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Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite



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Brief Communication: Sleep Curtailment in Healthy Young Men Is
Associated with Decreased Leptin Levels, Elevated Ghrelin Levels, and
Increased Hunger and Appetite
Karine Spiegel, PhD; Esra Tasali, MD; Plamen Penev, MD, PhD; and Eve Van Cauter, PhD
Background: Total sleep deprivation in rodents and in humans
has been associated with hyperphagia. Over the past 40 years,
self-reported sleep duration in the United States has decreased by
almost 2 hours.
Objective: To determine whether partial sleep curtailment, an
increasingly prevalent behavior, alters appetite regulation.
Design: Randomized, 2-period, 2-condition crossover clinical
Setting: Clinical Research Center, University of Chicago, Chi-
cago, Illinois.
Patients: 12 healthy men (mean age [±SD], 22 ± 2 years; mean
body mass index [±SD], 23.6 ± 2.0 kg/m
Measurements: Daytime profiles of plasma leptin and ghrelin
levels and subjective ratings of hunger and appetite.
Intervention: 2 days of sleep restriction and 2 days of sleep
extension under controlled conditions of caloric intake and phys-
ical activity.
Results: Sleep restriction was associated with average reductions
in the anorexigenic hormone leptin (decrease, 18%;
elevations in the orexigenic factor ghrelin (increase, 28%;
0.04), and increased hunger (increase, 24%;
<0.01) and appe-
tite (increase, 23%;
0.01), especially for calorie-dense foods
with high carbohydrate content (increase, 33% to 45%;
Limitations: The study included only 12 young men and did not
measure energy expenditure.
Conclusions: Short sleep duration in young, healthy men is
associated with decreased leptin levels, increased ghrelin levels,
and increased hunger and appetite.
Ann Intern Med. 2004;141:846-850.
For author affiliations, see end of text.
See editorial comment on pp 885-886.
Sleep plays an important role in energy balance. In ro-
dents, food shortage or starvation results in decreased
sleep (1), and, conversely, total sleep deprivation leads to
marked hyperphagia (2). Leptin and ghrelin are peripheral
signals that contribute to the central regulation of food
intake. Leptin, a hormone released by the adipocytes, pro-
vides information about energy status to hypothalamic reg-
ulatory centers (3). In humans, circulating leptin levels rap-
idly decrease or increase in response to acute caloric
shortage or surplus, respectively (4). These changes in lep-
tin levels have been associated with reciprocal changes in
hunger (4). Ghrelin, a peptide produced predominantly by
the stomach, is also involved in energy balance regulation,
but, in contrast to the anorexigenic effects of leptin, ghrelin
stimulates appetite (5). It has been proposed that leptin
and ghrelin “represent the ‘yin–yang’ of one regulatory sys-
tem that has developed to inform the brain about the cur-
rent energy balance state” (6).
Over the past 40 years, sleep duration in the U.S.
population has decreased by 1 to 2 hours (7–10). The
proportion of young adults sleeping fewer than 7 hours per
night has more than doubled between 1960 and 2001–
2002 (from 15.6% to 37.1%) (7–10). The effect of sleep
curtailment on the control of appetite and food intake is
not known. Because of the well-documented associations
between sleep and food intake (1, 2), we sought to deter-
mine whether sleep duration influences the daytime pro-
files of leptin and ghrelin.
Twelve healthy men (mean age [SD], 22 2 years];
mean body mass index [SD], 23.6 2.0 kg/m
) who
did not smoke or take any medications participated in the
study. All of the men were within 10% of ideal body
weight and had regular nocturnal time in bed of 7 to 9
hours. We excluded persons who had traveled across time
zones less than 4 weeks before the study.
Experimental Protocol
The Institutional Review Board of the University of
Chicago approved the protocol, and we obtained written
informed consent from all participants. During the week
preceding each study, we asked participants not to deviate
from a fixed time in bed (11:00 p.m. to 7:00 a.m.) by more
than 30 minutes. Naps were not allowed.
The men participated in 2 studies that were conducted
in a randomized order, were spaced at least 6 weeks apart,
and were performed in the Clinical Research Center at the
University of Chicago, Chicago, Illinois. Six of the 12 men
first performed the study with restricted time in bed, and
the remaining 6 men first performed the study with ex-
tended time in bed. Average weight did not change over
the time period separating the 2 study conditions (75.2 kg
in the sleep restriction condition vs. 75.4 kg in the sleep
extension condition; P0.2). We obtained blood samples
at 20-minute intervals from 8:00 a.m. to 9:00 p.m. after 2
consecutive nights of 10 hours in bed (10:00 p.m. to 8:00
846 © 2004 American College of Physicians
a.m.; sleep extension) and after 2 consecutive nights of 4
hours in bed (1:00 a.m. to 5:00 a.m.; sleep restriction).
Sleep was recorded every night. For both extension and
restriction conditions, each overnight stay began at 7:00
p.m. with a standard hospital dinner, and the first over-
night stay ended after breakfast, which was served at 8:00
a.m. We instructed the participants not to deviate from
their usual eating habits between breakfast and dinner, but
caloric intake was not otherwise monitored. Participants
were readmitted in the early evening and, after receiving a
standard hospital dinner at 7:00 p.m., remained at bed
rest. At 8:00 a.m. after the second night, the participants’
caloric intake was kept constant to avoid meal-related fluc-
tuations of hunger and satiety and consisted of an intrave-
nous glucose infusion at a constant rate of 5 g/kg of body
weight every 24 hours. There was no other source of calo-
ries. Every hour from 9:00 a.m. to 9:00 p.m., the men
completed validated visual analogue scales (0 to 10 cm) for
hunger (11) and appetite for various food categories (12).
To assess hunger, we asked participants to mark their re-
sponse to the question “How hungry do you feel right
now?” on a 10-cm scale (with “not at all hungry” on the
left and “extremely hungry” on the right). To assess appe-
tite, we asked participants to mark their response to how
much they would enjoy eating foods from 7 different food
categories on a 10-cm scale (with “not at all” on the left
and “very much” on the right). They were asked to provide
a score based only on their appetite at the moment, with-
out concern for calories, fat, or a healthy diet. The food
categories were sweets (such as cake, candy, cookies, ice
cream, and pastry); salty foods (such as chips, salted nuts,
pickles, and olives); starchy foods (such as bread, pasta,
cereal, and potatoes); fruits and fruit juices; vegetables;
meat, poultry, fish, and eggs; and dairy products (such as
milk, cheese, and yogurt).
We measured serum leptin levels in all samples by
using a human leptin radioimmunoassay kit (Linco Re-
search, St. Charles, Missouri) with a sensitivity of 0.5
ng/mL and an intra-assay coefficient of variation of 8.3%.
In 9 of the 12 participants, we also measured total ghrelin
levels at hourly intervals by radioimmunoassay (Linco Re-
search) with a sensitivity of 0.5 ng/mL and an intra-assay
coefficient of variation of 7.9%.
Statistical Analysis
We performed paired comparisons by using the Wil-
coxon matched-pairs signed-rank test. We calculated cor-
relations by using the Spearman coefficient. The mean rel-
ative changes in leptin, ghrelin, hunger, and appetite
between extended sleep (the reference category) and re-
stricted sleep were calculated by using the ratios of the
corresponding individual data and then deriving the mean
across all individuals.
Role of the Funding Sources
This work was partially supported by grants from the
National Institutes of Health, the European Sleep Research
Society, the Belgian Fonds de la Recherche Scientifique
Me´dicale, the University of Chicago Diabetes Research
and Training Grant, and The University of Chicago Gen-
eral Clinical Research Center. The funding sources had no
role in the design, conduct, and reporting of the study or
in the decision to submit the manuscript for publication.
Leptin levels were stable across the daytime period un-
der both sleep conditions, which was consistent with the
fact that calories were exclusively delivered in the form of a
constant glucose infusion. Average total sleep time was 9
hours and 8 minutes when the men spent 10 hours in bed
and 3 hours and 53 minutes when the men spent 4 hours
in bed (P0.01). When spending 4 hours in bed, the
participants had mean leptin levels that were 18% lower
(2.1 ng/mL vs. 2.6 ng/mL; P0.04) (Figure 1,part A)
and mean ghrelin levels that were 28% higher (3.3 ng/mL
vs. 2.6 ng/mL; P0.04) (Figure 1,part B) than when the
participants spent 10 hours in bed. The ratio of the con-
centrations of orexigenic ghrelin to anorexigenic leptin in-
creased by 71% (CI, 7% to 135%) with 4 hours in bed
compared with 10 hours in bed. Sleep restriction relative to
sleep extension was associated with a 24% increase in hun-
ger ratings on the 10-cm visual analogue scale (P0.01)
and a 23% increase in appetite ratings for all food catego-
ries combined (P0.01) (Figure 1,parts C and D, and
Table 1). The increase in appetite tended to be greatest for
calorie-dense foods with high carbohydrate content
(sweets, salty foods, and starchy foods: increase, 33% to
45%; P0.06) (Table 1). The increase in appetite for
fruits and vegetables was less consistent and of lesser mag-
nitude (increase, 17% to 21%) (Table 1). Appetite for
Studies in animals and humans suggest that sleep duration
is an important regulator of metabolism.
In this study, 12 young, healthy, normal-weight men ex-
hibited reductions in the satiety hormone leptin, increases
in the hunger hormone ghrelin, and increases in hunger
after 2 nights of only 4 hours of sleep compared with af-
ter 2 nights of 10 hours of sleep.
Inadequate sleep seems to influence the hormones that
regulate satiety and hunger in a way that could promote
excess eating.
–The Editors
ArticleLeptin, Ghrelin, Hunger, and Appetite during Sleep Loss 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11 847
protein-rich nutrients (meat, poultry, fish, eggs, and dairy
foods) was not significantly affected by sleep duration (Ta-
ble 1). When we considered the changes in ghrelin and
leptin in an integrated fashion by calculating the ghrelin-to-
leptin ratio, the increase in hunger was proportional to the
increase in ghrelin-to-leptin ratio (r0.87) (Figure 2). Al-
most 70% of the variance in increased hunger could be ac-
counted for by the increase in the ghrelin-to-leptin ratio.
We observed that sleep duration may affect the circu-
lating levels of neuroendocrine factors that regulate hunger
and appetite. Two days with 4 hours of time in bed each
night were associated with an 18% decrease in the levels of
the anorexigenic hormone leptin. By comparison, 3 days of
underfeeding by approximately 900 calories per day in
healthy lean volunteers has been reported to result in a
decrease of leptin levels averaging 22% (4). Sleep curtail-
ment was also associated with an almost 28% increase in
daytime levels of the orexigenic factor ghrelin. The recip-
rocal changes in leptin and ghrelin that we observed in
response to sleep restriction were associated with a 24%
increase in hunger and a 23% increase in appetite. Appetite
for calorie-dense nutrients with high carbohydrate content,
including sweets, salty snacks, and starchy foods, increased
by 33% to 45%. In contrast, appetite for fruits, vegetables,
and high-protein nutrients was less affected. The increase
in hunger during sleep restriction was strongly correlated
with the increase in the ghrelin-to-leptin ratio.
Our study involved intensive physiologic monitoring
under laboratory conditions in a relatively small group of
normal young men and will need to be replicated in a
larger sample. In addition, because age and sex may affect
neuroendocrine regulation of appetite (3, 5), our findings
may not readily apply to women and older adults. Recent
findings from a population study involving 1030 persons
are, however, in complete agreement with our observations
(13). In that study, restricted duration of sleep was associ-
ated with reduced leptin levels, increased ghrelin levels, and
elevated body mass index (13).
The alterations in appetite regulation that we observed
after sleep restriction may reflect a normal adaptation to
the increased caloric need associated with extended wake-
fulness. Our experimental protocol was designed to keep
energy intake and activity levels as constant as possible, and
the extra hours of wakefulness during sleep restriction were
spent lying in bed or sitting in a comfortable armchair.
Although several studies have indicated that differences in
energy expenditure between sleeping in bed compared with
quiet wakefulness are very small, if at all detectable (14,
15), it is not known whether sleep deprivation increases the
energy requirements of maintaining wakefulness. In studies
in rats in which the disk over water method achieved total
sleep deprivation, researchers observed a marked increase in
energy expenditure that resulted in overall weight loss de-
spite increased food intake (2). However, an increased en-
ergy demand is an intrinsic feature of this method of sleep
deprivation, which involves forced locomotion and re-
peated water immersions. Careful studies of energy balance
in sleep-restricted humans under comfortable sedentary
conditions will be necessary to determine whether in-
creased hunger will result in excessive food intake and
weight gain.
The causes of decreased leptin levels and increased
Figure 1. Effect of sleep duration on daytime leptin levels,
ghrelin levels, hunger, and appetite.
A. Mean (SE) daytime (9:00 a.m. to 9:00 p.m.) profiles of leptin after
2 days with 4 hours in bed or 2 days with 10 hours in bed. Mean leptin
levels were 18% lower when sleep was restricted. B. Mean (SE) day-
time (9:00 a.m. to 9:00 p.m.) profiles of ghrelin from 9 of the 12
participants after 2 days with 4 hours in bed or 2 days with 10 hours in
bed. Mean ghrelin levels were 28% higher in the afternoon and early
evening (12:00 noon to 9:00 p.m.) when sleep was restricted. Cand D.
Ratings of hunger (C) (0- to 10-cm visual analogue scale) and overall
appetite (D) (0- to 70-cm visual analogue scale) after 2 days with 4 hours
in bed or 2 days with 10 hours in bed. When sleep was restricted, ratings
of hunger and overall appetite increased by 24% and 23%, respectively.
Article Leptin, Ghrelin, Hunger, and Appetite during Sleep Loss
848 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11
ghrelin levels in a state of sleep loss remain to be deter-
mined. We have previously shown that 6 days of sleep
restriction in healthy adults resulted in an increase in car-
diac sympathovagal balance (16). Some, but not all, studies
have indicated that sleep loss is associated with increased
sympathetic nervous system outflow (17). Because leptin
release is inhibited by sympathetic nervous system activity
(18), decreased leptin levels, in the presence of a sleep debt,
may result from an inhibitory effect of increased sympa-
thetic outflow. Increased cardiac sympathovagal balance
could also reflect decreased vagal activity, which could ex-
plain increased ghrelin levels. Several studies have shown
that the vagus has a negative influence on ghrelin (5, 19,
Sleep loss due to voluntary curtailment of time in bed
has become a hallmark of modern society. Self-reported
sleep duration in the United States has decreased by 1 to 2
hours during the second half of the 20th century (7–10).
The proportion of young adults sleeping 8 to 8.9 hours per
night has decreased from 40.8% in 1960 to 23.5% in
2001–2002 (8–10). During the same time period, the in-
cidence of obesity has nearly doubled (21). Three epidemi-
ologic studies have found a relationship between higher
body mass index and shorter sleep duration (13, 22, 23).
This epidemiologic evidence, together with our experimen-
tal findings that sleep restriction affects leptin levels, ghre-
lin levels, hunger, and appetite, suggests that additional
studies should examine the possible role of chronic sleep
curtailment as a previously unrecognized risk factor for
From University of Chicago, Chicago, Illinois, and Universite´ Libre de
Bruxelles, Brussels, Belgium.
Acknowledgment: The authors thank Paul Rue for performing the lep-
tin assays, Miho Yoshida for performing the ghrelin assays, and Kristen
Knutson for providing statistical assistance. The authors also thank the
volunteers for their participation in this demanding study and the nurs-
ing staff of the University of Chicago General Clinical Research Center
for their expert assistance.
Grant Support: In part by grants from the National Institutes of Health
(DK-41814, AG-11412, and HL-72694), from the European Sleep Re-
search Society, from the Belgian Fonds de la Recherche Scientifique
Me´dicale (FRSM-3.4583.02), from the University of Chicago Diabetes
Research and Training Grant (NIH DK-20595), and from The Univer-
sity of Chicago General Clinical Research Center (NIH MO1-RR-
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Eve Van Cauter, PhD, Department of
Medicine, MC 1027, University of Chicago, 5841 South Maryland
Avenue, Chicago, IL 60637.
Figure 2. Association between the change in hunger ratings
and the change in ghrelin-to-leptin ratio during the 12:00 noon
to 9:00 p.m. time period when sleep is restricted as compared
with extended.
The changes in hunger ratings and in ghrelin-to-leptin ratio were calcu-
lated as the values obtained after 4 hours in bed minus the values ob-
tained after 10 hours in bed. For each of these variables, negative values
were obtained when the variable measured after 10 hours in bed was
higher than when measured after 4 hours in bed. The Spearman coeffi-
cient was 0.87 and the Pvalue was 0.01.
Table. Average Ratings of Appetite after 2 Days of Sleep Restriction or Sleep Extension
Food Category* Ratings for
Ratings for
Value Change,
Sweets (cake, candy, cookies, ice cream, and pastry) 5.4 6.6 0.03 33
Salty food (chips, salted nuts, pickles, and olives) 5.0 6.7 0.02 45
Starchy food (bread, pasta, cereal, and potatoes) 5.9 7.4 0.03 33
Fruits and fruit juices 6.4 7.2 0.07 17
Vegetables 5.6 6.6 0.02 21
Meat, poultry, fish, and eggs 5.9 6.9 0.11 21
Dairy (milk, cheese, and yogurt) 5.5 6.4 0.2 19
Overall appetite† 39.7 47.7 0.01 23
*Each category is rated on a 0- to 10-cm visual analogue scale.
Rated on a 0- to 70-cm visual analogue scale.
ArticleLeptin, Ghrelin, Hunger, and Appetite during Sleep Loss 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11 849
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Article Leptin, Ghrelin, Hunger, and Appetite during Sleep Loss
850 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11
Current Author Addresses: Dr. Spiegel: Laboratoire de Physiologie,
Centre d’Etude des Rythmes Biologiques (CERB), Universite´ Libre de
Bruxelles, Campus Hoˆpital Erasme–CPI 604, 808, Route de Lennik,
B-1070 Brussels, Belgium.
Drs. Tasali, Penev, and Van Cauter: Department of Medicine, MC
1027, University of Chicago, 5841 South Maryland Avenue, Chicago, IL
Author Contributions: Conception and design: K. Spiegel, E. Van Cau-
Analysis and interpretation of the data: K. Spiegel, E. Tasali, P. Penev, E.
Van Cauter.
Drafting of the article: K. Spiegel, E. Tasali, E. Van Cauter.
Critical revision of the article for important intellectual content: E.
Tasali, P. Penev, E. Van Cauter.
Final approval of the article: K. Spiegel, E. Tasali, P. Penev, E. Van
Provision of study materials or patients: E. Van Cauter.
Statistical expertise: E. Van Cauter.
Obtaining of funding: K. Spiegel, E. Van Cauter.
Administrative, technical, or logistic support: E. Van Cauter.
Collection and assembly of data: K. Spiegel, E. Tasali, E. Van Cauter. 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11 W-157
... Plusieurs études ont montré que les concentrations de leptine, hormone anorexigène sécrétée par le tissu adipeux, et de ghréline, hormone orexigène sécrétée par l'estomac, sont altérées en cas de privation de sommeil Leproult & Van Cauter, 2010;Spiegel et al., 2004). En effet, chez l'adulte, une restriction de sommeil (4 heures) diminue de 18% les niveaux de leptine et augmente de 28% ceux de ghréline, comparés aux concentrations mesurées lors d'une nuit de sommeil de 9 ...
... heures (Spiegel et al., 2004). Chez l'enfant, deux études se sont intéressées à la relation entre le temps de sommeil et la sécrétion de ces hormones adipocytaires et gastrointestinales mais les résultats sont divergents (Hart et al., 2013;Kjeldsen et al., 2014 (Greer et al., 2013;Spiegel et al., 2004). ...
... heures (Spiegel et al., 2004). Chez l'enfant, deux études se sont intéressées à la relation entre le temps de sommeil et la sécrétion de ces hormones adipocytaires et gastrointestinales mais les résultats sont divergents (Hart et al., 2013;Kjeldsen et al., 2014 (Greer et al., 2013;Spiegel et al., 2004). Chez l'adolescent, après cinq nuits de restriction de sommeil, la consommation d'aliments sucrés est augmentée comparée à celle évaluée après cinq nuits de sommeil de durée normale (Beebe et al., 2013). ...
Le sommeil, de par ses fonctions récupératrices, est essentiel à la vie. Pour autant, la modification du mode de vie et des comportements, tant sédentaires que nutritionnels, sont à l’origine d’une altération du sommeil, conduisant ensemble à des situations d’obésité. Cet excès pondéral s’accompagne fréquemment d’un syndrome d’apnées obstructives du sommeil (SAOS). Lorsque ces deux pathologies sont présentes, les troubles métaboliques s’aggravent et sont à l’origine d’une inflammation de bas grade. A notre connaissance, aucune étude ne s’est intéressée aux bénéfices d’un reconditionnement à l’exercice physique combiné à une modification des habitudes alimentaires, en dehors de ceux induits par la perte de poids, sur ces différents paramètres. L’objectif de ce travail de thèse a donc été, à partir d’une étude ancillaire, d’évaluer le sommeil d’adolescents obèses par polysomnographie (PSG) par comparaison à celui de sujets normo-pondérés. Dans l’étude principale, les effets d’un programme de 9 mois (reconditionnement à l’exercice, activités physiques adaptées, rééquilibre alimentaire) ont été évalués sur l’architecture et la durée du sommeil, le SAOS, les différents facteurs biologiques (inflammatoires, hormonaux, profils glucidique et lipidique) et sur les adaptations physiologiques à l’exercice musculaire, afin de mieux comprendre l’implication de l’endurance aérobie et des troubles du sommeil sur la santé cardio-métabolique. Trente-deux adolescents obèses (âge : 14,6 ans, z-score d’IMC= 4 ,7) ont été recrutés. Toutes les variables ont été analysées en pré et post-intervention. Les résultats montrent une durée de sommeil réduite chez les jeunes obèses avec un SAOS, diagnostiqué chez 58% d’entre eux, malgré une architecture du sommeil satisfaisante. En post-intervention, une perte de poids de 11 kg et une amélioration des paramètres d’adaptation à l’exercice maximal (PMA, VE, VO2pic…) ont été rapportées chez tous les sujets, que le SAOS soit encore, ou non, présent. En effet, ce syndrome s’est normalisé chez 46% d’entre eux. Par ailleurs, grâce à l’intervention, le sommeil s’est amélioré (qualité et quantité). Enfin, la protéine C-réactive basale du groupe SAOS, dont les valeurs atteignaient 11mg/l à l’admission, a considérablement diminué, accompagnée d’une baisse de la leptinémie et d’une hausse de l’adiponectinémie, pouvant expliquer le moindre risque cardio-métabolique. Nos résultats démontrent qu’à l’admission, l’inflammation est liée à l’obésité, alors qu’en post-intervention, sa baisse s’explique par l’augmentation de l’endurance aérobie, et ceci indépendamment du sexe, du poids, de la durée de sommeil et du SAOS. Bien que ce dernier n’ait pas été normalisé chez tous les sujets, sa prévention par l’exercice physique ainsi que celle des troubles métaboliques observés dans ces deux pathologies devrait faire partie intégrante de la prise en charge des jeunes obèses en vue d’atténuer le risque de morbi-mortalité cardiovasculaire à l’âge adulte
... Eptin pathway could explain the key mechanism via a modi cation effect [28]. Under some circumstances, the sleep deprivation could lead to disruption of insulin, leptin, cortisol and ghrelin expression [29,30]. After a period of sleep loss, people could experience a 24% increase in hunger with largely whetting the appetite for high carbohydrate foods [29]. ...
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Background: This study was designed to investigate the prevalence of sleep deprivation and explore the association between sleep duration and overweight or obesity in adolescents from middle school in Fuzhou, China. Methods: Questionaires focusing on sleep duration and overweight or obesity related factors were collected. A generalized linear hybrid model was used to evaluate the effects of sleep duration on overweight or obesity in school students. Results: The overall rates of overweight and obesity were 12.1% and 7.1%, respectively. The prevalence of sleep deprivation among students was 82.8%. The majority of high school students (92.5%) suffered from insufficient sleep. Compared with male children with a sleep duration of over 8 hrs a day, the odds ratios (95% CI) of overweight/obesity for those with a sleep duration of less than 6 h or 6 - 8 h, were 1.63 (1.25-2.13) and 1.06 (0.88-1.27). After adjusting social and demographic status, mental health and lifestyle factors, the odds ratios of female children were 1.38(0.99-1.93) and 1.04 (0.79-1.35), respectively. Conclusions: A large number of adolescents suffered from insufficient sleep. Sleep duration was negatively correlated with overweight or obesity among male children.
... Deprivation of sleep leads to a decrease in leptin and an increase in grehlin levels, thus promoting weight gain and obesity. 5 The role of calcium in the development of obesity is recently being recognized. Zemel et al 6 has observed an association with low intake of calcium with obesity, however, further research is needed to examine whether the relationship reported here persists among a broader socioeconomic group. ...
Background Small clinical studies have suggested that individuals with insufficient sleep could experience taste dysfunction. However, this notion has not been examined in a large-scale, population-based study. Objective This study aimed to examine whether overall sleep quality, as assessed by insomnia, daytime sleepiness, snoring, and sleep duration, was associated with the odds of having altered taste perception in a large population-based study. Design This was a cross-sectional study that used data from a subcohort of the Kailuan study, an ongoing multicenter cohort study that began in 2006 in Tangshan City, China. Participants/setting The participants were 11,030 adults aged 25 years or older (mean age 53.7 ± 10.7 years), who were free of neurodegenerative diseases. All the participants had undergone questionnaire assessments and medical examinations at Kailuan General Hospital from June 2012 to October 2013. Main outcome measures Altered taste and olfactory perception were assessed via a questionnaire with two questions regarding whether participants had any problems with sense of taste or smell for ≥3 months. Statistical analyses performed The association between sleep quality and altered taste/olfactory perception was examined using a logistic regression model, adjusting for age, sex, lifestyle factors (eg, obesity, smoking, alcohol intake, and physical activity) and health status (eg, lipid profiles, blood pressure, modification use, and presence of chronic diseases). Results Poor overall sleep quality was associated with a higher risk of having altered taste perception (adjusted odds ratio for low vs high sleep quality 2.03, 95% CI 1.42 to 2.91; P < 0.001). Specifically, insomnia, daytime sleepiness, and short sleep duration, but not prolonged sleep duration and snoring, were significantly associated with altered taste perception. A significant association between overall sleep quality and the risk of having altered olfactory perception was also observed (adjusted odds ratio for low vs high sleep quality 2.17, 95% CI 1.68 to 2.80; P < 0.001). Conclusions In this population-based study, poor sleep quality was associated with a high likelihood of altered taste perception.
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The aim of this study is to determine (a) whether short sleep is associated with the incidence of obesity and (b) whether interventions beneficial for sleep reduce weight gain in preschool children. We systematically searched PubMed, Embase, Web of Science and Cochrane up to 12/09/2019. (a) Studies that were included were prospective, had follow‐up ≥1 year, with sleep duration at baseline and required outcome measures. (b) Intervention trials with sleep intervention and measures of overweight or obesity were included. Data were extracted according to PRISMA guidelines. (a) The risk of developing overweight/obesity was greater in short sleeping children (13 studies, 42 878 participants, RR: 1.54; 95% CI, 1.33 to 1.77; p < 0.001). Sleep duration was associated with a significant change in BMI z‐score (10 studies, 11 cohorts and 29 553 participants) (mean difference: −0.02 unit per hour sleep; −0.03 to −0.01; p < 0.001). (b) Four of the five intervention studies reported improved outcomes: for BMI (−0.27 kg/m²; −0.50 to −0.03; p = 0.03); for BMI z‐score (−0.07 unit; −0.12 to −0.02; p = 0.006). Short sleep duration is a risk factor or marker of the development of obesity in preschool children. Intervention studies suggest that improved sleep may be beneficially associated with a reduced weight gain in these children.
Purpose: Previous studies have shown the connection between diet quality to sleep quality and weight status, although the relationship between Lifelines Diet Score (LLDS)-a fully food-based score that uses the 2015 Dutch Dietary Guidelines and underlying international literature-and sleep quality has not been evaluated in overweight and obese individuals yet. This observational study was conducted on overweight and obese adult females to assess the relationship between adherence to a LLDS pattern and sleep quality in Iran. Methods: A cohort of 278 overweight and obese women aged above 18 years was enrolled and their dietary intake was assessed using a 147-item, semi-quantitative, validated food frequency questionnaire. Pittsburgh Sleep Quality Index (PSQI), a self-reported questionnaire including 19-items, was applied to estimate sleep quality among the target population. Diet quality indices (LLDS) were calculated using the P.C. Vinke, et al. method, based on the 2015 Dutch Dietary Guidelines and the underlying literature. Results: Subjects in the highest LLDS tertile (those who had adhered closely to the food-based score) were older, compared to the lowest tertile (37.57 ± 7.77 versus 34.57 ± 9; p = 0.01). It was shown that about 25.5% of our subjects have poor quality sleep and 39% have better sleep quality which were mostly in the third tertile with greater LLDS. The parallel values in the first tertile were 29.9% and 46.8%, respectively (p = 0.02). Binary logistic regression was applied to evaluate the association between adherence of LLDS and sleep quality. The result has shown that the LLDS were correlated with lower risk poor sleep quality, wherein those who were in higher tertile (higher adherence to LLDS) had better sleep quality (odds ratio [OR]:0.586, 95% confidence interval [CI] (0.285-1.207), p = 0.009) and the result was not affected by adjusting for potential cofounders including age, education levels, and economic levels, sleep quality remained significantly associated with [OR]: 0.531, 95% confidence interval [CI] (0.248-1.138, p = 0.014). Conclusions: From this observational study, the higher LLDS can be related with better sleep quality in overweight and obese women. Level of evidence: Level IV, evidence obtained from multiple time series with or without the intervention, such as case studies.
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Fatigue and sleep deficiency among public safety personnel are threats to wellness, public and personal safety, and workforce retention. Napping strategies may reduce work‐related fatigue, improve safety and health, yet in some public safety organizations it is discouraged or prohibited. Our aim with this commentary is to define intra‐shift napping, summarize arguments for and against it, and to outline potential applications of this important fatigue mitigation strategy supported by evidence. We focus our discussion on emergency medical services (EMS); a key component of the public safety system, which is comprised of police, fire, and EMS. The personnel who work in EMS stand to benefit from intra‐shift napping due to frequent use of extended duration shifts, a high prevalence of personnel working multiple jobs, and evidence showing that greater than half of EMS personnel report severe fatigue, poor sleep quality, inadequate inter‐shift recovery, and excessive daytime sleepiness. The benefits of intra‐shift napping include decreased sleepiness and fatigue, improved recovery between shifts, decreased anxiety, and reduced feelings of burnout. Intra‐shift napping also mitigates alterations in clinician blood pressure associated with disturbed sleep and shift work. The negative consequences of napping include negative public perception, acute performance deficits stemming from sleep inertia, and the potential costs associated with reduced performance. While there are valid arguments against intra‐shift napping, we believe that the available scientific evidence favors it as a key component of fatigue mitigation and workplace wellness. We further believe that these arguments extend beyond EMS to all sectors of public safety.
Background Few studies reported the association of dietary patterns with obesity, central adiposity, and quality of sleep. We aimed to investigate the association between major dietary patterns and anthropometric indices in relation to obesity and quality of sleep among female students of Ahvaz Jundishapur University of Medical Sciences (AJUMS). Methods This cross-sectional study was conducted on 245 female university students aged 18–38 years. To assess sleep quality, we used a self-reported Pittsburgh sleep quality index (PSQI). Usual dietary intakes were assessed with the use of a 168 items food frequency questionnaire (FFQ). We used factor analysis to identify dietary patterns. Results Four major dietary patterns were identified: mixed, high protein, Western, and healthy dietary patterns. After adjustment for energy intake, subjects in the upper tertile of the mixed dietary pattern were more likely to have a high quality of sleep than those in the first tertile (odds ratio [OR]: 0.27; 95% CI: 0.13, 0.55). Individuals with greater adherence to Western dietary pattern had greater odds of having low quality of sleep compared to those in the first tertile (OR: 1.99; 95% CI: 1.04, 3.82). A healthy dietary pattern was associated with a higher quality of sleep; however, the association was no longer significant after adjustment for dietary energy intake. No significant association was found for high protein dietary patterns. Compared to the first tertile of the healthy dietary pattern, individuals in the upper tertile were less likely to be centrally obese (OR = 0.15; 95% CI = 0.50–0.52). Participants in the last tertile of the high protein dietary pattern were less likely to be generally obese (OR = 0.34; 95% CI = 0.12–0.99), whereas those in the upper tertile of the Western dietary pattern were more likely to be generally obese (OR = 1.84; 95% CI = 1.08–4.93). Conclusions Adherence to a mixed dietary pattern was associated with a high quality of sleep; however, the result was not significant for a high protein dietary pattern. While the high protein dietary pattern was negatively associated with general and central obesity, students in the upper tertile of the Western dietary pattern were more likely to be generally obese.
Growing evidence suggested that Sleep Disorders (SD) could increase the risk of developing obesity and could contribute to worsen obesity-related cardiovascular risk. Further, obesity per se has been reported to blunt sleep homeostasis. This happens through several mechanisms. First of all, the excessive adipose tissue at neck and chest levels could represent a mechanical obstacle to breathe. Moreover, the visceral adipose tissue is known to release cytokines contributing to low-grade chronic inflammation that could impair the circadian rhythm. Also, nutrition plays an important role in sleep homeostasis. High fat and/or high carbohydrate diets are known to have a negative impact on both sleep quality and duration. In addition, obesity predisposes to a condition called “obstructive sleep apnea” that has a detrimental effect on sleep. SD could increase the risk and/or could contribute to worsen cardiovascular risk usually associated with obesity. The chronic low grade inflammation associated with obesity has been reported to increase the risk of developing hypertension, type 2 diabetes and dyslipidemia. In turn, improving quality of sleep has been reported to improve the management of these cardiovascular risk factors. Thus, the aim of this manuscript is to provide evidence on the association of obesity and SD and on how they could contribute to the risk of developing cardiovascular risk factors such as hypertension, dyslipidemia and type 2 diabetes in obesity.
Continuous EEG recordings were performed in lean (240–250 g) rats, in large size (300–380 g) rats and in Ventromedial Hypothalamic (VMH) lesioned obese (450–470 g) rats, during 4 days of food deprivation and 3 days following food restitution. Though the daily amounts of both Slow Wave Sleep (SWS) and Paradoxical Sleep (PS) were dramatically decreased in lean rats (particularly during the dark phase of the day) by the food deprivation, they remained unchanged in large size rats and also in VMH obese rats. In the latter, there was even a tendency to an increase of SWS during the first two days of starvation. Food restitution brought about a significant rebound in SWS and PS (largely based upon an increase during the dark phase of the diurnal cycle) in lean rats, but had no effect on the sleep parameters of large size and VMH obese rats. Replacement by glucose infusions (100% of the normal daily caloric intake) via a cardiac catheter of oral nutrients in food deprived rats also resulted in a similar increase of sleep duration. These findings suggest that sleep is dependent on the degree of availability of metabolizable substances at the cellular level. In addition, possible causative relations between sleep and feeding are discussed.
Prospective epidemiologic data of the American Cancer Society disclosed that reported usual sleep durations among groups who complained of insomnia and sleeping pill use "often" overlapped with those of groups who had no complaints. Reports of insomnia were not consistently associated with increased mortality when several factors were controlled; however, men who reported usually sleeping less than four hours were 2.80 times as likely to have died within six years as men who reported 7.0 to 7.9 hours of sleep. The ratio for women was 1.48. Men and women who reported sleeping ten hours or more had about 1.8 times the mortality of those who reported 7.0 to 7.9 hours of sleep. Those who reported using sleeping pills "often" had 1.5 times the mortality of those who "never" used sleeping pills. These results do not prove that mortality could be reduced by altering sleep durations or by reducing hypnotic prescribing. Rather, studies are needed to determine the causes of these mortality risk factors.
Ten rats were subjected to total sleep deprivation (TSD) by the disk apparatus. All TSD rats died or were sacrificed when death seemed imminent within 11-32 days. No anatomical cause of death was identified. All TSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (TSC) rats remained healthy. Since dehydration was ruled out and several measures indicated accelerated use rather than failure to absorb nutrients, the food-weight changes in TSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all TSD rats increased EE, with mean levels reaching more than twice baseline values.
A nutritional survey, the Pittsburgh Appetite Test (PAT), was developed to study potential changes in appetite and food preference reported by patients during a depressive episode and during antidepressant treatment. We examined a group of 50 depressed outpatients who were drug-free for 2 weeks prior to treatment with imipramine and psychotherapy for 4 months. A significant increase in the desire for "sweets" (carbohydrate--fat-rich foods) was observed during a depressive episode, compared to periods when patients recalled feeling well (retrospective data). During imipramine treatment, no further changes were observed in preference for either "sweets" or carbohydrates when compared to the medication-free period. Alterations in patient self-reports of appetite and body weight change were noted during imipramine treatment.
The purpose of this study was to determine if overnight energy expenditure, the lowest energy expenditure sustained for 60 min during the night, measured and predicted basal metabolic rate are equivalent. Overnight energy expenditure (ON-EE), the lowest energy expenditure sustained for 60 min during sleep (LS-EE) and basal metabolic rate (BMR) were measured two to seven times in a room-sized indirect calorimeter in 69 adult subjects. Subjects' gender, age, weight and height were also used to predict BMR (FAO/WHO/UNU, 1985) (BMR-WHO). Beltsville Human Nutrition Research Center, Beltsville, MD, USA. The results from calorimetry measurements (mean +/- s.d.) included: ON-EE (6.87 +/- 0.99 MJ/d), LS-EE (6.18 +/- 0.94 MJ/d) and BMR (6.87 +/- 0.99 MJ/d). Predicted BMR mean was: BMR-WHO, 6.95 +/- 1.03. The mean within-subject difference for the calorimetry measurements were: ON-EE, 0.21 MJ/d; LS-EE, 0.16 MJ/d; and BMR, 0.34 MJ/d. Results indicate there was no significant difference between ON-EE, BMR and BMR-WHO. LS-EE was significantly lower (P < 0.0001) than ON-EE, BMR and BMR-WHO. These results indicate that while metabolic rate drops significantly below BMR during sleep, overnight metabolic rate and BMR are equivalent.
The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.
Chronic sleep debt is becoming increasingly common and affects millions of people in more-developed countries. Sleep debt is currently believed to have no adverse effect on health. We investigated the effect of sleep debt on metabolic and endocrine functions. We assessed carbohydrate metabolism, thyrotropic function, activity of the hypothalamo-pituitary-adrenal axis, and sympathovagal balance in 11 young men after time in bed had been restricted to 4 h per night for 6 nights. We compared the sleep-debt condition with measurements taken at the end of a sleep-recovery period when participants were allowed 12 h in bed per night for 6 nights. Glucose tolerance was lower in the sleep-debt condition than in the fully rested condition (p<0.02), as were thyrotropin concentrations (p<0.01). Evening cortisol concentrations were raised (p=0.0001) and activity of the sympathetic nervous system was increased in the sleep-debt condition (p<0.02). Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.
The discovery of leptin has enhanced understanding of the interrelationship between adipose energy stores and neuronal circuits in the brain involved in energy balance and regulation of the neuroendocrine axis. Leptin levels are dependent on the status of fat stores as well as changes in energy balance as a result of fasting and overfeeding. Although leptin was initially thought to serve mainly as an anti-satiety hormone, recent studies have shown that it mediates the adaptation to fasting. Furthermore, leptin has been implicated in the regulation of the reproductive, thyroid, growth hormone, and adrenal axes, independent of its role in energy balance. Although it is widely known that leptin acts on hypothalamic neuronal targets to regulate energy balance and neuroendocrine function, the specific neuronal populations mediating leptin action on feeding behavior and autonomic and neuroendocrine function are not well understood. In this review, we have discussed how leptin engages arcuate hypothalamic neurons expressing putative orexigenic peptides, e.g., neuropeptide Y and agouti-regulated peptide, and anorexigenic peptides, e.g., pro-opiomelanocortin (precursor of alpha-melanocyte-stimulating hormone) and cocaine- and amphetamine-regulated transcript. We show that leptin's effects on energy balance and the neuroendocrine axis are mediated by projections to other hypothalamic nuclei, e.g., paraventricular, lateral, and perifornical areas, as well as other sites in the brainstem, spinal cord, and cortical and subcortical regions.
Leptin plays a vital role in the regulation of energy balance in rodent models of obesity. However, less information is available about its homeostatic role in humans. The aim of this study was to determine whether leptin serves as an indicator of short-term energy balance by measuring acute effects of small manipulations in energy intake on leptin levels in normal individuals. The 12-day study was composed of four consecutive dietary-treatment periods of 3 days each. Baseline (BASE) [100% total energy expenditure (TEE)] feeding, followed by random crossover periods of overfeeding (130% TEE) or underfeeding (70% TEE) separated by a eucaloric (100% TEE) washout (WASH) period. The study participants were six healthy, nonobese subjects. Leptin levels serially measured throughout the study period allowed a daily profile for each treatment period to be constructed and a 24-h average to be calculated; ad libitum intake during breakfast "buffet" following each treatment period was also measured. Average changes in mesor leptin levels during WASH, which were sensitive to energy balance effected during the prior period, were observed. After underfeeding, leptin levels during WASH were 88 +/- 16% of those during BASE compared with 135 +/- 22% following overfeeding (P = 0.03). Leptin levels did not return to BASE during WASH when intake returned to 100% TEE, but instead were restored (104 +/- 21% and 106 +/- 16%; not significant) only after subjects crossed-over to complementary dietary treatment that restored cumulative energy balance. Changes in ad libitum intake from BASE correlated with changes in leptin levels (r2 = 0.40; P = 0.01). Leptin levels are acutely responsive to modest changes in energy balance. Because leptin levels returned to BASE only after completion of a complementary feeding period and restoration of cumulative energy balance, leptin levels reflect short-term cumulative energy balance. Leptin seems to maintain cumulative energy balance by modulating energy intake.