The Metabolic Consequences of Sleep Deprivation
TL;DR: The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.
About: This article is published in Sleep Medicine Reviews.The article was published on 2007-06-01 and is currently open access. It has received 1211 citations till now. The article focuses on the topics: Diabetes risk & Sleep deprivation.
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TL;DR: This review aims to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings.
Abstract: Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.
1,964 citations
Cites background from "The Metabolic Consequences of Sleep..."
...Sleep has been proposed as serving an energy-saving function (82, 1311), the restoration of energy resources and the repairing of cell tissue (875), thermoregulation (973), metabolic regulation (651, 1229), and adaptive immune functions (695)....
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TL;DR: Both short and long duration of sleep are significant predictors of death in prospective population studies as well as sensitivity analyses and publication bias are assessed.
Abstract: Background: Increasing evidence suggests an association between both short and long duration of habitual sleep with adverse health outcomes.
Objectives: To assess whether the population longitudinal evidence supports the presence of a relationship between duration of sleep and all-cause mortality, to investigate both short and long sleep duration and to obtain an estimate of the risk.
Methods: We performed a systematic search of publications using MEDLINE (1966-2009), EMBASE (from 1980), the Cochrane Library, and manual searches without language restrictions. We included studies if they were prospective, had follow-up >3 years, had duration of sleep at baseline, and all-cause mortality prospectively. We extracted relative risks (RR) and 95% confidence intervals (CI) and pooled them using a random effect model. We carried out sensitivity analyses and assessed heterogeneity and publication bias.
Results: Overall, the 16 studies analyzed provided 27 independent cohort samples. They included 1,382,999 male and female participants (follow-up range 4 to 25 years), and 112,566 deaths. Sleep duration was assessed by questionnaire and outcome through death certification. In the pooled analysis, short duration of sleep was associated with a greater risk of death (RR: 1.12; 95% CI 1.06 to 1.18; P <0.01) with no evidence of publication bias (P = 0.74) but heterogeneity between studies (P = 0.02). Long duration of sleep was also associated with a greater risk of death (1.30; [1.22 to 1.38]; P < 0.0001) with no evidence of publication bias (P = 0.18) but significant heterogeneity between studies (P < 0.0001).
Conclusion: Both short and long duration of sleep are significant predictors of death in prospective population studies.
1,549 citations
TL;DR: Quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes and the mechanisms underlying this relation may differ between short and long sleepers.
Abstract: OBJECTIVE - To assess the relationship between habitual sleep disturbances and the incidence of type 2 diabetes and to obtain an estimate of the risk.
RESEARCH DESIGN AND METHODS - We conducted a systematic search of publications using MEDLINE (1955-April 2009), EMBASE, and the Cochrane Library and manual searches Without language restrictions. We included studies if they were prospective with follow-up >3 years and had an assessment of sleep disturbances at baseline and incidence of type 2 diabetes. We recorded several characteristics for each study. We extracted quantity and quality of sleep, how they were assessed, and incident cases defined with different validated methods. We extracted relative risks (RRs) and 95% Cl and pooled them using random-effects models. We performed sensitivity analysis and assessed heterogeneity and publication bias.
RESULTS - we included 10 Studies (13 independent cohort Samples; 107,756 male and female participants, follow-up range 4.2-32 years, and 3,586 incident cases Of type 2 diabetes). In pooled analyses, quantity and quality of sleep predicted the risk of development Of type 2 diabetes. For short duration of sleep (: 8-9 h/night), the RR was 1.48 (1.13-1.96, P = 0.005); for difficulty in initiating sleep, the RR was 1.57 (1.25-1.97, P < 0.0001); and for difficulty in maintaining sleep, the RR was 1.84 (1.39-2.43, P < 0.0001).
CONCLUSIONS - Quantity and quality of sleep consistently and significantly predict the risk Of the development Of type 2 diabetes. The mechanisms Underlying this relation may differ between short and long sleepers.
1,299 citations
Cites background from "The Metabolic Consequences of Sleep..."
...These in turn would increase appetite and caloric intake, reduce energy expenditure (3,4), and facilitate the development of obesity (4,6) and impaired glycemic control (36), increasing cardiovascular risk....
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...Lack of sleep exerts deleterious effects on a variety of systems with detectable changes in metabolic (3,4), endocrine (5,6), and immune pathways (7)....
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TL;DR: Investment in understanding migraine leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.
Abstract: Plaguing humans for more than two millennia, manifest on every continent studied, and with more than one billion patients having an attack in any year, migraine stands as the sixth most common cause of disability on the planet. The pathophysiology of migraine has emerged from a historical consideration of the "humors" through mid-20th century distraction of the now defunct Vascular Theory to a clear place as a neurological disorder. It could be said there are three questions: why, how, and when? Why: migraine is largely accepted to be an inherited tendency for the brain to lose control of its inputs. How: the now classical trigeminal durovascular afferent pathway has been explored in laboratory and clinic; interrogated with immunohistochemistry to functional brain imaging to offer a roadmap of the attack. When: migraine attacks emerge due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the first, premonitory, phase that precedes headache, brain stem and diencephalic systems modulating afferent signals, light-photophobia or sound-phonophobia, begin to dysfunction and eventually to evolve to the pain phase and with time the resolution or postdromal phase. Understanding the biology of migraine through careful bench-based research has led to major classes of therapeutics being identified: triptans, serotonin 5-HT1B/1D receptor agonists; gepants, calcitonin gene-related peptide (CGRP) receptor antagonists; ditans, 5-HT1F receptor agonists, CGRP mechanisms monoclonal antibodies; and glurants, mGlu5 modulators; with the promise of more to come. Investment in understanding migraine has been very successful and leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.
1,036 citations
Cites background from "The Metabolic Consequences of Sleep..."
...While sleep can be affected by changes in energy homeostasis, changes in sleep patterns can likewise disturb endocrine regulation of energy homeostasis (475)....
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TL;DR: It is proposed that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms.
Abstract: Sleep and circadian rhythm disruption are frequently observed in patients with psychiatric disorders and neurodegenerative disease. The abnormal sleep that is experienced by these patients is largely assumed to be the product of medication or some other influence that is not well defined. However, normal brain function and the generation of sleep are linked by common neurotransmitter systems and regulatory pathways. Disruption of sleep alters sleep-wake timing, destabilizes physiology and promotes a range of pathologies (from cognitive to metabolic defects) that are rarely considered to be associated with abnormal sleep. We propose that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms. The stabilization of sleep may be a means by which to reduce the symptoms of--and permit early intervention of--psychiatric and neurodegenerative disease.
864 citations
References
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TL;DR: The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.
Abstract: Despite the prevalence of sleep complaints among psychiatric patients, few questionnaires have been specifically designed to measure sleep quality in clinical populations. The Pittsburgh Sleep Quality Index (PSQI) is a self-rated questionnaire which assesses sleep quality and disturbances over a 1-month time interval. Nineteen individual items generate seven "component" scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. The sum of scores for these seven components yields one global score. Clinical and clinimetric properties of the PSQI were assessed over an 18-month period with "good" sleepers (healthy subjects, n = 52) and "poor" sleepers (depressed patients, n = 54; sleep-disorder patients, n = 62). Acceptable measures of internal homogeneity, consistency (test-retest reliability), and validity were obtained. A global PSQI score greater than 5 yielded a diagnostic sensitivity of 89.6% and specificity of 86.5% (kappa = 0.75, p less than 0.001) in distinguishing good and poor sleepers. The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.
23,155 citations
TL;DR: Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.
3,322 citations
TL;DR: The prevalence of obesity and diabetes continues to increase among US adults, and interventions are needed to improve physical activity and diet in communities nationwide.
Abstract: ContextRecent reports show that obesity and diabetes have increased in the
United States in the past decade.ObjectiveTo estimate the prevalence of obesity, diabetes, and use of weight control
strategies among US adults in 2000.Design, Setting, and ParticipantsThe Behavioral Risk Factor Surveillance System, a random-digit telephone
survey conducted in all states in 2000, with 184 450 adults aged 18 years
or older.Main Outcome MeasuresBody mass index (BMI), calculated from self-reported weight and height;
self-reported diabetes; prevalence of weight loss or maintenance attempts;
and weight control strategies used.ResultsIn 2000, the prevalence of obesity (BMI ≥30 kg/m2) was
19.8%, the prevalence of diabetes was 7.3%, and the prevalence of both combined
was 2.9%. Mississippi had the highest rates of obesity (24.3%) and of diabetes
(8.8%); Colorado had the lowest rate of obesity (13.8%); and Alaska had the
lowest rate of diabetes (4.4%). Twenty-seven percent of US adults did not
engage in any physical activity, and another 28.2% were not regularly active.
Only 24.4% of US adults consumed fruits and vegetables 5 or more times daily.
Among obese participants who had had a routine checkup during the past year,
42.8% had been advised by a health care professional to lose weight. Among
participants trying to lose or maintain weight, 17.5% were following recommendations
to eat fewer calories and increase physical activity to more than 150 min/wk.ConclusionsThe prevalence of obesity and diabetes continues to increase among US
adults. Interventions are needed to improve physical activity and diet in
communities nationwide.
2,779 citations
TL;DR: In this study, 12 young, healthy, normal-weight men exhibited reductions in the satiety hormone leptin, increases in the hunger hormone ghrelin, and increases in hunger after 2 nights of only 4 hours of sleep compared with after two nights of 10 hours ofSleep, suggesting inadequate sleep seems to influence the hormones that regulate satiety and hunger.
Abstract: Sleep-deprived healthy persons experience increased hunger. They also have increased blood levels of leptin and decreased levels of ghrelin (hormones that regulate satiety and hunger). These hormon...
2,178 citations
TL;DR: Differences in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration, and changes in appetite regulatory hormones with sleep curtailment may contribute to obesity.
Abstract: Background Sleep duration may be an important regulator of body weight and metabolism. An association between short habitual sleep time and increased body mass index (BMI) has been reported in large population samples. The potential role of metabolic hormones in this association is unknown. Methods and Findings Study participants were 1,024 volunteers from the Wisconsin Sleep Cohort Study, a population-based longitudinal study of sleep disorders. Participants underwent nocturnal polysomnography and reported on their sleep habits through questionnaires and sleep diaries. Following polysomnography, morning, fasted blood samples were evaluated for serum leptin and ghrelin (two key opposing hormones in appetite regulation), adiponectin, insulin, glucose, and lipid profile. Relationships among these measures, BMI, and sleep duration (habitual and immediately prior to blood sampling) were examined using multiple variable regressions with control for confounding factors. A U-shaped curvilinear association between sleep duration and BMI was observed. In persons sleeping less than 8 h (74.4% of the sample), increased BMI was proportional to decreased sleep. Short sleep was associated with low leptin (p for slope = 0.01), with a predicted 15.5% lower leptin for habitual sleep of 5 h versus 8 h, and high ghrelin (p for slope = 0.008), with a predicted 14.9% higher ghrelin for nocturnal (polysomnographic) sleep of 5 h versus 8 h, independent of BMI.
2,111 citations