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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
... Some of them have reported that short sleep duration was significantly associated with the risk of MetS 52-56 , while conversely several studies showed that long sleep duration was associated with MetS 57,58 . Furthermore, some studies have reported a U-shaped association between sleep duration and MetS as both short and long sleeping hours were associated with the risk of MetS 58 [61][62][63] , sleep restriction can reduce leptin and increase ghrelin levels, leading to increased hunger and appetite specifically for carbohydrate-dense food 63 . The deficiency in melatonin secretion, as in shift-work associated with reductions in blood melatonin levels 64 .Recent studies indicates that melatonin has potential benefits for cardiovascular health and metabolic syndrome by influencing on blood pressure regulation, lipid metabolism, and glucose homeostasis 64,65 . ...
... Some of them have reported that short sleep duration was significantly associated with the risk of MetS 52-56 , while conversely several studies showed that long sleep duration was associated with MetS 57,58 . Furthermore, some studies have reported a U-shaped association between sleep duration and MetS as both short and long sleeping hours were associated with the risk of MetS 58 [61][62][63] , sleep restriction can reduce leptin and increase ghrelin levels, leading to increased hunger and appetite specifically for carbohydrate-dense food 63 . The deficiency in melatonin secretion, as in shift-work associated with reductions in blood melatonin levels 64 .Recent studies indicates that melatonin has potential benefits for cardiovascular health and metabolic syndrome by influencing on blood pressure regulation, lipid metabolism, and glucose homeostasis 64,65 . ...
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... Spiegel ve ark. kısa vadeli uyku kısıtlanmasının Leptin ve Ghrelin gibi iştah metabolizmasında önemli bazı hormonların değişimini de beraberinde getirdiğini göstermiştir (37). Yapılan başka bir çalışmaya göre ise uyku süresindeki her 1 saatlik azalmanın obezite riskinde %24'lük artışa neden olduğu saptanmıştır (35). ...
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Amaç: Bu çalışmada Toros Üniversitesi’nde öğrenim gören öğrencilerin depresyon, beslenme durumları ve bazı antropometrik özellikleri ile uyku kaliteleri arasındaki ilişkilerin değerlendirilmesi amaçlanmıştır. Gereç ve Yöntemler: Çalışma Kasım-Aralık 2022 tarihleri arasında Toros Üniversitesi Sağlık Bilimleri Fakültesi’nde okuyan 200 öğrenci ile gerçekleştirilmiştir. Çalışmaya dahil edilme kriterleri 19-40 yaş arası ve çalışmaya gönüllü katılım sağlamış olmaları iken gebe ve emzikliler, kronik hastalığı olanlar, herhangi ilaç, vitamin-mineral ve besin desteği kullanan ve yeme davranış bozukluğu olan öğrenciler çalışma dışında bırakılmışlardır. Çalışmada öğrencilerle yapılan yüz yüze görüşmelerde öğrencilerin; tanımlayıcı özellikleri (yaş, cinsiyet, medeni durum, çalışma durumu, beslenme alışkanlıkları ve fiziksel aktivite kayıtları) sorgulanırken, genel ve santral obezite durumlarının değerlendirilmesi için bazı antropometrik ölçümleri (vücut ağırlığı, boy uzunluğu, bel ve kalça çevresi ölçümleri) ve beslenme durumlarının değerlendirebilmesi içinde 24 saatlik besin tüketim kayıtları alınmıştır. Ayrıca öğrencilerin uyku kalitelerini değerlendirebilmesi için Pittsburgh Uyku Kalite Ölçeği (PUKİ), depresyon durum ve şiddetini saptanabilmesi için de Beck Depresyon Ölçeği (BDÖ) uygulanmıştır. Bulgular: Çalışmada kötü uyku kalitesine sahip olan öğrencilerin vücut ağırlıkları uyku kalitesi iyi olan öğrencilere göre anlamlı düzeyde daha fazla olduğu bulunurken, vücut ağırlığındaki bir birimlik artışın uyku kalitesinin iyi olma düzeyini %3.6 oranında azalttığı saptanmıştır (p
... Dallman suggests that stress reduces the individual's response and cognitive level, stimulating the production of glucocorticoids and insulin, thereby increasing food intake and leading to undesired weight gain [45]. Besides, excessive stress has been associated with poor sleep and changes in serum leptin and ghrelin levels, leading to increased hunger and appetite [46]. Air pollution may thus exacerbate this process as it directly increases the risk of overweight and indirectly affects the individual's psychological health [47]. ...
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Abstract Background Overweight is a known risk factor for various chronic diseases and poses a significant threat to middle-aged and elderly adults. Previous studies have reported a strong association between overweight and air pollution. However, the spatial relationship between the two remains unclear due to the confounding effects of spatial heterogeneity. Methods We gathered height and weight data from the 2015 China Health and Retirement Long-term Survey (CHARLS), comprising 16,171 middle-aged and elderly individuals. We also collected regional air pollution data. We then analyzed the spatial pattern of overweight prevalence using Moran's I and Getis-Ord Gi* statistics. To quantify the explanatory power of distinct air pollutants for spatial differences in overweight prevalence across Southern and Northern China, as well as across different age groups, we utilized Geodetector's q-statistic. Results The average prevalence of overweight among middle-aged and elderly individuals in each city was 67.27% and 57.39%, respectively. In general, the q-statistic in southern China was higher than that in northern China. In the north, the prevalence was significantly higher at 54.86% compared to the prevalence of 38.75% in the south. SO2 exhibited a relatively higher q-statistic in middle-aged individuals in both the north and south, while for the elderly in the south, NO2 was the most crucial factor (q = 0.24, p
... In older adults, sleep fragmentation is associated with all-cause mortality due to the aforementioned immune system and inflammation outcomes of sleep loss as well as sleep's relationship with obesity and cardiovascular disease (Smagula et al., 2016). In the United States, the prevalence of obesity is 41.9% (Centers for Disease Control and Prevention, 2022), and obesity is crosssectionally related to sleep loss via a decrease in leptin and increase in ghrelin, as well as an increased risk for type II diabetes and impaired glucose tolerance Spiegel et al., 2004). Weight loss can improve sleep quality and quantity, as well as decrease inflammation and improve overall physical health (Romero-Corral et al., 2010). ...
... A convincing body of literature reported that visceral adiposity may dispose towards OSA, and this situation could be reversed by weight loss [63]. Factors like physical activity and reduction of high caloric diet especially refined carbohydrates should be promoted in order to minimize obesity induced OSA [64]. ...
... Te correlation across three diferent unhealthy behaviors (smoking, sleeping <7 hours, and no leisure-time physical activity) suggests that unhealthy behaviors tend to cluster. Tere are also known pathophysiologic pathways for obesity with, for example, poor sleep through decreased leptin, increased ghrelin, and other mediators (glucagon-like peptide-1 and peptide YY) [4,45,46]. Journal of Obesity ...
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Introduction. Limited access to healthy food in areas that are predominantly food deserts or food swamps may be associated with obesity. Other unhealthy behaviors may also be associated with obesity and poor food environments. Methods. We calculated Modified Retail Food Environment Index (mRFEI) to assess food retailers. Using data collected from the Behavioral Risk Factor Surveillance System (BRFSS) survey, the NJ Department of Health (NJDOH), and the US Census Bureau, we conducted a cross-sectional analysis of the interaction of obesity with the food environment and assessed smoking, leisure-time physical activity (LPA), and poor sleep. Results. There were 17.9% food deserts and 9.3% food swamps in NJ. There was a statistically significant negative correlation between mRFEI and obesity rate (Pearson’s r −0.13, p < 0.001 ), suggesting that lack of access to healthy food is associated with obesity. Regression analysis was significantly and independently associated with increased obesity prevalence (adjusted R square 0.74 and p = 0.008 ). Obesity correlated positively with unhealthy behaviors. Each unhealthy behavior was negatively correlated with mRFEI. The mean prevalence for smoking, LPA, and sleep <7 hours was 15.4 (12.5–18.6), 26.5 (22.5–32.3), and 37.3 (34.9–40.4), respectively. Conclusion. Obesity tracks with food deserts and especially food swamps. It is also correlated with other unhealthy behaviors (smoking, LPA, and poor sleep).
... There are evidences suggesting that sleep is a major component in cognition [14], learning and memory consolidation [15], well-being [16] cell growth and repair [17], glucose metabolism leptin [18] and ghrelin secretion [19] and immune system function [20]. Apparently, improved quality of sleep in athletes is of utmost importance for recovery and energy conservation objectives [21]. ...
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Background: The COVID-19 pandemic is global pandemic leading to home confinement all over the world. Aim: the purpose of this study was to compare lifestyle of vaccinated versus unvaccinated international elite athletes during the covid-19 pandemic. Methods: An online survey was conducted from March to October 2021. The questionnaires were including Socio-individual information of athletes, International Physical Activity Questionnaire IPAQ, Rapid Eating Assessment for Participants (REAP-S) and Petersburg Sleep Quality Questionnaire (PSQI). 581 Elite athlete in the range of 18-35 years from 4 continents (Europe, Asia, Africa and America) and different countries were recruited voluntarily. Results: The results indicated that there was a significant difference between the level of physical activity and eating behavior of vaccinated versus unvaccinated elite athletes (p<0.001). However, no significant difference was found between quality of sleep among vaccinated and unvaccinated elite athletes (p=0.270). Conclusion: It was shown that in spite of unvaccinated status of some elite athletes (49.9%), their physical activity levels were more than that of vaccinated elite athletes during the covid-19 pandemic. Additionally, eating behavior of vaccinated elite athletes was better than that of unvaccinated elite athletes during the covid-19 pandemic; however, quality of sleep was not significantly different in the groups. Keywords Covid-19 elite athlete vaccination
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Introducción. La prevalencia del sobrepeso, obesidad y la somnolencia se incrementan cada vez más en la población joven mexicana, sin embargo, esta relación ha sido escasamente estudiada en universitarios, por lo que, el objetivo de este estudio fue analizar la relación del Índice de Masa Corporal (IMC) con la somnolencia en una población estudiantil de pregrado en Tabasco, México. Metodología. Se realizó un estudio transversal analítico en 155 estudiantes, determinándose en ellos el IMC, mientras que la somnolencia se evaluó mediante la Escala de Somnolencia Epworth (ESE). Los datos obtenidos se analizaron de manera independiente y fueron conjuntados para poder analizar la posible relación entre ellos. La validez estadística de este estudio se obtuvo a través de análisis desarrollados en el software SPSS statistics versión 21. Resultados. El 69,7% de la población estudiada la conformaron los hombres. La presencia de sobrepeso y obesidad se presentó en casi la mitad de la población con el 41,2%, siendo el grupo de las mujeres quienes presentan medias del IMC mayores en comparación con los hombres [media 25,9 kg/m2 (DE: 4,7) vs media 24,1kg/m2 (DE: 3,9)] p<0,01). Con la ESE se pudo observar que el 37,4% de los estudiantes presentan algún tipo de somnolencia, siendo el grupo de los hombres el que se observó con mayores afectaciones. En cuanto al análisis del IMC con la somnolencia se mostró una p=0,00 con nivel de confianza del 95% que confirma una relación entre estos factores, con un coeficiente de correlación bajo. Conclusión. El grado de IMC tiende aumentar el nivel de somnolencia.
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هدفت هذه الحروف الأدبية إلى استعراض أهم المرجعيات العلمية التي تناولت التأثيرات الحيوية لقلة النوم وجودته على الكتلة الجسمية في صورة البدانة كجائحة عالمية لدى فئات الأطفال، بما في ذلك المراهقين. فمن خلال (74) مرجع علمي مجمع، تم الخروج برأي علمي مفاده أن تأثير النوم على البدانة يخضع في الأساس إلى جملة من المسارات الحيوية المتداخلة؛ أين يمتد ذلك بين الطاقة المتناولة إلى الأكل المضطرب والخمول الحركي والبدني. وقد برر ذلك بأن مدة النوم أكثر أهمية للمشاكل والاضطرابات النفسية عن جودة النوم من أجل التسبب بالمشاكل البدنية. كما وجد له دور مباشر من أجل هرمونات الجوع والشبع بما قد يدفع الطفل إلى تفضيل الطعام الغني بالسكريات. ومن أجل ذلك يقرح المؤلفان جملة من المقترحات المهمة ذات الصلة في آخر الدراسة. These literary letters aimed to present the most important scientific backgrounds that dealt with the biological effects of lack of sleep and its quality on body mass in the form of obesity as a global epidemic among groups of children, including adolescents. Through (74) scientific references collected, a scientific opinion has been reached that the effect of sleep on obesity is mainly governed by a set of overlapping biological pathways. Where does that lie between energy intake, disordered eating, and lack of physical activity. This was justified by the fact that the duration of sleep is more important for mental problems and disorders than the quality of sleep in order to cause physical problems. It also found a direct role for the hunger and satiety hormones that may lead a child to prefer foods rich in sugar. For this, the authors make a number of important and relevant proposals.
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.