Metabolic consequences of sleep and sleep loss
Open accessAbstract
Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health.
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How much television people watch and how long they sleep might affect energy intake, energy output, or both.
“In addition, the duration of television viewing and of sleep may influence energy consumption, energy expenditure, or both.15–19”
From Changes in diet and lifestyle and long-term weight gain in women and men (2011) · cites this paper as [19]
In short-term trials, reduced sleep alters leptin, ghrelin, subjective hunger, and preferences for calorie-dense, refined-carbohydrate foods.
“In short-term trials, reduced sleep alters leptin, ghrelin, subjective hunger, and preferences for calorie-dense, refined-carbohydrate foods.19”
From Changes in diet and lifestyle and long-term weight gain in women and men (2011) · cites this paper as [19]
Decreases in sleep duration are concordant with the U.S. obesity epidemic.
“Decreases in sleep duration are concordant with the U.S. obesity epidemic.18,19,53”
From Changes in diet and lifestyle and long-term weight gain in women and men (2011) · cites this paper as [19]
Insufficient sleep duration is associated with weight gain and obesity.
“short sleep duration (6 hours or less), and especially very short sleep duration (less than 5 hours) is associated with increased cardiometabolic morbidity and mortality, including weight gain and obesity, hypertension, hyperlipidemia, and diabetes.”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [28]
Insufficient sleep is linked to lower energy expenditure, altered glucose homeostasis, and alterations in hormones that mediate hunger.
“insufficient sleep has been linked to lower energy expenditure, altered glucose homeostasis and alterations in hormones that mediate hunger(24, 25, 27-31).”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [28]
Physiologic studies show that sleep loss can influence metabolism through changes in metabolic hormones, adipocyte function, and beta-cell function.
“Physiologic studies also show that sleep loss can influence metabolism through changes in metabolic hormones,60,61 adipocyte function,62 and beta-cell function.63”
From Sleep, Health, and Society (2017) · cites this paper as [60]
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- Authors
- Van Cauter, E., Spiegel, K., Tasali, E., & Leproult, R.
- Affiliations
- Lyon 1 Université (FR)
- University of Chicago (US)
- Venue
- Sleep Medicine
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 9
- Pages
- S23-S28
- ISSN
- 1389-9457 (ISSN-L)
- PMC
- PMC4444051
- OpenAlex
- W2013252791
- Cited by
- 812
- References
- 48
- Citations by year
- 2026: 37 · 2025: 53 · 2024: 54 · 2023: 54 · 2022: 62 · 2021: 56 · 2020: 56 · 2019: 49 · 2018: 52 · 2017: 46 · 2016: 39 · 2015: 46 · 2014: 51 · 2013: 48 · 2012: 42
- FWCI
- 11.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Sleep Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (P01-AG11412., P01AG011412)
- National Heart, Lung, and Blood Institute (R01HL075079)
- National Institute of Diabetes and Digestive and Kidney Diseases (P60DK20595, P60DK020595)
- National Center for Research Resources (P41RR013642)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Keywords
- sleep deprivation, sleep duration, metabolic effects, slow-wave sleep, growth hormone, cortisol, leptin, ghrelin, appetite regulation, energy expenditure, obesity, type 2 diabetes, metabolic syndrome, glucose regulation, cardiovascular function, sleep restriction
- MeSH terms
- Diabetes Mellitus, Type 2, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Sleep Initiation and Maintenance Disorders, Obesity, Pituitary-Adrenal System, Risk Factors, Sleep, REM, Human Growth Hormone, Carbohydrate Metabolism
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