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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
study.
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
2
).
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%;
P
0.04),
elevations in the orexigenic factor ghrelin (increase, 28%;
P
<
0.04), and increased hunger (increase, 24%;
P
<0.01) and appe-
tite (increase, 23%;
P
0.01), especially for calorie-dense foods
with high carbohydrate content (increase, 33% to 45%;
P
0.02).
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. www.annals.org
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.
METHODS
Participants
Twelve healthy men (mean age [SD], 22 2 years];
mean body mass index [SD], 23.6 2.0 kg/m
2
) 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
Article
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).
Assays
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.
RESULTS
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
Context
Studies in animals and humans suggest that sleep duration
is an important regulator of metabolism.
Contribution
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.
Implications
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
www.annals.org 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.
DISCUSSION
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 www.annals.org
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,
20).
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
obesity.
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-
00055).
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
10hinBed
(
n
12)
Ratings for
4hinBed
(
n
12)
P
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
www.annals.org 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11 849
Current author addresses and author contributions are available at www
.annals.org.
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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 www.annals.org
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
60637.
Author Contributions: Conception and design: K. Spiegel, E. Van Cau-
ter.
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
Cauter.
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.
www.annals.org 7 December 2004 Annals of Internal Medicine Volume 141 • Number 11 W-157
... Ao avaliarmos os militares de acordo com a quantidade de sono, encontramos diferenças entre os militares no IMC e na CC, demonstrando maior probabilidade de risco para os militares que dormem menos que 7 horas por noite. Alguns estudos já observaram que a redução do sono está associada a dois comportamentos endócrinos capazes de alterar a ingestão alimentar como a diminuição do hormônio anorexígeno leptina (Taheri et al., 2004;Mullington et al., 2003;Spiegel et al., 2003;Spiegel et al., 2004b) e o aumento do hormônio anorexígeno grelina (Spiegel et al., 2004;Taheri et al., 2004;Bodosi et al., 2004), resultando, assim, no aumento da fome e da ingestão alimentar (Spiegel et al., 2004). Flier, (2004 apontou que alterações do sono promove efeito no apetite devido a ação da leptina e da grelina devido envolvimento de circuitos neurais de centros hipotalâmicos que liberam neuropeptídeos e receptores que têm papéis importantes na homeostase da massa corporal. ...
... Ao avaliarmos os militares de acordo com a quantidade de sono, encontramos diferenças entre os militares no IMC e na CC, demonstrando maior probabilidade de risco para os militares que dormem menos que 7 horas por noite. Alguns estudos já observaram que a redução do sono está associada a dois comportamentos endócrinos capazes de alterar a ingestão alimentar como a diminuição do hormônio anorexígeno leptina (Taheri et al., 2004;Mullington et al., 2003;Spiegel et al., 2003;Spiegel et al., 2004b) e o aumento do hormônio anorexígeno grelina (Spiegel et al., 2004;Taheri et al., 2004;Bodosi et al., 2004), resultando, assim, no aumento da fome e da ingestão alimentar (Spiegel et al., 2004). Flier, (2004 apontou que alterações do sono promove efeito no apetite devido a ação da leptina e da grelina devido envolvimento de circuitos neurais de centros hipotalâmicos que liberam neuropeptídeos e receptores que têm papéis importantes na homeostase da massa corporal. ...
... Adicionalmente, é possível considera que a diminuição dos níveis de leptina após a restrição de sono seja uma adaptação do aumento da necessidade calórica pelo aumento do tempo de vigília (Spiegel et al., 2004c) bem como uma associação negativa entre as mudanças nos níveis da leptina e do cortisol (envolvido no aumento do estresse) é bem documentada na literatura durante a restrição de sono, e pode indicar um efeito supressivo da leptina no eixo hipotálamopituitária-adrenal (Flier, 2004;Wauters et al., 2000). Em relação a grelina evidências mostram que os níveis da grelina são maiores em indivíduos com restrição de sono, em comparação aos com adequação do sono (Spiegel et al., 2004;Taheri et al., 2004). Spiegel et al., (2004) demonstraram que restrição do sono de 4 horas por um período de 2 dias foi associado com um aumento aproximadamente 28% dos níveis diurnos da grelina. ...
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Introdução: a análise do sono de militares ainda é pouco compreendida, principalmente pelas características das atividades laborais dos agentes de segurança pública pertencentes a grupos de operações especiais. Objetivo: o objetivo deste estudo foi avaliar e associar indicadores antropométricos, nível de atividade física e horas de sono de policiais militares da Companhia de Operações de Choque do Batalhão de Missões Especiais do Espírito Santo (BME-ES). Métodos: 61 policiais militares foram distribuídos em dois grupos de acordo com o número de horas de sono, sendo suficiente (S, n:20) e insuficiente (I, n:41). Foram avaliados percepção geral de saúde, indicadores ocupacionais e tempo de atividade física semanal. Resultados: Não foram encontradas diferenças na idade e no tempo de serviço entre os militares. O número de horas de sono diferiu (p<0,001) entre os grupos I (5,46±0,9) e S (7,70±0,4). Foram encontradas diferenças significativas (p<0,05) entre os grupos na massa corporal, IMC, % de gordura, massa gorda e circunferência da cintura, mas não na massa magra e atividade física. Correlação negativa fraca entre horas de sono e percentual de gordura e massa gorda. Conclusão: a maioria dos militares apresentou boa percepção geral dos indicadores de saúde, com alta prevalência de atividade física mesmo com excesso de peso e distribuição moderada de gordura corporal. Palavras-chave: segurança pública, polícia militar, atividade física, antropometria
... As discussed above, OSA and obesity are associated with high levels of leptin, several studies have found that short sleep duration is associated with decreased levels of leptin and increased levels of ghrelin. [26] Spiegel et al. [27] reported that a 2-day sleep restriction is associated with an 18% reduction in circulating leptin and a 28% elevation in ghrelin, concomitant with an increase in appetite. Although Nedeltcheva et al. [28] found no significant differences in serum leptin and ghrelin after sleep restriction, as did Spiegel et al., they did report increased appetite for high-calorie and highcarbohydrate foods in the sleep-deprived subjects. ...
... In a study of sleep restriction, Spiegel et al. [27] concluded that sleep modulates the neuroendocrine control of appetite, reporting a decrease in mean and maximal levels as well as in the rhythm amplitude of leptin (−19%, −26%, and −20%, respectively), concomitant with SNS activation, during sleep restriction compared with sleep extension. This finding may be at least partially explained by the stressful effect of sleep restriction that activates the SNS, which, in turn, inhibits plasma leptin secretion by adipocytes. ...
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Diabetes mellitus (DM) is the most prevalent endocrine disorder globally. DM is under-evaluated and less efficiently managed in terms of ruling out comorbid conditions associated with it and predisposing factors resulting in poor outcomes. Sleep disorders are more common than usually diagnosed due to less awareness in the community regarding the importance of timely diagnosis and the impact of interventions related to proper sleep hygiene and sleep structure. Obstructive sleep apnea (OSA) is independently associated with cardiovascular and cardiometabolic risk in several large epidemiological studies. OSA leads to several physiological disturbances, such as intermittent hypoxia, sleep fragmentation, and an increase in autonomic tone. Metabolic syndrome (MS) is an adverse outcome that is typically associated with obesity. It is a cluster of metabolic risk factors for type 2 DM (T2DM) and cardiovascular diseases (CVDs), including central obesity, hypertension, hyperglycemia, insulin resistance, and dyslipidemia. T2DM is often associated with OSA, and a bidirectional relationship may exist between the two diseases, mediated by both weight-and physiology-dependent mechanisms. OSA is highly associated with T2DM, and treatment of OSA may have a positive impact on the cardiometabolic profile. In this review, we have attempted to summarize the impact of sleep disorders on MS and DM, and vice versa, with special emphasis on newer medical options in the management of DM and cardiometabolic syndrome.
... Sleep aff ects many processes in the body including immune system function, energy metabolism, learning, memory, appetite regulation and gene expression (9)(10)(11)(12)(13)(14). Gais et al. suggest that sleep enhances creativity by facilitating mental restructuring that is critical to insight (15). ...
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Recent studies on children with cerebral palsy indicate that this population is at a higher risk of sleep disorders. Although sleep dysfunction seems to be frequent in cerebral palsy, there are few studies assessing sleep dysfunction and its risk in children. Also, the prevalence of sleep apnea has not been formally assessed in children with cerebral palsy. Risk factors for sleep dysfunction include comorbid epilepsy, mental retardation, visual impairment and degree of functional motor impairment. Contractures and spasticity can adversely contribute to positioning during sleep. We analyzed motor, cognitive and functional impairment, as well as the existence of comorbidity and results of brain imaging and electroencephalography in 21 children with cerebral palsy and correlated them with the presence of sleep disorders. Sleep disorder was evaluated by electroencephalography/polysomnography. About 57% of children in our study had sleep disorders. The most common motor impairment was spastic diplegia. Most children had peri ventricular hyperintensities and cortical atrophy on neuroimaging. Diffi culty in initiating and maintaining sleep (microarousals), fragmented sleep, and sleep breathing disorders were frequently identifi ed problems and were evaluated by polysomnography. Children with abnormal electroencephalography had more sleep disturbances than those with normal electroencephalography. Disorders of initiation and maintenance of sleep were more frequent in children with spastic quadriplegia. It is known that the consequences of sleep disorders in children aff ect both the child and the family. Prospective studies in a larger sample and proper methodology are needed to determine whether improvement in sleep quality of children with cerebral palsy leads to improvement in their life quality.
... Short sleep duration may lead to hyperactivity of the sympathetic nerve, an increased inflammatory reaction and oxidative stress, and damage the activity of the coagulation system, thus increasing the risk of PVD (92-94). Short sleep time may also change the circulating levels of leptin and ghrelin (95,96), thus increasing the risk of obesity (96,97) by increasing appetite and calorie intake and reducing energy consumption (97,98), leading to hypertension (99), impaired glycemic control (100), and endothelial dysfunction (101), and thus increasing the risk of PVD. Moreover, results from various metaanalyses have indicated a link between a shorter sleep duration and an increased risk of several health conditions, such as obesity, hypertension, and type 2 diabetes. ...
... Importantly, these health behaviors are interrelated. Insufficient sleep is associated with decreased leptin and elevated ghrelin levels, which can cue increased food intake (Spiegel et al., 2004). Decreased sleep is also associated with greater intake of processed foods and high-sugar refined foods (Godos et al., 2021) and less physical activity (Mead et al., 2019;Semplonius & Willoughby, 2018). ...
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... Two meta-analyses have shown that leptin and ghrelin were not affected by sleep restriction (Capers et al., 2015;Zhu et al., 2019), despite increases in subjective hunger and caloric intake (Zhu et al., 2019). Several controlled laboratory studies in small groups of healthy young participants showed that short-term sleep restriction (one to six nights of 4 hours) led to decreased insulin sensitivity and impaired glucose tolerance symptomatic of a pre-diabetic state (Donga et al., 2010;Reynolds et al., 2012;Schmid et al., 2011;Spiegel et al., 1999Spiegel et al., , 2004Van Leeuwen et al., 2010;Zhu et al., 2019). ...
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... Further, workers in rotating shift work (especially women, who report greater levels of time spent on household activities) report the most difficulties in managing work-home conflict (Gignac et al., 2012). Sleep deficiency is associated with obesity and chronic diseases (Buxton & Marcelli, 2010;Cappuccio et al., 2010;McAllister et al., 2009), and early death (Grandner et al., 2010;Wingard & Berkman, 1983), with some probable mechanisms including impacts on hormones, metabolism, food cravings, and calorie consumption (Brondel et al., 2010;Buxton et al., 2012;Greer et al., 2013;McAllister et al., 2009;Spiegel et al., 2004). Interestingly, there is increasing evidence that the timing of what we eat matters, especially relative to our biological clock time, which is largely driven by light exposure. ...
... For example, a study by the University of Pittsburgh found that sleep-deprived people are more likely to experience symptoms of depression. [37] Increased risk of suicide: Sleep deprivation has been linked to an increased risk of suicide. For example, a study by the University of Pennsylvania found that people who are sleep-deprived are more likely to attempt suicide. ...
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Social networking sites (SNSs) are virtual spaces where users can connect with others based on shared interests, create public profiles, and interact with real-life friends. They offer a variety of benefits, such as access to academic resources, learning opportunities, entertainment, social connection, news and information, and networking opportunities. However, SNSs can also have harmful effects, such as addiction, cyberbullying, body image issues, reduced productivity, and increased risk of depression.Ayurveda considers sleep (nidra) to be one of the three pillars of health, along with diet (ahara) and exercise (vyayama). Nidra is essential for physical and mental well-being. It helps to restore the body's energy, improve cognitive function, and boost the immune system. There are four types of nidra: tamasika, swabhaviki, vaikarika, and kalaswabhavaj. The physiology of sleep is explained by four theories: tamoguna theory, kapha dosha theory, depression theory, and svabhava theory.The text provides a comprehensive overview of social networking and sleep in the context of Ayurveda. It discusses the benefits and harmful effects of SNSs, as well as the importance of nidra for physical and mental health. The text also provides an overview of the four theories that explain the physiology of sleep.
... Evidence indicates that short sleep duration is associated with enhanced sympathetic activity [33], a well-known crucial factor for high blood pressure [34], while also inhibits leptin release, contributing to the central regulation of food intake [35]. Indeed, sleep deficit or deprivation is linked to reduced leptin and increased ghrelin levels, which control body weight and resulting in obesity [36,37]. Considering the global increase in short sleep duration and obesity among adolescents, which poses a growing public health concern, further research is needed to investigate the role of chronic short sleep as a previously unrecognized risk factor for subsequent development of obesity and its contribution to hypertension. ...
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Prevalence of hypertension in adolescents has increased worldwide and is considered a risk factor for hypertension and cardiovascular disease in adulthood. Although obesity and sleep deficiency increase this risk, the combined effects of these factors on hypertension remain unclear. This study aimed to examine the combined effects of obesity and sleep duration on hypertension in adolescents. This study was conducted using data from the 2016 to 2018 Korean National Health and Nutrition Examination Survey, which included a study population of 1272 adolescents. The participants were categorized into four groups based on sleep duration and body mass index (BMI) percentiles: normal sleep and normal body mass group (reference; normal), only short sleep group (short sleep), only overweight/obesity group (overweight/obesity), and short sleep and overweight/obesity group (short sleep and overweight/obesity). Short sleep duration was defined as <8 h of average sleep duration, and overweight/obesity was defined as a BMI ≥ 85th percentile. Hypertension in adolescents was defined as a systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥80 mmHg. The prevalence of hypertension was 9.2% among Korean adolescents. Short sleep duration with overweight/obesity were associated with a significantly increased risk of hypertension (odds ratio = 6.57; 95% confidence interval: 3.27–13.20) in adolescents, and controlling for the potential confounding variables only partially attenuated this relationship (odds ratio = 5.28; 95% confidence interval: 2.28–12.26). This study demonstrated that the coexistence of short sleep duration and obesity was associated with an increased risk of hypertension in Korean adolescents.
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Introduction: Obesity and overweight are major global health challenges. One of the bad effects of noise that has been recently expressed is the effect of noise on obesity. This study aimed to investigate the effect of high-frequency noise exposure on obesity, food intake, and abdominal visceral fat in adult male guinea pigs. Material and Methods: The animals in this study were 24 adult male guinea pigs randomly divided into 3 groups (control and two case groups). Each case group was separately exposed to high-frequency white noise with sound pressure levels in 65 dB and 85 dB for 5 days per week in 30 days. The food intake was measured daily. The weight of animals was measured at the start and on days 6, 12, 18, 24, and at the end of exposure period. The abdominal visceral fat was extracted and weighted at the end of the study period. The data were assessed using SPSS V.22 software. Results: ANOVA analysis showed that exposure to high-frequency noise at 65dB and 85dB had a significant effect on weight gain, food intake, and abdominal visceral fat weight (P-value< 0.05) which in the group exposed to the noise with 65 dB was more than other groups. Conclusion: Based on this study, exposure to high-frequency noise may be an effective factor in obesity and increasing abdominal visceral fat. Further studies are needed to investigate the mechanism affecting weight status following noise exposure.
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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.
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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.
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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.
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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.
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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.