que des hommes « lâchés » dans un supermarché , avec un budget fixé par les expérimentateurs (50 USD) achetaient davantage d'aliments caloriques après privation de sommeil qu'après une nuit de sommeil normal [87]. ...
... Une étude a même observé que des hommes « lâchés » dans un supermarché , avec un budget fixé par les expérimentateurs (50 USD) achetaient davantage d'aliments caloriques après privation de sommeil qu'après une nuit de sommeil normal [87]. En ce qui concerne les variations hormonales induites par la privation de sommeil, certains travaux ont noté une augmentation [66,74,75,78,81,88,89], d'autres une absence de variation [61,64,65,90], d'autres enfin, une diminution [91] de la ghrélinémie. La leptinémie a diminué dans certaines études [60,88,[92][93][94][95], n'a pas changé [61,64,65,74,75,78,90] ou a augmenté dans d'autres [65,71,82,83,96]. ...
Notre rythme de vie actuel a entraîné une diminution progressive du temps alloué au sommeil. En France, une personne sur 3 dormirait moins de 7 heures par nuit. Dans le même temps, le nombre de patients souffrant d’obésité a augmenté. De nombreuses études épidémiologiques soulignent le lien entre la faible durée du temps de sommeil et la prise de poids. En parallèle, les études expérimentales ont observé que la privation de sommeil modifiait le comportement alimentaire en augmentant la sensation de faim et la prise alimentaire. Le cycle nycthéméral induit par l’alternance lumière–obscurité a une influence majeure sur le sommeil mais aussi sur le comportement alimentaire : la lumière agit sur les noyaux suprachiasmatiques, puis secondairement sur les noyaux préoptiques et les noyaux latéraux de l’hypothalamus d’où l’augmentation des orexines. Plusieurs théories tentent d’expliquer l’augmentation de la prise alimentaire : la première, phylogénétique, serait liée aux variations de la durée du sommeil au cours des saisons ; la deuxième concernerait l’adaptation anticipatoire face à l’éveil ; la dernière serait liée à une modification du contrôle hédonique de la prise alimentaire. De nombreuses pathologies altèrent la relation physiologique sommeil–comportement alimentaire, comme par exemple le syndrome d’apnée du sommeil. Il est donc nécessaire de mieux comprendre cette relation pour améliorer la prise en charge des personnes obèses et pour prévenir le développement du surpoids par le respect d’un rythme du sommeil adapté à l’enfant.
... Les effets d'une privation ou d'une perturbation du sommeil sur la prise alimentaire ont été étudiés aussi bien chez l'Homme que chez l'animal. De manière générale, une diminution de la qualité du sommeil entraîne une augmentation de la prise alimentaire aussi bien chez les adultes (Hogenkamp et al., 2013) que chez les enfants (Tatone-Tokuda et al., 2012). Cette augmentation se traduit par l'augmentation des portions afin d'apporter les éléments nécessaires pour rester éveillé. ...
... Cette augmentation se traduit par l'augmentation des portions afin d'apporter les éléments nécessaires pour rester éveillé. Toutefois cet apport est supérieur à la quantité nécessaire pour compenser les dépenses énergétiques engendrées par la perturbation du sommeil (Hogenkamp et al., 2013;Markwald et al., 2013). Les personnes ayant subi une restriction de sommeil peuvent donc présenter une augmentation jusqu'à 20 % supérieure à la prise journalière habituelle (Bosy-Westphal et al., 2008;Brondel et al., 2010). ...
Avec le développement des nouvelles technologies, l'exposition aux champs électromagnétiques est de plus en plus importante. En marge de ce développement, nos sociétés ont vu émerger des personnes présentant des symptômes qu'ils attribuent à une exposition aux champs électromagnétiques. Les résultats des études expérimentales antérieurs restant à controverse, l'objectif de ce travail est de voir si une exposition conjointe entre les champs électromagnétiques et le bruit conduit à une apparition ou une exacerbation des symptômes des champs électromagnétiques. Cette étude s'est portée sur différentes fonctions physiologiques chez une population juvénile : le sommeil, le système immunitaire, la prise alimentaire, la respiration et le comportement. Nos résultats montrent un comportement anxieux, une diminution de la locomotion ainsi qu'une augmentation du poids des animaux, associé à des variations dans le pattern alimentaire. Le sommeil et la respiration sont peu modifiés chez les animaux exposés aux champs électromagnétiques. Le système immunitaire des animaux exposés aux champs électromagnétiques présente des altérations au niveau du système immunitaire acquis avec une redistribution des sous-populations lymphocytaires en faveur d'une activation des cellules et de l'immunité humorale, mais sans variation du système immunitaire inné. L'altération de ce dernier système est observée lors de la co-exposition mais est différente de celle d'une exposition au bruit. Ce travail de thèse a permis de mettre en évidence différents effets des CEM, notamment un comportement anxieux et des variations immunitaire
... Improving sleep quality appears as an important point of intervention, which can enhance effectiveness of obesity therapy including effectiveness of bariatric surgery associated weight loss. The evidence of adverse effects of poor sleep on dietary intake is based mainly on studies of experimental reduction of sleep duration [34,35], and there is a lack of studies in which objective measures of sleep were used. For the present study, we hypothesized that sleep problems as assessed by Athens Insomnia Scale (AIS) are associated with unhealthy eating habits in bariatric surgery candidates. ...
... However, the Finnish study was unable to confirm any associations probably due to general questions on food habits and suggestive categorization of food habits as healthy or unhealthy. On the other hand, an experimental reduction of sleep duration was accompanied by increased intake of calories from snacks [34,48], increased food purchasing in normal-weight men [35], and increased hunger and appetite, especially for calorie-dense foods with high carbohydrate content [5]. These associations seem to be related to the alterations in appetitive brain signaling [49]. ...
Background:
Alongside obesity, insomnia and depression are common public health problems. Sleep problems are currently believed to be associated with excessive food intake and metabolic disturbances. Therefore, we aimed to explore a relationship between insomnia, depressive symptoms and eating habits as well as metabolic parameters in bariatric surgery candidates.
Methods:
A total of 361 unrelated obese subjects were included in this study. Severity of sleep problems was measured with Athens Insomnia Scale (AIS) and the severity of depressive symptoms was assessed with the Beck Depression Inventory (BDI-II). Obstructive sleep apnea (OSA) was assessed by the Apnea Hypopnoea Index (AHI). Information was obtained about demographics, eating habits and lifestyle. Blood samples were collected to measure concentration of lipids (cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol), and glucose.
Results:
The median (interquartile range) score for AIS in the study participants was 5 (3-8) with a range of 0-24 and 47% (171) participants scored ≥6 (met criteria for diagnosis of insomnia). Statistically significant correlations were found between the AIS scores and serum triglycerides and glucose concentrations, and BDI-II total scores. The highest scores on AIS and BDI-II were found in participants with high frequency of snack food consumption, in physically inactive individuals as well as in those who self-reported eating at night or who declared more than 3 intense emotions associated with a desire-to-eat. Adjusted multivariate logistic regression analysis revealed that clinical insomnia was most strongly associated with daily consumption of snack foods, with the odds ratio of 3.26 (95% CI: 1.74-6.11), while depressive symptoms were strongly associated with both eating in response to ≥3 specific emotions with OR = 2.93 (95% CI: 1.26-6.78) as well as with daily consumption of snack foods with OR = 2.87 (95% CI: 1.16-5.14).
Conclusions:
The results indicate that insomnia and depression in obese individuals are associated with eating habits, and suggest that in some patients these associations appears as major factors affecting obesity development.
... In addition,Hollands et al. (2017)suggest that biological state may influence food selection. Research unrelated to proximity studies show that hunger (Furst, Connors, Bisogni, Sobal, & Falk, 1996;Hoefling & Strack, 2010), tiredness (Brondel, Romer, Nougues, Touyarou, & Davenne, 2010;Hogenkamp et al., 2013), and stress (VanBlyderveen et al., 2016;Zellner et al., 2006) influence food selection, with higher levels of each of these factors inducing unhealthier food selection.Bucher et al. (2016)highlight that the participants' BMI does not moderate the proximity effect. Further, a current study protocol outlines an investigation into whether executive functioning moderates the proximity effect, with the hypothesis that the effect is consistent regardless of executive functioning level (Hunter, Hollands, Couturier, & Marteau, 2016). ...
... Consumption from healthy proximal and unhealthy distal conditions will fare in between the aforementioned food placements. H4) Higher subjective tiredness, stress, and hunger ratings will positively correlate with chocolate consumption, as past research suggests that higher levels of each factor increase unhealthier food selection (Greer, Goldstein, & Walker, 2013;Hoefling & Strack, 2010;Hogenkamp et al., 2013;Van Blyderveen et al., 2016). Further, BMI, age, food preference/liking (Bucher et al., 2016), acceptability (Petrescu et al., 2016) and executive functioning (Hunter et al., 2016) are all expected to not significantly moderate food consumption. ...
... Sleep loss generally increases the preference for foods with a high carbohydrate content including sweets, salty, and starchy foods compared to vegetables, fruit, and high protein foods [51][52][53][54]. Across two weeks of sleep restriction (i.e., 5 h sleep per night) [55] or following one night of total sleep deprivation [56], participants increased their ad-libitum food and energy intake, particularly through increased snacking. Sleep restriction also impacts food- The diets of shiftworkers have been reviewed by Lowden et al. [50]. ...
... Sleep loss generally increases the preference for foods with a high carbohydrate content including sweets, salty, and starchy foods compared to vegetables, fruit, and high protein foods [51][52][53][54]. Across two weeks of sleep restriction (i.e., 5 h sleep per night) [55] or following one night of total sleep deprivation [56], participants increased their ad-libitum food and energy intake, particularly through increased snacking. Sleep restriction also impacts food-purchasing behaviours, influencing longer-term food intake. ...
(1) Background: About one in four workers undertake shift rosters that fall outside the traditional 7 a.m.–6 p.m. scheduling. Shiftwork alters workers’ exposure to natural and artificial light, sleep patterns, and feeding patterns. When compared to the rest of the working population, shiftworkers are at a greater risk of developing metabolic impairments over time. One fundamental component of metabolic health is skeletal muscle, the largest organ in the body. However, cause-and-effect relationships between shiftwork and skeletal muscle health have not been established; (2) Methods: A critical review of the literature was completed using online databases and reference lists; (3) Results: We propose a conceptual model drawing relationships between typical shiftwork consequences; altered light exposure, sleep patterns, and food and beverage consumption, and drivers of skeletal muscle health—protein intake, resistance training, and hormone release. At present, there is no study investigating the direct effect of shiftwork on skeletal muscle health. Instead, research findings showing that acute consequences of shiftwork negatively influence skeletal muscle homeostasis support the validity of our model; (4) Conclusion: Further research is required to test the potential relationships identified in our review, particularly in shiftwork populations. Part of this testing could include skeletal muscle specific interventions such as targeted protein intake and/or resistance-training.
... Experimental studies have shown that subjects under sleep restriction had increased food, energy and fat intake and consumed larger food portions and more calories from snacks. [6][7][8][9][10][11] Some of these studies further support the hypothesis that sleep has an impact on metabolic and hormonal changes. In case of sleep deprivation, levels of the appetite-stimulating hormone ghrelin were increased, whereas levels of the appetitesuppressing hormone leptin were reduced. ...
... Different studies have shown that due to an increased feeling of hunger and appetite, subjects under sleep restriction consumed larger portions, more energy-dense foods and preferred foods high in fat or carbohydrates, compared with subjects with adequate sleep duration. 6,9,12 The higher intake of carbonated beverages among short duration sleepers might be another example how energy and to a certain amount caffeine (for example, in coke energy drinks) could be supplied quickly. The explanation for a higher intake of tap water among short duration sleepers remains unclear. ...
Background/objectives:
Only few epidemiologic studies examined sleep characteristics in relation to dietary behaviour. Our aim was to analyse associations of sleep duration, midpoint of sleep and sleep quality with dietary intake among the Bavarian population.
Subjects/methods:
Within the cross-sectional Bavarian Food Consumption Survey II, 1050 subjects aged 13-81 years were recruited. Dietary intake was assessed with three 24-h dietary recalls by telephone (EPIC-Soft). In our study, 814 participants aged 18 years or older, who completed at least two 24-h dietary recalls and who had complete and plausible information on sleep characteristics were analysed. Dietary intake was described by the consumption of main food groups, energy-proving nutrients and energy intake. Sleep was measured by the Pittsburgh Sleep Quality Index Questionnaire, from which categories of self-reported usual sleep duration in half-h-steps per night, midpoint of sleep and overall sleep quality were derived.
Results:
Sleep duration was associated with intake of non-alcoholic beverages (P<0.01), carbonated beverages (P=0.04), water (P=0.04) and coffee/black tea (P=0.01) with higher intake among short duration sleepers. No association was found between the consumption of other main food groups, energy-proving nutrients or total daily energy intake and sleep duration. Midpoint of sleep was associated with intake of carbonated beverages (P=0.02, highest intake among subjects with early midpoint of sleep). No association between sleep quality and dietary intake was detected.
Conclusions:
Our findings demonstrate only specific associations between sleep characteristics and dietary intake, and mainly sleep duration was associated with beverage intake.European Journal of Clinical Nutrition advance online publication, 11 January 2017; doi:10.1038/ejcn.2016.264.
... In healthy adults, sleep restriction (curtailed sleep across multiple consecutive days) leads to increases in caloric intake [1][2][3][4][5][6][7][8][9][10], snacking [7,11], fat and carbohydrate consumption [2,5,7,8,10,11], late-night eating/delayed meal timing [1,2,10] and weight gain [1][2][3]. Similarly, during total sleep deprivation (one night of continuous wakefulness), adults consume a large number of calories during the overnight period [12], consume more fat the following day [12], make more food purchases [13], consume larger portion sizes [14] and eat more calories from snacks [14]. This increased consumption of energy (via food/drink) [9] exceeds the additional energy required to sustain the extended wakefulness associated with either type of sleep loss [1,[15][16][17]. ...
... In healthy adults, sleep restriction (curtailed sleep across multiple consecutive days) leads to increases in caloric intake [1][2][3][4][5][6][7][8][9][10], snacking [7,11], fat and carbohydrate consumption [2,5,7,8,10,11], late-night eating/delayed meal timing [1,2,10] and weight gain [1][2][3]. Similarly, during total sleep deprivation (one night of continuous wakefulness), adults consume a large number of calories during the overnight period [12], consume more fat the following day [12], make more food purchases [13], consume larger portion sizes [14] and eat more calories from snacks [14]. This increased consumption of energy (via food/drink) [9] exceeds the additional energy required to sustain the extended wakefulness associated with either type of sleep loss [1,[15][16][17]. ...
Experimental studies have shown that sleep restriction (SR) and total sleep deprivation (TSD) produce increased caloric intake, greater fat consumption, and increased late-night eating. However, whether individuals show similar energy intake responses to both SR and TSD remains unknown. A total of N = 66 healthy adults (aged 21–50 years, 48.5% women, 72.7% African American) participated in a within-subjects laboratory protocol to compare daily and late-night intake between one night of SR (4 h time in bed, 04:00–08:00) and one night of TSD (0 h time in bed) conditions. We also examined intake responses during subsequent recovery from SR or TSD and investigated gender differences. Caloric and macronutrient intake during the day following SR and TSD were moderately to substantially consistent within individuals (Intraclass Correlation Coefficients: 0.34–0.75). During the late-night period of SR (22:00–04:00) and TSD (22:00–06:00), such consistency was slight to moderate, and participants consumed a greater percentage of calories from protein (p = 0.01) and saturated fat (p = 0.02) during SR, despite comparable caloric intake (p = 0.12). Similarly, participants consumed a greater percentage of calories from saturated fat during the day following SR than TSD (p = 0.03). Participants also consumed a greater percentage of calories from protein during recovery after TSD (p < 0.001). Caloric intake was greater in men during late-night hours and the day following sleep loss. This is the first evidence of phenotypic trait-like stability and differential vulnerability of energy balance responses to two commonly experienced types of sleep loss: our findings open the door for biomarker discovery and countermeasure development to predict and mitigate this critical health-related vulnerability.
... 9,10 Studies have attempted to understand the mechanisms between sleep and obesity, but have been limited to clinical studies among adults in controlled environments. This research suggests that sleep disruption increases a homeostatic drive to eat 11 and that sleep restriction results in subsequent increased caloric intake from energy-dense foods and larger portion sizes. [11][12][13][14] Additionally, studies of adults have also shown that insufficient sleep (less than 7 h) and oversleeping (more than 9-10 h) may increase risk for obesity, type 2 diabetes, heart disease, stroke, and depression. ...
... This research suggests that sleep disruption increases a homeostatic drive to eat 11 and that sleep restriction results in subsequent increased caloric intake from energy-dense foods and larger portion sizes. [11][12][13][14] Additionally, studies of adults have also shown that insufficient sleep (less than 7 h) and oversleeping (more than 9-10 h) may increase risk for obesity, type 2 diabetes, heart disease, stroke, and depression. [15][16][17] Research on children has found a relationship between sleep patterns and dietary patterns as early as age 2. 18 Sleep diffi- culties in infancy may influence irregular eating patterns at ages 2-4 years. ...
Study objective:
Short sleep duration is a risk factor for childhood obesity. Mechanisms are unclear, but may involve selection of high carbohydrate foods. This study examined the association between estimated sleep duration and macronutrient intake as percentages of total energy among Mexican American (MA) 9-11 year olds.
Methods:
This cross-sectional study measured diet using two 24-hour recalls and estimated sleep duration using hip-worn accelerometry in MA children (n=247) who were part of a cohort study. Child and maternal anthropometry were obtained; mothers reported on demographic information. Using linear regression, we examined the relationship of sleep duration with energy intake, sugar intake, and the percentage of energy intake from carbohydrates, fat and protein.
Results:
Children were 47% male; mean age was 10 (SD=0.9) years. Mean sleep duration was 9.6 (SD=0.8) hours; 53% were overweight/obese, with a mean energy intake of 1759 (SD=514) calories. Longer sleep duration was independently associated with a lower percentage of energy intake from carbohydrates (B= -0.22, P< 0.01) and a higher percentage of energy from fat (B=0.19, P< 0.01), driven by the percentage of energy from polyunsaturated fatty acids (PUFA; B=0.17, P< 0.05). No association was found with the intake of energy or total sugars, or the percent of calories from protein.
Conclusions:
MA children who slept longer consumed diets with a lower percentage of calories from carbohydrates and a higher percentage from fat, especially from PUFA. Short sleep duration may be a risk factor for food cravings that are high in carbohydrate content, and may displace heart-healthy dietary fat, and thereby increase obesity risk among children.
... Therefore, if similar effects of poor sleep on decision-making and risk-taking behaviors are observed with SSD, one might expect that individuals with poor sleep quality or SSD would also make poor decisions with respect to their food choices. Hogenkamp et al. (2013) explored the effects of sleep deprivation on a computer-based task to self-select portion sizes for a meal relative to a night of 8-h TIB. Young, normal-weight, healthy men underwent one night of 8-h TIB followed by 1 day of a fixed meal and food intake diet before being randomly allocated to the TSD or 8-h TIB night. ...
... However, food intake was not measured in this study, and it is unknown whether participants would have actually consumed what they reported they would in the portion task. Nevertheless, based on data from studies of food intake, one would expect that the results obtained by Hogenkamp et al. (2013) would be reflective of actual consumption patterns. One study has been conducted to investigate the association between the results of this task and actual and concluded that screen-based measures of portion-size selections were a valid method to assess energy intake in humans ( Wilkinson et al., 2012). ...
There is a consistent epidemiological association between short sleep duration and obesity. It is increasingly clear from intervention studies that restricting sleep increases food intake. However, the control mechanisms of food intake that are disturbed by sleep duration remain somewhat unknown. There are some data supporting a homeostatic mechanism implicating alterations in ghrelin and leptin concentrations, but there are also data supporting changes in hedonistic controls of food intake. This chapter focuses on the latter and examines the state of science relating sleep duration to changes in food appeal and food choice. Food stimuli seem to elicit greater neuronal reactivity in reward and pleasure centers of the brain under conditions of sleep restriction, which could lead to poor food choices, overeating, and weight gain over time. The effects of sleep duration on food intake are clearly complex, and more research is necessary to disentangle the roles of the environment and biology.
... This is also the time that many eating disorders, such as binge eating disorder, become apparent, possibly due to issues related to self-esteem and body image. Many studies have found an asso- ciation between sleep deprivation and food choices [48][49][50][51][52][53]. Sleep-deprived individuals appear more prone to choose unhealthy foods high in energy and fat content [48][49][50][51][52][53]. ...
... Many studies have found an asso- ciation between sleep deprivation and food choices [48][49][50][51][52][53]. Sleep-deprived individuals appear more prone to choose unhealthy foods high in energy and fat content [48][49][50][51][52][53]. Also, sleep-deprived individuals are reported to have more frequent meals or snacks between meals compared with individuals who had sufficient sleep [50]. ...
Insulin resistance (IR) occurs in a transient manner during puberty. Obese adolescents may be at risk for persistent IR during puberty. The objective of the study is to review the literature on the association of the anthropometry and lifestyle characteristics with insulin sensitivity in overweight and obese adolescents, and include data from a new study. Relevant papers were selected and reviewed. In addition, 137 overweight and obese adolescents (42 male/95 female, age 14.4 ± 2.3 years, BMI z-score +3.3 ± 0.7, HOMA-IR 3.4 ± 1.8) from the Centre for Overweight Adolescent and Children's Healthcare (MUMC+) were included in this study. Anthropometrics, Tanner stages, sleep characteristics, food intake behaviour and physical activity were determined, and possible associations with homeostasis model assessment of insulin resistance (HOMA-IR) were tested.
Overweight and obese adolescents with unfavourable fat partitioning and family history of NIDDM are at risk for persistent IR. Overweight and obese adolescents from the new cohort showed a higher HOMA-IR postpubertally. BMI z-score, age, pubertal stage and prepubertally total sleeping time (TST) and sleep efficiency (SE) were identified as significant contributors. Overweight and obese adolescents showed a persistently higher instead of transiently higher HOMA-IR during puberty, associated with BMI z-score, age, pubertal stage and prepubertally less TST and SE.
© 2015 John Wiley & Sons Ltd.
... In addition to the homeostatic system, the hedonic system also plays an important role in regulating food intake. After one night of TSD, 16 healthy normal-weight men choose larger food portions (+14%, p = 0.02) in correspondence with an increased hunger status [59]. The portions of snacks consumed after breakfast also increased (+16%, p = 0.02). ...
... While ghrelin and leptin levels remain unchanged in some studies [46,47,49,50], a few others have shown significant changes after sleep deprivation. A randomized crossover study of 16 healthy normal-weight men resulted in an increase in hunger ratings parallel to an increase in morning plasma ghrelin levels (+13%, p = 0.04) after one night of TSD when compared to 8 h in bed sleep opportunity [59]. A similar study with 14 men also showed elevations in morning ghrelin levels (p < 0.02) following the night after TSD [33]. ...
Background:
Cardiometabolic diseases, which include obesity, diabetes, hypertension, and cardiovascular disease, are associated with reduced quality of life and reduced life expectancy. Unfortunately, there are racial/ethnic and socioeconomic disparities associated with these diseases such that minority populations, such as African Americans and Hispanics, and those of lower socioeconomic status, experience a greater burden. Several reports have indicated that there are differences in sleep duration and quality that mirror the disparities in cardiometabolic disease. The goal of this paper is to review the association between sleep and cardiometabolic disease risk because of the possibility that suboptimal sleep may partially mediate the cardiometabolic disease disparities.
Methods:
We review both experimental studies that have restricted sleep duration or impaired sleep quality and examined biomarkers of cardiometabolic disease risk, including glucose metabolism and insulin sensitivity, appetite regulation and food intake, and immune function. We also review observational studies that have examined the association between habitual sleep duration and quality, and the prevalence or risk of obesity, diabetes, hypertension, and cardiovascular disease.
Conclusion:
Many experimental and observational studies do support an association between suboptimal sleep and increased cardiometabolic disease risk.
... Obesity rates have more than doubled since 1980, and in 2008 more than 1.4 billion adults were categorically overweight or obese [1]. There are a variety of lifestyle factors that have been proposed to contribute to this obesity pandemic [2]–[4]. For example, several epidemiological and laboratory studies have linked television (TV) watching to both increases in acute food intake, and subsequent weight gain and adiposity [2], [5]–[7]. ...
... Obesity rates have more than doubled since 1980, and in 2008 more than 1.4 billion adults were categorically overweight or obese [1]. There are a variety of lifestyle factors that have been proposed to contribute to this obesity pandemic234. For example, several epidemiological and laboratory studies have linked television (TV) watching to both increases in acute food intake, and subsequent weight gain and adiposity [2,567. ...
Obesity is a serious and growing health concern worldwide. Watching television (TV) represents a condition during which many habitually eat, irrespective of hunger level. However, as of yet, little is known about how the content of television programs being watched differentially impacts concurrent eating behavior. In this study, eighteen normal-weight female students participated in three counter-balanced experimental conditions, including a ‘Boring’ TV condition (art lecture), an ‘Engaging’ TV condition (Swedish TV comedy series), and a no TV control condition during which participants read (a text on insects living in Sweden). Throughout each condition participants had access to both high-calorie (M&Ms) and low-calorie (grapes) snacks. We found that, relative to the Engaging TV condition, Boring TV encouraged excessive eating (+ 52 % g, P=0.009). Additionally, the Engaging TV condition actually resulted in significantly less concurrent intake relative to the control ‘Text’ condition (- 35 % g, P=0.05). This intake was driven almost entirely by the healthy snack, grapes; however, this interaction did not reach significance (P=0.07). Finally, there was a significant correlation between how bored participants were across all conditions, and their concurrent food intake (beta= 0.317, P=0.02). Intake as measured by kcals was similarly patterned but did not reach significance. These results suggest that, for women, different TV programs elicit different levels of concurrent food intake, and that the degree to which a program is engaging (or alternately, boring) is related to that intake. Additionally, they suggest that emotional content (e.g. boring vs. engaging) may be more associated than modality (e.g. TV vs. text) with concurrent intake.
... At the same time, more than 500 million people are currently obese (2). Epidemiological evidence supports a link between sleep duration and obesity (3), and insufficient sleep has been linked to cognitive and metabolic mechanisms promoting weight gain (4)(5)(6)(7)(8). ...
... Impulsivity as a trait-measured by self-reported assessments and a behavioral task-has been linked to increased food intake even in subjects of normal weight (17). Sleep deprivation has not only been linked to increased feelings of hunger (5,7,27), but also to increased portion sizes and food purchasing (6,7). The latter could serve as a proxy for increased impulsive-like or riskier behavior following sleep loss, especially in light of other findings of altered and increased risk behavior following TSD (28). ...
Objective: To investigate whether acute sleep deprivation (TSD) leads to decreased cognitive control when food cues are presented during a task requiring active attention, by assessing the ability to cognitively inhibit prepotent responses.
Methods: Fourteen males participated in the study on two separate occasions in a randomized, crossover within-subject design: one night of TSD versus normal sleep (8.5 hours). Following each nighttime intervention, hunger ratings and morning fasting plasma glucose concentrations were assessed before performing a go/no-go task.
Results: Following TSD, participants made significantly more commission errors when they were presented “no-go” food words in the go/no-go task, as compared with their performance following sleep (+56%; P<0.05). In contrast, response time and omission errors to “go” non-food words did not differ between the conditions. Self-reported hunger after TSD was increased without changes in fasting plasma glucose (fPG). The increase in hunger did not correlate with the TSD-induced commission errors.
Conclusions: Our results suggest that TSD impairs cognitive control also in response to food stimuli in healthy young men. Whether such loss of inhibition or impulsiveness is food cue-specific as seen in obesity – thus providing a mechanism through which sleep disturbances may promote obesity development – warrants further investigation.
... Epidemiological observations indicate that short sleep is associated with an increased
risk to develop obesity and type 2 diabetes.1, 2 Respective experimental studies have provided evidence
that acute sleep loss increases food intake3, 4 and impairs glucose tolerance and insulin
sensitivity.5 The intestinal hormone
glucagon-like peptide 1 (GLP-1) acts as an incretin, that is secreted after oral nutrient
intake and enhances insulin release,6 and
moreover reduces food intake in humans.7
Therefore, some of the detrimental metabolic sequelae of sleep curtailment might involve
an effect on GLP-1 signaling. ...
... Considering that GLP-1 infusion increases postprandial satiety in normal
weight7 as well as obese humans,14 a delay in the postprandial GLP-1 response might affect
food intake regulation and in particular impact inter-meal snacking that has been shown to
be augmented after sleep loss.4, 15 Accordingly, our group has demonstrated that TSD enhances the
brain's response to high-calorie food stimuli presented after a caloric
preload.16 ...
Objective: Previous experiments have demonstrated that acute sleep loss impairs glucose homeostasis and increases food intake in humans. The incretin hormone glucagon-like peptide 1 (GLP-1) enhances postprandial insulin secretion and promotes satiety. Hypothesizing that the detrimental metabolic effects of sleep curtailment imply alterations in GLP-1 signaling, we investigated 24-h serum total GLP-1 concentrations during total sleep deprivation and a normal sleep/wake cycle (comprising ~8 hours of sleep) in 12 healthy young men.
Methods: Sessions started at 1800 h, and subjects were provided with standardized meals. Assessments of serum GLP-1 took place in 1.5- to 3-h intervals, focusing on the response to breakfast intake (3.8 MJ).
Results: Across conditions, 24-h concentration profiles of GLP-1 were characterized by the expected postprandial increases (P<0.001). While there were no differences in magnitude between conditions (P>0.11), the postprandial GLP-1 peak response to breakfast intake was delayed by approximately 90 min following sleep loss in comparison to regular sleep (P<0.02).
Conclusions: Results indicate that acute total sleep deprivation exerts a mild, but discernible effect on the postprandial dynamics of circulating GLP-1 concentrations in healthy men.
... Several mechanisms could explain the association between altered sleep patterns and changes in food intake. Shorter sleep duration may provide more opportunities for individuals to consume food, change the timing of food consumption, and induce hedonic eating (16)(17)(18)(19)(20) . Additionally, sleep deprivation may be linked to increased concentrations of the hunger-stimulating hormone ghrelin and decreased levels of the appetite-suppressing hormone leptin (21)(22) . ...
To analyse the association between sleep duration and quality with food intake, chrononutrition patterns, and weight gain during pregnancy. A prospective cohort study was conducted with 100 pregnant women. Data collection occurred once during each gestational trimester. The assessment of sleep quality and duration was performed using the Pittsburgh Sleep Quality Index. Food intake was assessed using three 24-hour recalls in each trimester. Body weight was measured during the three trimesters, and height was measured only once to calculate the Body Mass Index (BMI). Linear regression analyses were performed to associate sleep duration and quality with food consumption and weight gain variables. Longer sleep duration was associated with a later dinner in the first trimester (β=0.228,p=0.025) and earlier in the third trimester (β=-0.223,p=0.026), in addition to a later morning snack in the second trimester (β=0.315,p=0.026). Worse sleep quality was associated with higher total energy intake (β=0.243,p=0.044), total fat (β=0.291,p=0.015), and with the chrononutrition variables such as a higher number of meals (β=0.252,p=0.037), higher caloric midpoint (β=0.243,p=0.044), and shorter fasting time (β=-0.255,p=0.034) in the third trimester. Sleep quality was also associated with a higher BMI in the first trimester of pregnancy (β=0.420,p=<0.001). Most of the associations found in the present study show that poor sleep is associated with higher calorie and fat intake and higher BMI. Longer sleep duration was associated with a later dinner in early pregnancy and an earlier dinner in late pregnancy, as well as with a later morning snack in the second trimester of pregnancy.
... For example, experiments using an ad libitum feeding paradigm have demonstrated that sleep curtailment increases energy intake, even when appetite-stimulating hormones are not elevated [18,19], suggesting that the relationship between insufficient sleep and excess energy intake is driven more by hedonic rather than homeostatic factors [15]. Further, when a meal is provided to minimize caloric deficit after sleep curtailment, individuals maintain an increased desire for excess intake from snacks [20], suggesting that changes in food reward processing after curtailment are not driven exclusively by hunger. Because hedonic evaluation of foods and beverages is based on sensory input from gustatory, olfactory, and somatosensory systems [21], altered sensory perception after short sleep may contribute to changes in food choice. ...
Short sleep duration increases preferences for high-carbohydrate and high-fat foods. It is unclear if insufficient sleep-induced changes in food preference are mediated by changes in taste perception and if these changes are related to sweetener type (sucrose or sucralose) or sweet liking phenotype. The primary objective of this study was to determine if sleep curtailment results in changes in sweet taste perception after sleep curtailment. Forty participants used a single-channel electroencephalograph to record both a habitual and curtailed night (33% reduction) of sleep at home. The following morning, multiple dimensions of sweet taste perception were measured, including preferred sweetener concentrations, patterns of sweet liking, and intensity perception over a range of concentrations. After curtailment, a significant increase in preferred concentration for both sucrose and sucralose (p < 0.001 for both) was observed. The slope of sucrose sweet liking increased after curtailment (p = 0.001). The slope of sucralose liking also increased, but this was not significant (p = 0.129). Intensity perception of the sweeteners was not altered by curtailment. Hierarchical cluster analysis was used to classify participants by sweet liking phenotype. Phenotypes were found to predict preferred sweetener concentration. These findings illustrate a possible need to control for sleep in food sensory studies and suggest a potential mechanism by which insufficient sleep can lead to excess energy intake.
... Furthermore, sleep restriction reduced leptin by 18% and increased ghrelin by 28% in 12 healthy men [67]. Other laboratory studies indicated an increase of ghrelin after sleep restriction [161][162][163][164]. However, the effects of sleep restriction on ghrelin and leptin are contradictory [164][165][166][167][168][169] with a suggestion of sex differences [170]. ...
A substantial burden of disease and mortality globally is attributable to both sleep disruption and low intakes of fruit and vegetable (FV) and there is increasing mechanistic and epidemiological evidence to support a reciprocal relationship between the two. This review provides an overview of experimental and observational studies assessing the relations between sleep and FV consumption from 52 human adult studies. Experimental studies are currently limited and show inconsistent results. Observational studies support a non-linear association with adults sleeping the recommended 7–9 hours/day having the highest intakes of FV. The potential mechanisms linking sleep and FV consumption are highlighted. Disrupted sleep influences FV consumption through homeostatic and non-homeostatic mechanisms. Conversely, FV consumption may influence sleep through polyphenol content via several potential pathways. Few human experimental studies have examined the effects of FV items and their polyphenols on sleep and there is a need for more studies to address this. An appreciation of the relationship between sleep and FV consumption may help optimize sleep and FV consumption and may reduce the burden of chronic diseases. This review provides implications for public health and directions for future work.
... From another point of view, short sleep causes metabolic change, which increases ghrelin and decreased leptin secretion [8]. Experimental studies corroborate that metabolic change caused by sleep deprivation results in several hedonic food choices [28], which may also explain the increased high GI food, such as sugar beverage. In our study, we also affirmed an association between increased SBI and SSD/MSD. ...
Background
The relationship between sleep duration and food intake is unclear. This study aims to examine the relationship among children aged 6–17 years in China.
Methods
The sample consisted of 70,519 children aged 6–17 years, which were randomly selected from 7 representative areas from China, from September to November, 2013. In the structured questionnaire, children reported daily sleep hours (less than 7 h, 7–9 h and more than 9 h), weekly food intake amount (including vegetables, fruit, sugar beverages and meat), physical activity and sedentary time. The relationship of sleep duration with vegetable, sugar beverage, fruit and meat intake was evaluated by multi-nominal logistic regression and multi-variable adjusted.
Results
A total of 62,517 children (51.6% boys) completed the study. Short sleep duration (SSD, < 7 h) was independently associated with increased sugar beverage intake (SBI, Odd Ratio, OR: 1.29, 95% CI: 1.19–1.40) but decreased vegetable (VI, OR: 0.94, 95% CI: 0.90–0.98) & fruit intake (FI, OR: 0.94, 95% CI: 0.88–0.99). Stratified by age and gender, SSD increased SBI for boys of both young (6–12 years) & older (13–17 years) groups and older girls (ORs: 1.25, 1.25, 1.49, 95% CI: 1.08–1.44, 1.04–1.50, 1.22–1.81, respectively), but decreased VI and FI for older girls (ORs: 0.84& 0.81, 95% CI: 0.74–0.96& 0.68–0.96, respectively).
Conclusions
Among school-aged children in China, short sleep duration was associated with increased risks of more sugar beverage intake among those younger and boys but less vegetable & fruit intake among those older and girls. Longitudinal research is needed to clarify the causation in between.
... Thus, we cannot rule out inverse causation regarding the association between low milk and dairy product consumption and better sleep initiation. For example, previous studies have shown alterations in food intake after sleep loss, indicating higher total energy and fat intake [26] and increased portion size [27]. ...
To date, little is known about how dietary patterns may link to measures of sleep quality in older subjects, who often suffer from sleep problems. Here, we investigated, in an older male population from Sweden (n = 970; aged 71 ± 1 year), whether adherence to the Healthy Diet Indicator (HDI; based on recommendations from the World Health Organization) or the Mediterranean Diet (MD) is linked to sleep disturbances. The diet scores were calculated using a seven-day food diary, and self-reported sleep initiation or maintenance problems were assessed by questionnaires. When adjusted for potential confounders, no associations between dietary scores and sleep parameters were found. In contrast, low consumption of milk and dairy products —one of the dietary features of the MD —was associated with better subjective sleep initiation. This association was, however, not found in men with adequate reports of daily energy intake (~54% of the cohort). To summarize, our findings do not suggest that older men can mitigate perceived difficulties to fall and stay asleep by adhering to either the HDI or MD. Whether low consumption of milk and dairy products can facilitate sleep initiation must be confirmed in future studies by utilizing objective measures of sleep such as polysomnography. Finally, when investigating associations between dietary patterns and sleep, particular attention should be paid to the potential confounder of inadequate reporting of energy intake.
... Beyond dietary intake itself, sleep might also alter eating behaviors possibly leading to concurrent changes in dietary intake and the risk of chronic disease. It has been reported that sleep deprivation or short sleep duration (<6 h) increases portion size, the likelihood of main meal skipping, and was associated with greater energy intake from snacks and longer eating periods [11][12][13][14]. ...
Evidence on the association between sleep, diet, and eating behaviors in pregnant women is lacking. We examine this in a cohort of apparently healthy pregnant women. At 26–28 weeks gestation, 497 participants completed the Pittsburgh Sleep Quality Index to assess sleep and a 24-h recall to assess dietary intake. Diet quality was assessed by the Healthy Eating Index for pregnant women in Singapore (HEI-SGP) score and previously derived dietary patterns (vegetables-fruit-rice, seafood-noodles, and pasta-cheese-meat pattern). Eating behaviors studied included the longest night-time fasting interval, frequency of consumption occasions, energy from discretionary foods, and nighttime eating. Adjusted means were estimated between poor/good quality and short/normal sleepers using linear regressions, including covariates. Good sleep quality versus poor sleep quality, was associated with better diet quality (mean HEI-SGP 54.6 vs. 52.0; p = 0.032), greater adherence to the vegetables-fruit-rice pattern (mean 0.03 vs. −0.15; p = 0.039), lesser adherence to the seafood-noodle pattern (mean −0.14 vs. 0.03; p = 0.024), and a trending lower calories from discretionary foods (mean 330.5 vs. 382.6 kcal; p = 0.073), after adjusting for covariates. After additional adjustment for anxiety, only sleep quality and the seafood-noodle pattern remained significantly associated (p = 0.018). Short sleep was not associated with any diet or eating behavior. In conclusion, good sleep quality is associated with a better diet quality and a greater adherence to the vegetable-fruit-rice pattern, but with lesser adherence to the seafood-noodle diets in pregnant women.
... Furthermore, administration of 2AG into the shell of the nucleus accumbens, an extra-hypothalamic area strongly linked to eating motivation increases food intake (Kirkham et al., 2002 ). With these findings in mind, it could therefore be hypothesized that the rise in plasma 2AG (and the sum with its isomer 1AG) may offer a possible molecular mechanism for findings of previous studies, which have demonstrated that sleep restriction increases craving and intake of food during morning hours (Benedict et al., 2012; Cedernaes et al., 2014; Chapman et al., 2013; Hogenkamp et al., 2013; St-Onge et al., 2011 ), and possibly also a reason for the previously observed elevated risk of long term weight gain and obesity in those who chronically suffer from insufficient sleep (Cappuccio et al., 2008). However, three nights of partial sleep loss increased plasma concentrations of 2AG only shortly after awakening in the present study (i.e., 8:30 a.m.), which is therefore not likely to represent the main mechanism that promotes overeating across 24-h in sleep-deprived people (St-Onge et al., 2011) – unless it is able to produce a more long-lasting effect at the behavioral or energy homeostasis level. ...
Following binding to cannabinoid receptors, endocannabinoids regulate a variety of central nervous system processes including appetite and mood. Recent evidence suggests that the systemic release of these lipid metabolites can be altered by acute exercise and that their levels also vary across the 24-hr sleep-wake cycle. The present study utilized a within-subject design (involving 16 normal-weight men) to determine whether daytime circulating endocannabinoid concentrations differ following three nights of partial sleep deprivation (4.25-hr sleep opportunity, 2:45-7am each night) vs. normal sleep (8.5-hr sleep opportunity, 10:30pm-7am each night), before and after an acute bout of ergometer cycling in the morning. In addition, subjective hunger and stress were measured. Pre-exercise plasma concentrations of 2-arachidonoylglycerol (2AG) were 80% higher 1.5 hr after awakening (vs. normal sleep, p<0.05) when participants were sleep-deprived. This coincided with increased hunger ratings (+25% vs. normal sleep, p<0.05). Moreover, plasma 2AG was elevated 15 min post-exercise (+44%, p<0.05). Sleep duration did not however modulate this exercise-induced rise. Finally, subjective stress was generally lower on the day after three nights of short sleep vs. normal sleep, especially after exercise (p<0.05). Given that activation of the endocannabinoid system has been previously shown to acutely increase appetite and mood, our results could suggest that behavioral effects of acute sleep loss, such as increased hunger and transiently improved psychological state, may partially result from activation of this signaling pathway. In contrast, more pronounced exercise-induced elevations of endocannabinoids appear to be less affected by short sleep duration.
... Insulin may also play a role; there is mounting evidence that sleep loss is associated with decreased insulin sensitivity ( Schmid et al., 2011) and intranasal insulin administration decreases food intake in men but not women (Benedict et al., 2008). In addition, St-Onge et al. (2012b) found that experimental sleep restriction with controlled feeding increased the orexigenic hormone ghrelin in men but not women, and noted that this finding was consistent with previous studies showing a significant effect of sleep restriction on ghrelin in men (Spiegel et al., 2004b; Hogenkamp et al., 2013) but not women (Bosy-Westphal et al., 2008). In rats, ghrelin administration increased food intake to a greater degree in males than females (Asarian and Geary, 2013). ...
Habitual short sleep duration is consistently associated with weight gain and increased risk for obesity. The objective of this dissertation was to elucidate how chronic sleep restriction impacts components of energy balance, namely, weight gain, energy intake, and energy expenditure. Healthy adults (21-50 y) participated in controlled isolated laboratory protocols for 14-18 days and were randomized to either an experimental condition (baseline sleep followed by sleep restriction [5 consecutive nights of 4 hours time-in-bed [TIB] per night] and recovery sleep) or control condition (no sleep restriction: 10 hours TIB per night for all nights). Sleep-restricted subjects exhibited significant weight gain, increased caloric intake, greater consumption of fat, delayed meal timing and decreased resting metabolic rate (the largest component of energy expenditure) during sleep restriction but these changes returned to baseline levels after one night of recovery sleep (12 hours TIB). Control subjects did not exhibit a significant change in weight, caloric intake or resting metabolic rate across corresponding protocol days. Notably, there were significant gender and race differences in the energy balance response to sleep restriction. Men gained more weight, increased caloric intake to a greater degree during sleep restriction and consumed a larger percentage of calories during late-night hours than women. Relative to Caucasians, African Americans consumed a comparable amount of calories during baseline and sleep restriction but exhibited marked energy expenditure deficits after baseline sleep, sleep restriction and recovery sleep, and gained more weight during the study. In the largest, most diverse healthy sample of adults studied to date under controlled laboratory conditions, sleep restriction promoted weight gain and positive energy balance. Collectively, these results highlight the importance of obtaining sufficient sleep for regulating energy balance and maintaining a healthy weight, particularly in men and African Americans.
... The books were presented to the participants in a random order. This approach is based on software that has been used widely in the lab of two of the authors (Brunstrom & Rogers, 2009) and elsewhere (Farah, Brunstrom, & Gill, 2012;Ferriday & Brunstrom, 2008;Hogenkamp et al., 2013). ...
Objective:
This study investigated whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner.
Methods:
A total of 44 participants (mean age 24.9 years; 20 women; 19 with obesity) participated in a crossover design, including one night of sleep deprivation and one night of sleep in the laboratory. After each night, fasting blood was collected.
Results:
After sleep deprivation, fasting levels of leptin were lower (mean [SE], vs. sleep: 17.3 [2.6] vs. 18.6 [2.8] ng/mL), whereas those of ghrelin and adiponectin were higher (839.4 [77.5] vs. 741.4 [63.2] pg/mL and 7.5 [0.6] vs. 6.8 [0.6] μg/mL, respectively; all p < 0.05). The changes in leptin and adiponectin following sleep loss were more pronounced among women. Furthermore, the ghrelin increase was stronger among those with obesity after sleep loss. Finally, the sleep loss-induced increase in adiponectin was more marked among normal-weight participants.
Conclusions:
Acute sleep deprivation reduces blood concentrations of the satiety hormone leptin. With increased blood concentrations of ghrelin and adiponectin, such endocrine changes may facilitate weight gain if persisting over extended periods of sleep loss. The observed sex- and weight-specific differences in leptin, ghrelin, and adiponectin call for further investigation.
Background
Inconsistent sleep patterns may promote excess weight gain by increasing food cravings and loss-of-control (LOC)-eating; however, these relationships have not been elucidated in youth.
Objective
We tested whether sleep duration and timing were associated with food cravings and LOC-eating.
Method
For 14 days, youths wore actigraphy monitors to assess sleep and reported severity of food cravings and LOC-eating using ecological momentary assessment. Generalized linear mixed models tested the associations between weekly and nightly shifts in facets of sleep (i.e., duration, onset, midpoint, and waketime) and next-day food cravings and LOC-eating. Models were re-run adjusting for relevant covariates (e.g., age, sex, adiposity).
Results
Among 48 youths (12.88 ± 2.69 years, 68.8% female, 33.3% with overweight/obesity), neither weekly nor nightly facets of sleep were significantly associated with food cravings (ps = 0.08–0.93). Youths with shorter weekly sleep duration (est. ß = −0.31, p = 0.004), earlier weekly midpoints (est. ß = −0.47, p = 0.010) and later weekly waketimes (est. ß = 0.49, p = 0.010) reported greater LOC-eating severity; findings persisted in adjusted models.
Conclusions
In youth, weekly, but not nightly, shifts in multiple facets of sleep were associated with LOC-eating severity; associations were not significant for food cravings. Sleep should be assessed as a potentially modifiable target in paediatric LOC-eating and obesity prevention programs.
Introduction
To examine the association of sleep duration, insomnia, and obstructive sleep apnea (OSA) with hemoglobin A1c (HbA1c) in a cohort of patients with type 2 diabetes (T2D) on glucose-lowering medications.
Research design and methods
13 346 patients with T2D were included in the present analysis (mean age: 60.2 years; 56.6% were on antidiabetic drug monotherapy; 43.4% received at least two glucose-lowering medications). Sleep duration (short: ≤6 hours/day; normal: 7–8 hours/day; long: ≥9 hours/day) and frequency of insomnia symptoms were self-reported. The risk of OSA was considered high if at least two of the following conditions were fulfilled: regular snoring, frequent daytime sleepiness, and either obesity (≥30 kg/m ² ) or hypertension (systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg). Associations between sleep variables and HbA1c were investigated by analysis of covariance or linear regression (adjusted for, eg, participants’ age, sex, ethnic background, and systolic blood pressure).
Results
Long sleep duration and a high risk for OSA were independently associated with higher HbA1c values (long vs normal sleep duration: +0.10% (95% CI 0.03 to 0.18); high vs low risk for OSA: +0.07% (95% CI 0.02 to 0.11), both p=0.004). No robust association was found of short sleep duration and frequent insomnia symptoms with HbA1c. Finally, a positive dose–response association between the number of sleep problems per subject (range: 0–3) and HbA1c was observed (β=0.04% (0.02 to 0.06), p=0.002). However, all significant associations were small.
Conclusion
Screening for and treatment of sleep problems may help lower HbA1c levels in patients with T2D on glucose-lowering medications.
In the current study, a systematic review and meta‐analysis were conducted to summarize and assess whether short sleep duration is associated with appetite‐regulating hormones and adipokine levels. Reference databases were searched for studies related to sleep and appetite‐regulating hormones and adipokines. Qualitative and quantitative syntheses were conducted to evaluate the relationship between sleep duration and the level of appetite‐regulating hormones and adipokines, including leptin, ghrelin, adiponectin, resistin, and orexin. Twenty‐one of 3536 studies, covering a total of 2250 participants, met the inclusion criteria. Leptin, ghrelin, and adiponectin were included in the meta‐analysis. Ghrelin levels were higher in the short sleep group (standard mean difference [SMD] = 0.14, 95% CI [0.03, 0.25], p = 0.01). Significant differences between the short sleep group and recommended sleep group were also noted in leptin level experimental subgroup studies (SMD = 0.19, 95% CI [0.03, 0.35], p = 0.02) and ghrelin level cross‐sectional subgroup studies (SMD = 0.14, 95% CI [0.02, 0.27], p = 0.03). A rise in leptin and ghrelin levels were also observed in sleep deprivation groups (SMD = 0.24, 95% CI [0.10, 0.39], p = 0.001 and SMD = 0.18, 95% CI [0.04, 0.33], p = 0.01, respectively). In conclusion, short sleep duration is associated with an increased ghrelin level, while sleep deprivation had a significant effect on the levels of both leptin and ghrelin.
Background
In adults, poor sleep quality is associated with increased obesogenic eating behaviors; less is known about this relationship in youth. The objectives of this study were to assess the strength of association between fatigue‐related quality of life (QoL) and eating behaviors among youth and to describe the associations in participants with percent body fat (%BF) above and below the 90th percentile for sex and age.
Methods
Caregiver‐reported measures of fatigue (Pediatric QoL Multidimensional Fatigue Scale) and eating behaviors (Child Eating Behavior Questionnaire) were obtained on participants, aged 8‐17 years. %BF was measured by iDXA and grouped by sex‐and age‐percentiles. Multiple linear regression adjusting for age, sex, and race/ethnicity was used.
Results
Of the 352 participants (49% male), 44.6% had %BF >90th percentile. General, Sleep/Rest, and Cognitive Fatigue QoL was inversely associated with Food Approach Behaviors: Food Responsiveness, Enjoyment of Food, Emotional Overeating, and Desire to Drink. For participants with %BF >90th percentile, higher General Fatigue QoL was associated with higher Satiety Responsiveness (0.13; 95% CI (0.03, 0.24)). For participants with %BF <90th percentile, higher General Fatigue QoL was associated with less Satiety Responsiveness (‐0.16; 95% CI (‐0.31, ‐0.01).
Conclusion
Less fatigue symptoms were associated with less behaviors associated with food approach among pediatric participants. For participants with %BF >90th percentile, less symptoms of general fatigues corresponded with more satiety. Though causation has yet to be established, youth with elevated %BF should be screened for fatigue symptoms and offered counseling on sleep hygiene or a sleep medicine referral to help mitigate weight gain.
Background
Self‐reported short sleep duration is associated with greater risk for metabolic syndrome (MetS), obesity, and higher energy intake (EI). However, studies of these associations in children using objective methods are sparse.
Objectives
The study aims to determine the associations for sleep patterns with MetS indices, body composition, and EI using objective measures in children.
Methods
Free‐living sleep and physical activity were measured in 125 children (aged 8‐17 years, BMI z = 0.57 ± 1.0, 55% female) using wrist‐worn actigraphs for 14 nights. Blood pressure, fasting blood levels of lipids, insulin, glucose, waist circumference, and body composition (dual‐energy X‐ray absorptiometry [DXA]) were obtained during outpatient visits. EI was assessed during an ad libitum buffet meal.
Results
Later weekday and weekend bedtimes were associated with higher systolic blood pressure (Ps < 0.05). Sleep duration and bedtime were not significantly associated with other components of MetS, body composition, or EI. Short sleepers (duration less than 7 hours) consumed a greater percentage of carbohydrates than those with adequate (greater than or equal to 7 hours) sleep (P < 0.05).
Conclusion
Indicators of sleep duration were variably associated with children's eating patterns and risk for chronic disease. Prospective data are needed to determine whether these indicators of sleep quality represent unique or shared risk factors for poor health outcomes.
Overweight and obesity are highly prevalent throughout the world and can adversely affect the nutritional status of individuals. Studies have shown that many people with obesity have inadequate intake of iron, calcium, magnesium, zinc, copper, folate and vitamins A and B12, likely as a result of poor diet quality. Nutritional inadequacies or deficiencies may also occur due to altered pharmacokinetics in the individual with obesity and due to interactions in those with overweight or obesity with various pharmaceuticals. However, it has been demonstrated that the adult population in the United States as a whole is deficient in certain micronutrients as a result of the availability and overconsumption of high-calorie, low-nutrient processed foods. Poor nutrition may contribute to the development of certain chronic conditions, such as type 2 diabetes, which is already more prevalent in those with obesity. Clinicians need to be aware of these gaps, particularly in those individuals with obesity who are undergoing bariatric surgery or taking pharmaceutical products long term to facilitate weight loss. Patients with overweight or obesity likely struggle to achieve a balanced diet and may benefit from consultation with a dietitian. Along with providing recommendations for healthy eating and exercise, supplementation with specific micronutrients or multivitamins should be considered for individuals at the highest risk for or with established deficiencies. Further research is needed to understand the factors underlying nutritional inadequacies in individuals with overweight or obesity, as well as the outcomes of treatment strategies employed to address them.
Objectives
The metabolic burden of inadequate sleep has not been determined in healthy individuals outside laboratories. This study aims to investigate the impact of sleep duration on five metabolic syndrome components in a healthy adult cohort.
Methods
162,121 adults aged 20–80 (men 47.4%) of the MJ Health Database, who were not obese and free from major diseases, were recruited and followed up from 1996 to 2014. Sleep duration and insomnia symptoms were assessed by a self-administered questionnaire. Incident cases of five metabolic syndrome components were identified by follow-up medical examinations. Cox proportional hazard ratios (HRs) were calculated for three sleep duration categories “< 6 hours/day (short),” “6–8 hours/day (regular),” and “> 8 hours/day (long)” with adjustment for potential confounding factors. Analyses were stratified by insomnia symptoms to assess whether insomnia symptoms modified the association between sleep duration and metabolic syndrome.
Results
Compared to regular sleep duration, short sleep significantly (P < 0.001) increased the risk for central obesity by 12% (adjusted HR 1.12 [1.07–1.17]), for elevated fasting glucose by 6% (adjusted HR 1.06 [1.03–1.09]), for high blood pressure by 8% (adjusted HR 1.08 [1.04–1.13]), for low HDL-C by 7% (adjusted HR 1.07 [1.03–1.11]), for hypertriglyceridaemia by 9% (adjusted HR 1.09 [1.05–1.13]), and for metabolic syndrome by 9% (adjusted HR 1.09 [1.05–1.13]). Long sleep decreased the risk of hypertriglyceridaemia (adjusted HR 0.89 [0.84–0.94]) and metabolic syndrome (adjusted HR 0.93 [0.88–0.99]). Insomnia symptoms did not modify the effects of sleep duration.
Conclusions
Sleep duration may be a significant determinant of metabolic health.
Short sleep duration has been associated with obesity in numerous epidemiological studies. However, such association studies cannot establish evidence of causality. Clinical intervention studies, on the other hand, can provide information on a causal effect of sleep duration on markers of weight gain: energy intake and energy expenditure. Herein is an overview of the science related to the impact of sleep restriction, in the context of clinical intervention studies, on energy intake, energy expenditure and body weight. Additionally, studies that evaluate the impact of sleep restriction on weight loss and the impact of sleep extension on appetite are discussed. Information to date suggests that weight management is hindered when attempted in the context of sleep restriction, and the public should be made aware of the negative consequences of sleep restriction for weight regulation.
Study objectives:
To determine the relationship between an ecologically-relevant change in sleep behavior and its subsequent effects on daytime alertness and feeding behavior.
Methods:
Fifty healthy, young participants (10 male, 40 female) completed two 3-hour study sessions that were at least five days apart. The first session was a baseline evaluation. On the night prior to Session 2, the amount of time in bed was manipulated to be 60-130% of the individual's habitual sleep time. Within both sessions, subjective (Stanford Sleepiness Scale) and objective (Psychomotor Vigilance Test) alertness were measured. During the middle of each session, a 40-minute ad libitum meal opportunity allowed participants to eat from eight different food items. Food healthfulness, caloric density, distribution and number of calories were measured and compared to alertness levels.
Results:
The induced variation in time in bed resulted in induced variation in both subjective and objective (p<0.05) measures of alertness. Decreased subjective alertness was associated with increased total caloric consumption (p<0.05), and a greater number of calories consumed from less healthy food (p<0.05), as rated by both the investigators and by the participant. Decreased objective alertness was associated with less healthy food choices (p<0.05), and the consumption of more food from the calorically-dense items (p<0.05).
Conclusions:
Ecologically-relevant impairments in subjective and objective alertness are associated with increased caloric intake and dysfunctional eating decisions. People experiencing reduced alertness after modest sleep loss may be more willing to eat food they recognize as less healthful, and appear to prefer more calorically dense foods.
The relation between sleep duration and weight status is well established, and growing evidence suggests this relation is causal. However, the mechanisms underlying the sleep/obesity relation remain controversial. We have previously reviewed the evidence relating sleep restriction to energy balance regulation, uncovering much discrepancy in physiological/hormonal explanations. Herein, we perform an in-depth assessment of the evidence, published since 2012, of the impact of sleep restriction on energy balance regulation. Increased energy intakes as a result of sleep curtailment are consistently observed, but effects on its hormonal regulators are debatable. Future studies should continue to enroll women, perform hormonal measurements under controlled, weight maintenance feeding conditions, and lengthen the intervention period beyond five nights to elucidate the mechanism linking sleep and obesity.
Sleep is increasingly recognized as an important lifestyle contributor to health. However, this has not always been the case, and an increasing number of Americans choose to curtail sleep in favor of other social, leisure, or work-related activities. This has resulted in a decline in average sleep duration over time. Sleep duration, mostly short sleep, and sleep disorders have emerged as being related to adverse cardiometabolic risk, including obesity, hypertension, type 2 diabetes mellitus, and cardiovascular disease. Here, we review the evidence relating sleep duration and sleep disorders to cardiometabolic risk and call for health organizations to include evidence-based sleep recommendations in their guidelines for optimal health.
Obesity is associated with an array of adverse
physiological, psychological, and social consequences.
Tackling obesity remains difficult, given the challenges
of maintaining positive behavior changes. Obesity occurs
from persistent positive energy (excessive energy intake
with insufficient counteractive energy expenditure), but
several biological, psychological, and environmental factors
influence energy balance. It has recently emerged that
sleep duration is an important factor that impinges on energy
balance and could be a potential overlooked behavior
predisposing to obesity. We highlight and review the recent
evidence surrounding sleep in relation to obesity from epidemiological
studies to experimental work.
In unserer modernen 24-Stunden-Gesellschaft zeigt sich ein zunehmender Trend zu verkurztem und unregelmasigem Schlaf. Parallel hierzu nimmt die Pravalenz des metabolischen Syndroms mit seinen Kernkomponenten Adipositas und Typ-2-Diabetes mellitus stetig zu, wie eine Vielzahl epidemiologischer Arbeiten belegen. Experimentelle kurzzeitige Interventionsstudien weisen auf einen kausalen Zusammenhang zwischen Schlafdauer und -qualitat und Energiemetabolismus hin und haben zugrundeliegende Mechanismen identifiziert. Insbesondere Veranderungen in der neuroendokrinen Regulation des Glukosestoffwechsels, der zirkadianen Rhythmik sowie von Appetit und Essverhalten scheinen die negativen Auswirkungen von unzureichendem Schlaf auf den Energiehaushalt zu vermitteln. Auch wenn langfristige Interventionsstudien bislang fehlen, kann davon ausgegangen werden, dass eine Verbesserung der Schlafhygiene einen attraktiven Ansatz in der Pravention und Therapie metabolischer Erkrankungen darstellt.
Although insufficient sleep is a well-recognized risk factor for overeating and weight gain, the neural mechanisms underlying increased caloric (particularly fat) intake after sleep deprivation remain unclear. Here we used resting-state functional magnetic resonance imaging and examined brain connectivity changes associated with macronutrient intake after one night of total sleep deprivation (TSD). Compared to the day following baseline sleep, healthy adults consumed a greater percentage of calories from fat and a lower percentage of calories from carbohydrates during the day following TSD. Subjects also exhibited increased brain connectivity in the salience network from the dorsal anterior cingulate cortex (dACC) to bilateral putamen and bilateral anterior insula (aINS) after TSD. Moreover, dACC-putamen and dACC-aINS connectivity correlated with increased fat and decreased carbohydrate intake during the day following TSD, but not during the day following baseline sleep. These findings provide a potential neural mechanism by which sleep loss leads to increased fat intake.
Objectives:
To examine the association between short sleep duration and obesity among adolescents (mean age 16 years) transitioning into young adulthood (mean age 21 years) in the National Longitudinal Study of Adolescent Health (N = 10,076).
Study design:
Self-reported sleep duration was categorized as <6, 6-8, or >8 hours. Obesity status, using measured height and weight, was defined as body mass index ≥95th percentile in adolescence and body mass index ≥30 kg/m(2) in young adulthood.
Results:
Cross-sectionally, short sleep duration was associated with obesity in adolescent males (prevalence ratio 1.8 [95% CI, 1.3-2.4]) but not in females (prevalence ratio 1.0 [95% CI, 0.7-1.4]). In longitudinal analyses, short sleep duration in adolescence was associated with incident obesity in both males and females (risk ratio 1.2 [95% CI, 1.0-1.6]) in young adulthood. No interactions by sex were noted.
Conclusions:
Analyzing the association of sleep duration and obesity longitudinally resolved sex discrepancies observed in earlier cross-sectional analyses. Optimizing sleep duration during adolescence may be an effective intervention to prevent excess weight gain in young adults.
Short sleep duration has been shown to be associated with elevated body mass index (BMI) in many epidemiological studies. Several pathways could link sleep deprivation to weight gain and obesity, including increased food intake, decreased energy expenditure, and changes in levels of appetite-regulating hormones, such as leptin and ghrelin. A relatively new factor that is contributing to sleep deprivation is the use of multimedia (e.g. television viewing, computer, and internet), which may aggravate sedentary behavior and increase caloric intake. In addition, shift-work, long working hours, and increased time commuting to and from work have also been hypothesized to favor weight gain and obesity-related metabolic disorders, because of their strong link to shorter sleep times. This article reviews the epidemiological, biological, and behavioral evidence linking sleep debt and obesity.
In parallel with the increasing prevalence of obesity and type 2 diabetes, sleep loss has become common in modern societies. An increasing number of epidemiological studies show an association between short sleep duration, sleep disturbances, and circadian desynchronisation of sleep with adverse metabolic traits, in particular obesity and type 2 diabetes. Furthermore, experimental studies point to distinct mechanisms by which insufficient sleep adversely affects metabolic health. Changes in the activity of neuroendocrine systems seem to be major mediators of the detrimental metabolic effects of insufficient sleep, through favouring neurobehavioural outcomes such as increased appetite, enhanced sensitivity to food stimuli, and, ultimately, a surplus in energy intake. The effect of curtailed sleep on physical activity and energy expenditure is less clear, but changes are unlikely to outweigh increases in food intake. Although long-term interventional studies proving a cause and effect association are still scarce, sleep loss seems to be an appealing target for the prevention, and probably treatment, of metabolic disease.
Short sleep duration among children and adolescents has been reported to be associated with elevated BMI and other adverse health outcomes. Food choices are one proposed mechanism through which this association may occur. In the present study, we examined whether self-reported habitual sleep duration is associated with vegetable and fruit consumption and fast food consumption. Using cross-sectional data from the National Longitudinal Study of Adolescent Health (n 13 284), we estimated three nested logistic regression models for two outcome variables: daily vegetable and fruit consumption and previous week's fast food consumption. The adjusted models included demographic and social/behavioural covariates. Self-reported habitual short sleep duration ( < 7 h/night) was associated with reduced odds of vegetable and fruit consumption compared with the recommended sleep duration (>8 h/night) (OR 0·66, P <0·001), even after adjusting for demographic and social/behavioural factors (OR 0·75, P <0·001). Short sleep duration was also associated with increased odds of fast food consumption (OR 1·40, P <0·001) even after adjustment (OR 1·20, P <0·05). Food choices are significantly associated with sleep duration and may play an important role in the mediation of the association between sleep and health among adolescents.
Background/Objectives
The extent to which alterations in energy expenditure (EE) in response to sleep restriction contribute to the short sleep-obesity relationship is not clearly defined. Short sleep may induce changes in resting metabolic rate (RMR), thermic effect of food (TEF), and postprandial substrate oxidation.
Subjects/Methods
Ten females (age and BMI: 22-43 y and 23.4-28 kg/m2) completed a randomized, crossover study assessing the effects of short (4 h/night) and habitual (8 h/night) sleep duration on fasting and postprandial RMR and respiratory quotient (RQ). Measurements were taken after 3 nights using whole-room indirect calorimetry. The TEF was assessed over a 6-h period following consumption of a high-fat liquid meal.
Results
Short vs. habitual sleep did not affect RMR (1.01 ± 0.05 and 0.97 ± 0.04 kcal/min; p=0.23). Fasting RQ was significantly lower after short vs. habitual sleep (0.84 ± 0.01 and 0.88 ± 0.01; p=0.028). Postprandial EE (short: 1.13 ± 0.04 and habitual: 1.10 ± 0.04, p=0.09) and RQ (short: 0.88 ± 0.01 and habitual: 0.88 ± 0.01, p=0.50) after the high-fat meal were not different between conditions. TEF was similar between conditions (0.24 ± 0.02 kcal/min in both; p=0.98), as was the ~6-h incremental area under the curve (1.16 ± 0.10 and 1.17 ± 0.09 kcal/min x 356 min after short and habitual sleep, respectively; p=0.92).
Conclusions
Current findings observed in non-obese healthy premenopausal women do not support the hypothesis that alterations in TEF and postprandial substrate oxidation are major contributors to the higher rate of obesity observed in short sleepers. In exploring a role of sleep duration on EE, research should focus on potential alterations in physical activity to explain the increased obesity risk in short sleepers.
There is increasing evidence showing that sleep has an influence on eating behaviors. Short sleep duration, poor sleep quality, and later bedtimes are all associated with increased food intake, poor diet quality, and excess body weight. Insufficient sleep seems to facilitate the ingestion of calories when exposed to the modern obesogenic environment of readily accessible food. Lack of sleep has been shown to increase snacking, the number of meals consumed per day, and the preference for energy-rich foods. Proposed mechanisms by which insufficient sleep may increase caloric consumption include: (1) more time and opportunities for eating, (2) psychological distress, (3) greater sensitivity to food reward, (4) disinhibited eating, (5) more energy needed to sustain extended wakefulness, and (6) changes in appetite hormones. Globally, excess energy intake associated with not getting adequate sleep seems to be preferentially driven by hedonic rather than homeostatic factors. Moreover, the consumption of certain types of foods which impact the availability of tryptophan as well as the synthesis of serotonin and melatonin may aid in promoting sleep. In summary, multiple connections exist between sleep patterns, eating behavior and energy balance. Sleep should not be overlooked in obesity research and should be included as part of the lifestyle package that traditionally has focused on diet and physical activity.
Background:
Lack of sleep and increased consumption of energy-dense foods and sugar-sweetened beverages (SSBs) have all been suggested as factors contributing to the increased prevalence of overweight and obesity.
Objective:
To evaluate whether objectively measured sleep duration (average and day-to-day variability) as well as parent-reported sleep problems are independently associated with proposed dietary risk factors for overweight and obesity in 8-11-year-old children.
Design:
In this cross-sectional study, data on sleep duration and day-to-day variability in sleep duration were measured in 676 Danish, apparently healthy children by an objective measure (actigraphy) for 8 nights, and the Children's Sleep Habits Questionnaire (CSHQ) was filled out by the parents. Diet was recorded using a web-based food record for 7 consecutive days. Fasting blood samples were obtained for measurements of plasma leptin and ghrelin levels.
Results:
Sleep duration (h per night) was negatively associated with energy density (ED) of the diet (β = -0.32 kJ g(-1)), added sugar (β = -1.50 E%) and SSBs (β = -1.07 E%) (all P ≤ 0.003). Furthermore, variability in sleep duration (10-min per night) was positively associated with SSBs (β = 0.20 E%, P = 0.03), independent of sleep duration, and CSHQ score was positively associated with ED (β = 0.16 kJ g(-1), P = 0.04). All of these associations were independent of potential confounders (age, sex, pubertal status, height, weight, screen time, moderate-to-vigorous physical activity and parental education and ethnicity).
Conclusion:
Our study suggests that short sleep duration, high sleep duration variability and experiencing sleep problems are all associated with a poor, obesity-promoting diet in children.
Objective:
To investigate if acute sleep deprivation affects food purchasing choices in a mock supermarket.
Design and methods:
On the morning after one night of total sleep deprivation (TSD) or after one night of sleep, 14 normal-weight men were given a fixed budget (300 SEK-approximately 50 USD). They were instructed to purchase as much as they could out of a possible 40 items, including 20 high-caloric foods (>2 kcal/g) and 20 low-caloric foods (<2 kcal/g). The prices of the high-caloric foods were then varied (75%, 100% (reference price), and 125%) to determine if TSD affects the flexibility of food purchasing. Before the task, participants received a standardized breakfast, thereby minimizing the potential confound produced by hunger. In addition, morning plasma concentrations of the orexigenic hormone ghrelin were measured under fasting conditions.
Results:
Independent of both type of food offered and price condition, sleep-deprived men purchased significantly more calories (+9%) and grams (+18%) of food than they did after one night of sleep (both P < 0.05). Morning plasma ghrelin concentrations were also higher after TSD (P < 0.05). However, this increase did not correlate with the effects of TSD on food purchasing.
Conclusions:
This experiment demonstrates that acute sleep loss alters food purchasing behavior in men.
To determine the hormonal effects of reducing sleep duration under controlled feeding conditions.
Randomized, crossover study.
Inpatient.
Twenty-seven normal weight, 30- to 45-yr-old men and women habitually sleeping 7-9 hr/night.
PARTICIPANTS WERE STUDIED UNDER TWO SLEEP CONDITIONS: short (4 hr in bed) or habitual (9 hr in bed) sleep. A controlled diet was provided for each 4-day study period.
Fasting blood samples were obtained daily and frequent blood samples were obtained throughout day 4. The main outcomes measures included glucose, insulin, leptin, ghrelin, adiponectin, total glucagon-like peptide 1 (GLP-1) and peptide YY(3-36) (PYY(3-36)) concentrations. Body weights were reduced by 2.2 ± 0.4 lb and 1.7 ± 0.4 lb during the habitual and short sleep phases, respectively (both P < 0.0001). There was no effect of sleep duration on glucose, insulin, and leptin profiles (all P > 0.05). Ghrelin and GLP-1 responses differed by sex. Short sleep increased fasting (P = 0.054) and morning (08:00-12:00) (P = 0.042) total ghrelin in men but not women. The reverse was observed for GLP-1: afternoon levels (12:30-19:00) were lower (P = 0.016) after short sleep compared with habitual sleep in women but not men.
These data suggest that, in the context of negative energy balance, short sleep does not lead to a state of increased insulin resistance, but may predispose to overeating via separate mechanisms in men and women.
Trial registration on http://www.clinicaltrials.gov. #NCT00935402. CITATION: St-Onge MP; O'Keeffe M; Roberts AL; RoyChoudhury A; Laferrère B. Short sleep duration, glucose dysregulation and hormonal regulation of appetite in men and women. SLEEP 2012;35(11):1503-1510.
Voluntary sleep restriction is a lifestyle feature of modern societies that may contribute to obesity and diabetes. The aim of the study was to investigate the impact of partial sleep deprivation on the regulation of energy balance and insulin sensitivity.
In a controlled intervention, 14 healthy women (age 23-38 years, BMI 20.0-36.6 kg/m(2)) were investigated after 2 nights of >8 h sleep/night (T0), after 4 nights of consecutively increasing sleep curtailment (7 h sleep/night, 6 h sleep/night, 6 h sleep/night and 4 h sleep/night; T1) and after 2 nights of sleep recovery (>8 h sleep/night; T2). Resting and total energy expenditure (REE, TEE), glucose-induced thermogenesis (GIT), physical activity, energy intake, glucose tolerance and endocrine parameters were assessed.
After a decrease in sleep du-ration, energy intake (+20%), body weight (+0.4 kg), leptin/fat mass (+29%), free triiodothyronine (+19%), free thyroxine (+10%) and GIT (+34%) significantly increased (all p < 0.05). Mean REE, physical activity, TEE, oral glucose tolerance, and ghrelin levels remained unchanged at T1. The effect of sleep loss on GIT, fT3 and fT4 levels was inversely related to fat mass.
Short-term sleep deprivation increased energy intake and led to a net weight gain in women. The effect of sleep restriction on energy expenditure needs to be specifically addressed in future studies using reference methods for total energy expenditure.
Obesity is emerging as the most significant health concern of the 21st century. Although this is attributable in part to changes in our environment-including the increased prevalence of energy-dense food-it also appears that several lifestyle factors may increase our vulnerability to this calorie-rich landscape. Epidemiologic studies have begun to show links between adiposity and behaviors such as television watching, alcohol intake, and sleep deprivation. However, these studies leave unclear the direction of this association. In addition, studies that investigated the acute impact of these factors on food intake have reported a wide variety of effect sizes, from highly positive to slightly negative.
The purpose of this article was to provide a meta-analysis of the relation between lifestyle choices and increases in acute food intake.
An initial search was performed on PubMed to collect articles relating television watching, sleep deprivation, and alcohol consumption to food intake. Only articles published before February 2012 were considered. Studies that took place in a controlled, laboratory setting with healthy individuals were included. Studies were analyzed by using 3 meta-analyses with random-effects models. In addition, a 1-factor ANOVA was run to discover any main effect of lifestyle.
The 3 most prominent lifestyle factors-television watching, alcohol intake, and sleep deprivation-had significant short-term effects on food intake, with alcohol being more significant (Cohen's d = 1.03) than sleep deprivation (Cohen's d = 0.49) and television watching (Cohen's d = 0.2).
Our results suggest that television watching, alcohol intake, and sleep deprivation are not merely correlated with obesity but likely contribute to it by encouraging excessive eating. Because these behaviors are all known to affect cognitive functions involved in reward saliency and inhibitory control, it may be that they represent common mechanisms through which this eating is facilitated.
There is growing recognition that a large number of individuals living in Western society are chronically sleep deprived. Sleep deprivation is associated with an increase in food consumption and appetite. However, the brain regions that are most susceptible to sleep deprivation-induced changes when processing food stimuli are unknown.
Our objective was to examine brain activation after sleep and sleep deprivation in response to images of food.
Twelve normal-weight male subjects were examined on two sessions in a counterbalanced fashion: after one night of total sleep deprivation and one night of sleep. On the morning after either total sleep deprivation or sleep, neural activation was measured by functional magnetic resonance imaging in a block design alternating between high- and low-calorie food items. Hunger ratings and morning fasting plasma glucose concentrations were assessed before the scan, as were appetite ratings in response to food images after the scan.
Compared with sleep, total sleep deprivation was associated with an increased activation in the right anterior cingulate cortex in response to food images, independent of calorie content and prescan hunger ratings. Relative to the postsleep condition, in the total sleep deprivation condition, the activation in the anterior cingulate cortex evoked by foods correlated positively with postscan subjective appetite ratings. Self-reported hunger after the nocturnal vigil was enhanced, but importantly, no change in fasting plasma glucose concentration was found.
These results provide evidence that acute sleep loss enhances hedonic stimulus processing in the brain underlying the drive to consume food, independent of plasma glucose levels. These findings highlight a potentially important mechanism contributing to the growing levels of obesity in Western society.
Evidence suggests a relation between short sleep duration and obesity.
We assessed energy balance during periods of short and habitual sleep in normal-weight men and women.
Fifteen men and 15 women aged 30-49 y with a body mass index (in kg/m(2)) of 22-26, who regularly slept 7-9 h/night, were recruited to participate in this crossover inpatient study. All participants were studied under short (4 h/night) and habitual (9 h/night) sleep conditions, in random order, for 5 nights each. Food intake was measured on day 5, and energy expenditure was measured with the doubly labeled water method over each period.
Participants consumed more energy on day 5 during short sleep (2813.6 ± 593.0 kcal) than during habitual sleep (2517.7 ± 593.0 kcal; P = 0.023). This effect was mostly due to increased consumption of fat (20.7 ± 37.4 g; P = 0.01), notably saturated fat (8.7 ± 20.4 g; P = 0.038), during short sleep. Resting metabolic rate (short sleep: 1455.4 ± 129.0 kcal/d; habitual sleep: 1486.5 ± 129.5 kcal/d; P = 0.136) and total energy expenditure (short sleep: 2589.2 ± 526.5 kcal/d; habitual sleep: 2611.1 ± 529.0 kcal/d; P = 0.832) did not differ significantly between sleep phases.
Our data show that a reduction in sleep increases energy and fat intakes, which may explain the associations observed between sleep and obesity. If sustained, as observed, and not compensated by increased energy expenditure, the dietary intakes of individuals undergoing short sleep predispose to obesity. This trial is registered at clinicaltrials.gov as NCT00935402.
Epidemiologic evidence indicates that chronic sleep curtailment increases risk of developing obesity, but the mechanisms behind this relation are largely unknown.
We examined the influence of a single night of total sleep deprivation on morning energy expenditures and food intakes in healthy humans.
According to a balanced crossover design, we examined 14 normal-weight male subjects on 2 occasions during a regular 24-h sleep-wake cycle (including 8 h of nocturnal sleep) and a 24-h period of continuous wakefulness. On the morning after regular sleep and total sleep deprivation, resting and postprandial energy expenditures were assessed by indirect calorimetry, and the free-choice food intake from an opulent buffet was tested in the late afternoon at the end of the experiment. Circulating concentrations of ghrelin, leptin, norepinephrine, cortisol, thyreotropin, glucose, and insulin were repeatedly measured over the entire 24-h session.
In comparison with normal sleep, resting and postprandial energy expenditures assessed on the subsequent morning were significantly reduced after sleep deprivation by ≈5% and 20%, respectively (P < 0.05 and P < 0.0001). Nocturnal wakefulness increased morning plasma ghrelin concentrations (P < 0.02) and nocturnal and daytime circulating concentrations of thyreotropin, cortisol, and norepinephrine (P < 0.05) as well as morning postprandial plasma glucose concentrations (P < 0.05). Changes in food intakes were variable, and no differences between wake and sleep conditions were detected.
Our findings show that one night of sleep deprivation acutely reduces energy expenditure in healthy men, which suggests that sleep contributes to the acute regulation of daytime energy expenditure in humans.
Appetite and meal energy intake (MEI) following aerobic (AEx) and resistance (REx) exercises were evaluated in 19 young, active adults. The participants completed duplicate 35-min sessions of AEx, REx, and sedentary control, and consumed an ad libitum pasta meal 30min postsession. Hunger transiently decreased after AEx but was not influenced by REx. MEI was 14% to 18% higher after AEx and REx than control. These findings are consistent with exercise-stimulated ingestive behavior, not anorexia of exercise.
Sleep loss can modify energy intake and expenditure.
To determine whether sleep restriction attenuates the effect of a reduced-calorie diet on excess adiposity.
Randomized, 2-period, 2-condition crossover study.
University clinical research center and sleep laboratory.
10 overweight nonsmoking adults (3 women and 7 men) with a mean age of 41 years (SD, 5) and a mean body mass index of 27.4 kg/m² (SD, 2.0).
14 days of moderate caloric restriction with 8.5 or 5.5 hours of nighttime sleep opportunity.
The primary measure was loss of fat and fat-free body mass. Secondary measures were changes in substrate utilization, energy expenditure, hunger, and 24-hour metabolic hormone concentrations.
Sleep curtailment decreased the proportion of weight lost as fat by 55% (1.4 vs. 0.6 kg with 8.5 vs. 5.5 hours of sleep opportunity, respectively; P = 0.043) and increased the loss of fat-free body mass by 60% (1.5 vs. 2.4 kg; P = 0.002). This was accompanied by markers of enhanced neuroendocrine adaptation to caloric restriction, increased hunger, and a shift in relative substrate utilization toward oxidation of less fat.
The nature of the study limited its duration and sample size.
The amount of human sleep contributes to the maintenance of fat-free body mass at times of decreased energy intake. Lack of sufficient sleep may compromise the efficacy of typical dietary interventions for weight loss and related metabolic risk reduction.
National Institutes of Health.
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. This trial was registered at clinicaltrials.gov as NCT00986492.
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.
The prevalence of overweight and obesity has increased. A strong environmental factor contributing to the obesity epidemic is food portion size. This review of studies into the effects of portion size on energy intake shows that increased food portion sizes lead to increased energy intake levels. Important mechanisms explaining why larger portions are attractive and lead to higher intake levels are value for money and portion distortion. This review also shows that few intervention studies aiming to reverse the negative influence of portion size have been conducted thus far, and the ones that have been conducted show mixed effects. More intervention studies targeted at portion size are urgently needed. Opportunities for further interventions are identified and a framework for portion size interventions is proposed. Opportunities for intervention include those targeted at the individual as well as those targeted at the physical, economic, political and socio-cultural environment.
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.
Large portions of food may contribute to excess energy intake and greater obesity. However, data on the effects of portion size on food intake in adults are limited.
We examined the effect of portion size on intake during a single meal. We also investigated whether the response to portion size depended on which person, the subject or the experimenter, determined the amount of food on the plate.
Fifty-one men and women were served lunch 1 d/wk for 4 wk. Lunch included an entrée of macaroni and cheese consumed ad libitum. At each meal, subjects were presented with 1 of 4 portions of the entrée: 500, 625, 750, or 1000 g. One group of subjects received the portion on a plate, and a second group received it in a serving dish and took the amount they desired on their plates.
Portion size significantly influenced energy intake at lunch (P < 0.0001). Subjects consumed 30% more energy (676 kJ) when offered the largest portion than when offered the smallest portion. The response to the variations in portion size was not influenced by who determined the amount of food on the plate or by subject characteristics such as sex, body mass index, or scores for dietary restraint or disinhibition.
Larger portions led to greater energy intake regardless of serving method and subject characteristics. Portion size is a modifiable determinant of energy intake that should be addressed in connection with the prevention and treatment of obesity.
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.
Using self-refilling soup bowls, this study examined whether visual cues related to portion size can influence intake volume without altering either estimated intake or satiation.
Fifty-four participants (BMI, 17.3 to 36.0 kg/m2; 18 to 46 years of age) were recruited to participate in a study involving soup. The experiment was a between-subject design with two visibility levels: 1) an accurate visual cue of a food portion (normal bowl) vs. 2) a biased visual cue (self-refilling bowl). The soup apparatus was housed in a modified restaurant-style table in which two of four bowls slowly and imperceptibly refilled as their contents were consumed. Outcomes included intake volume, intake estimation, consumption monitoring, and satiety.
Participants who were unknowingly eating from self-refilling bowls ate more soup [14.7+/-8.4 vs. 8.5+/-6.1 oz; F(1,52)=8.99; p<0.01] than those eating from normal soup bowls. However, despite consuming 73% more, they did not believe they had consumed more, nor did they perceive themselves as more sated than those eating from normal bowls. This was unaffected by BMI.
These findings are consistent with the notion that the amount of food on a plate or bowl increases intake because it influences consumption norms and expectations and it lessens one's reliance on self-monitoring. It seems that people use their eyes to count calories and not their stomachs. The importance of having salient, accurate visual cues can play an important role in the prevention of unintentional overeating.
Physiologic studies suggest that sleep restriction has metabolic effects that predispose to weight gain. The authors investigated the association between self-reported usual sleep duration and subsequent weight gain in the Nurses' Health Study. The 68,183 women who reported habitual sleep duration in 1986 were followed for 16 years. In analyses adjusted for age and body mass index, women sleeping 5 hours or less gained 1.14 kg (95% confidence interval (CI): 0.49, 1.79) more than did those sleeping 7 hours over 16 years, and women sleeping 6 hours gained 0.71 kg (95% CI: 0.41, 1.00) more. The relative risks of a 15-kg weight gain were 1.32 (95% CI: 1.19, 1.47) and 1.12 (95% CI: 1.06, 1.19) for those sleeping 5 and 6 hours, respectively. The relative risks for incident obesity (body mass index: >30 kg/m(2)) were 1.15 (95% CI: 1.04, 1.26) and 1.06 (95% CI: 1.01, 1.11). These associations remained significant after inclusion of important covariates and were not affected by adjustment for physical activity or dietary consumption. These data suggest that short sleep duration is associated with a modest increase in future weight gain and incident obesity. Further research is needed to understand the mechanisms by which sleep duration may affect weight.
Humans have expectations about the satiety that is likely to develop after consuming particular foods. These expectations are potentially important, because they may influence decisions about meal size. Despite this, very little is known about the basis on which satiety expectations are formulated. This work introduces a methodology (based on a method of constant stimuli) that quantifies differences in expectations across foods. In Experiment 1 (N = 52) and Experiment 2 (N = 76) we compared expectations across 4 and 18 common foods, respectively. We discovered that a considerable mismatch occurs between satiety expectations and the energy content of foods (e.g., 200 kcal of pasta and 894 kcal of cashew nuts are expected to deliver equal satiety). This difference may reflect physical or macronutrient characteristics of these foods – energy-dense and high-fat foods have significantly lower ‘ratios of expected satiety.’ We also found a highly significant relationship between food familiarity and expected satiety (r = 0.86, p < 0.001), suggesting that expected-satiety judgements are learned. Across experiments, we were able to confirm both the reliability and robustness of our empirical approach. Future use of this methodology is discussed, both in relation to our understanding of portion-size decisions and its application more generally.
Epidemiologic evidence shows an increase in obesity concurrent with a reduction in average sleep duration among Americans. Although clinical studies propose that restricted sleep affects hormones related to appetite, neuronal activity in response to food stimuli after restricted and habitual sleep has not been investigated.
The objective of this study was to determine the effects of partial sleep restriction on neuronal activation in response to food stimuli.
Thirty healthy, normal-weight [BMI (in kg/m²): 22-26] men and women were recruited (26 completed) to participate in a 2-phase inpatient crossover study in which they spent either 4 h/night (restricted sleep) or 9 h/night (habitual sleep) in bed. Each phase lasted 6 d, and functional magnetic resonance imaging was performed in the fasted state on day 6.
Overall neuronal activity in response to food stimuli was greater after restricted sleep than after habitual sleep. In addition, a relative increase in brain activity in areas associated with reward, including the putamen, nucleus accumbens, thalamus, insula, and prefrontal cortex in response to food stimuli, was observed.
The findings of this study link restricted sleep and susceptibility to food stimuli and are consistent with the notion that reduced sleep may lead to greater propensity to overeat.
The customary approach to the study of meal size suggests that 'events' occurring during a meal lead to its termination. Recent research, however, suggests that a number of decisions are made before eating commences that may affect meal size. The present study sought to address three key research questions around meal size: the extent to which plate-cleaning occurs; prevalence of pre-meal planning and its influence on meal size; and the effect of within-meal experiences, notably the development of satiation. To address these, a large-cohort internet-based questionnaire was developed. Results showed that plate-cleaning occurred at 91% of meals, and was planned from the outset in 92% of these cases. A significant relationship between plate-cleaning and meal planning was observed. Pre-meal plans were resistant to modification over the course of the meal: only 18% of participants reported consumption that deviated from expected. By contrast, 28% reported continuing eating beyond satiation, and 57% stated that they could have eaten more at the end of the meal. Logistic regression confirmed pre-meal planning as the most important predictor of consumption. Together, our findings demonstrate the importance of meal planning as a key determinant of meal size and energy intake.
Non‐technical summary
One of the proposed functions of sleep is to conserve energy. We determined the amount of energy conserved by sleep in humans, how much more energy is expended when missing a night of sleep, and how much energy is conserved during recovery sleep. Findings support the hypothesis that a function of sleep is to conserve energy in humans. Sleep deprivation increased energy expenditure indicating that maintaining wakefulness under bed‐rest conditions is energetically costly. Recovery sleep after sleep deprivation reduced energy use compared to baseline sleep suggesting that human metabolic physiology has the capacity to make adjustments to respond to the energetic cost of sleep deprivation. The finding that sleep deprivation increases energy expenditure should not be interpreted that sleep deprivation is a safe or effective strategy for weight loss as other studies have shown that chronic sleep deprivation is associated with impaired cognition and weight gain.
Systemic glucose utilization declines during sleep in man. We tested the hypothesis that this decline in utilization is largely accounted for by reduced brain glucose metabolism. 10 normal subjects underwent internal jugular and radial artery cannulation to determine cerebral blood flow by N2O equilibrium technique and to quantitate cross-brain glucose and oxygen differences before and every 3 h during sleep. Sleep stage was graded by continuous electroencephalogram, and systemic glucose turnover was estimated by isotope dilution. Brain glucose metabolism fell from 33.6 +/- 2.2 mumol/100 g per min (mean +/- SE) before sleep (2300 h) to a mean nadir of 24.3 +/- 1.1 mumol/100 g per min at 0300 h during sleep (P = 0.001). Corresponding rates of systemic glucose utilization fell from 13.2 +/- 0.8 to 11.0 +/- 0.5 mumol/kg per min (P = 0.003). Diminished brain glucose metabolism was the product of a reduced arteriovenous glucose difference, 0.643 +/- 0.024 to 0.546 +/- 0.020 mmol/liter (P = 0.002), and cerebral blood flow, 50.3 +/- 2.8 to 44.6 +/- 1.4 cc/100 g per min (P = 0.021). Brain oxygen metabolism fell commensurately from 153.4 +/- 11.8 to 128.0 +/- 8.4 mumol/100 g per min (P = 0.045). The observed reduction in brain metabolism occurred independent of stage of central nervous system electrical activity (electroencephalographic data), and was more closely linked to duration of sleep. We conclude that a decline in brain glucose metabolism is a significant determinant of falling rates of systemic glucose utilization during sleep.
To investigate whether effects on food intake are seen in obese subjects receiving exogenous administration of ghrelin.
Randomised, double-blind, placebo-controlled study of intravenous ghrelin at doses 1 pmol/kg/min and 5 pmol/kg/min.
In all, 12 healthy lean subjects (mean body mass index (BMI) 20.5+/-0.17 kg/m(2)) and 12 healthy overweight and obese subjects (mean BMI 31.9+/-1.02 kg/m(2)).
Food intake, appetite and palatability of food, ghrelin and other obesity-related hormones, growth hormone.
Low-dose infusion of ghrelin increased ad libitum energy intake at a buffet meal in the obese group only (mean increase 36.6+/-9.4%, P<0.01.) High-dose ghrelin infusion increased energy intake in both groups (mean increase 20.1+/-10.6% in the lean and 70.1+/-15.5% in the obese, P<0.01 in both cases.) Ghrelin infusion increased palatability of food in the obese group.
Ghrelin increases food intake in obese as well as lean subjects. Obese people are sensitive to the appetite-stimulating effects of ghrelin and inhibition of circulating ghrelin may be a useful therapeutic target in the treatment of obesity.
Increased heat generation from biological processes is inherent to homeothermy. Homeothermic species produce more heat from sustaining a more active metabolism as well as from reducing fuel efficiency. This article reviews the mechanisms used by homeothermic species to generate more heat and their regulation largely by thyroid hormone (TH) and the sympathetic nervous system (SNS). Thermogenic mechanisms antecede homeothermy, but in homeothermic species they are activated and regulated. Some of these mechanisms increase ATP utilization (same amount of heat per ATP), whereas others increase the heat resulting from aerobic ATP synthesis (more heat per ATP). Among the former, ATP utilization in the maintenance of ionic gradient through membranes seems quantitatively more important, particularly in birds. Regulated reduction of the proton-motive force to produce heat, originally believed specific to brown adipose tissue, is indeed an ancient thermogenic mechanism. A regulated proton leak has been described in the mitochondria of several tissues, but its precise mechanism remains undefined. This leak is more active in homeothermic species and is regulated by TH, explaining a significant fraction of its thermogenic effect. Homeothermic species generate additional heat, in a facultative manner, when obligatory thermogenesis and heat-saving mechanisms become limiting. Facultative thermogenesis is activated by the SNS but is modulated by TH. The type II iodothyronine deiodinase plays a critical role in modulating the amount of the active TH, T(3), in BAT, thereby modulating the responses to SNS. Other hormones affect thermogenesis in an indirect or permissive manner, providing fuel and modulating thermogenesis depending on food availability, but they do not seem to have a primary role in temperature homeostasis. Thermogenesis has a very high energy cost. Cold adaptation and food availability may have been conflicting selection pressures accounting for the variability of thermogenesis in humans.
Feeding behavior is often separated into homeostatic and hedonic components. Hedonic feeding, which can be triggered by visual or olfactory food cues, involves brain regions that play a role in reward and motivation, while homeostatic feeding is thought to be under the control of circulating hormones acting primarily on the hypothalamus. Ghrelin is a peptide hormone secreted by the gut that causes hunger and food consumption. Here, we show that ghrelin administered intravenously to healthy volunteers during functional magnetic resonance imaging increased the neural response to food pictures in regions of the brain, including the amygdala, orbitofrontal cortex, anterior insula, and striatum, implicated in encoding the incentive value of food cues. The effects of ghrelin on the amygdala and OFC response were correlated with self-rated hunger ratings. This demonstrates that metabolic signals such as ghrelin may favor food consumption by enhancing the hedonic and incentive responses to food-related cues.
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.