The DOI matches its Crossref record; 227 of the 230 references it cites were found in a registry or an index; 10 of the 197 sources its claims cite were checked for support.
Sleep and metabolic function
Open accessAbstract
Evidence for the role of sleep on metabolic and endocrine function has been reported more than four decades ago. In the past 30 years, the prevalence of obesity and diabetes has greatly increased in industrialized countries, and self-imposed sleep curtailment, now very common, is starting to be recognized as a contributing factor, alongside with increased caloric intake and decreased physical activity. Furthermore, obstructive sleep apnea, a chronic condition characterized by recurrent upper airway obstruction leading to intermittent hypoxemia and sleep fragmentation, has also become highly prevalent as a consequence of the epidemic of obesity and has been shown to contribute, in a vicious circle, to the metabolic disturbances observed in obese patients. In this article, we summarize the current data supporting the role of sleep in the regulation of glucose homeostasis and the hormones involved in the regulation of appetite. We also review the results of the epidemiologic and laboratory studies that investigated the impact of sleep duration and quality on the risk of developing diabetes and obesity, as well as the mechanisms underlying this increased risk. Finally, we discuss how obstructive sleep apnea affects glucose metabolism and the beneficial impact of its treatment, the continuous positive airway pressure. In conclusion, the data available in the literature highlight the importance of getting enough good sleep for metabolic health.
Overview
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Written from the paper’s full text.
TL;DR
This review summarizes evidence that sleep duration and quality modulate glucose homeostasis, appetite-regulating hormones, and risk of diabetes and obesity, with obstructive sleep apnea (OSA) as an additional metabolic risk. It concludes that sufficient good-quality sleep is important for metabolic health, while CPAP effects on glycemic control remain less clear-cut than for other cardiovascular risk factors.
Key findings
- Prospective epidemiologic studies indicate that short sleep (≤5–6 h/night), long sleep (>8–9 h/night), and sleep disturbances predict incident type 2 diabetes; pooled relative risks were 1.28 for short sleep, 1.48 for long sleep, 1.57 for difficulty initiating sleep, and 1.84 for difficulty maintaining sleep.
- Experimental partial sleep deprivation impaired insulin sensitivity in 7 of 11 studies and beta-cell dysfunction in 5 of 11; in one classic study, sleep debt decreased glucose tolerance by >40%, SI/AIRg/SG by ~25%, and disposition index by 50%.
- Sleep restriction altered appetite regulation: two nights of 4 h vs. 10 h in bed decreased leptin by 18%, increased ghrelin by 28%, increased the ghrelin/leptin ratio by >70%, and increased hunger by 23% and high-carbohydrate appetite by 33%.
- OSA is highly prevalent in type 2 diabetes (58–86% in polysomnography studies), and 17 of 35 studies reported improvement in at least one glucose-homeostasis parameter after CPAP, most consistently insulin sensitivity, though only five controlled studies existed and results were mixed.
Methods
- Narrative review of epidemiologic and experimental laboratory literature on sleep, glucose regulation, appetite hormones, obesity/diabetes risk, and OSA.
- Synthesizes cross-sectional, prospective, total sleep deprivation, partial sleep deprivation, sleep-fragmentation, and CPAP studies, with results presented in Tables 1–3 and figures.
- No primary data collection or formal systematic review methodology is described.
Limitations
- The paper states that future prospective epidemiologic studies need objective sleep measures, and that more controlled studies are necessary to evaluate CPAP effects on glucose homeostasis.
- The paper notes inconsistent leptin/ghrelin findings across studies and attributes these partly to differences in sample size, severity of sleep restriction, body composition, and OSA prevalence.
- Evident from the text: as a narrative review, it does not describe a systematic search strategy, inclusion criteria, or formal quality assessment of included studies.
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Claims the paper makes
105 Not checked yet · 18 Own interpretation · 7 No basis given · 4 Partly supported · 1 Supported · 1 Supported so far · 1 Own result · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Such phenomenon is observed for other weight promoting behaviors, notably physical inactivity and overeating, both of which are reinforced by weight gain [158].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Partly supportedcites [158] Sorensen TI (2009) Conference on “Multidisciplinary approaches to nutritional problems”. Symposium on “Diabetes and health”. Challenges in the study of causation of obesity. Proc Nutr Soc 68:43–54 sourceExperimental — accuracy not yet measured
The “Self-promoting weight gain” section reports that weight gain is associated with a subsequent decline in physical activity and increased food intake. But it describes continued self-promoting weight gain as a possible theoretical scenario, not an established vicious circle, and characterizes the increased intake as meeting higher energy needs rather than necessarily overeating. Page information is unavailable in our copy. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Partly supportedcites [80] Knutson KL (2010) Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab 24:731–743 sourceExperimental — accuracy not yet measured
The “Sleep and BMI, obesity and appetite regulation” section (page not provided) reports that many prospective studies in children and adults linked shorter sleep with later weight gain, obesity, or changes in body size. It does not report a tally of 28 longitudinal studies or say that 22 found an association; the follow-up periods it describes also vary, including a 16-year study. (LLM, conf=0.88)
- Partly supportedcites [8] Bo S et al (2011) Contributors to the obesity and hyperglycemia epidemics. A prospective study in a population-based cohort. Int J Obes. doi: 10.1038/ijo.2011.5 sourceExperimental — accuracy not yet measured
The Sleep restriction section (p. 11) reports that short sleep was associated with obesity at follow-up in this cohort and says other epidemiological studies have found an association. It does not report a review of 28 longitudinal studies, the 22-study count, or findings spanning children and adults, weight gain, and fat mass. (LLM, conf=0.86)
- Partly supportedcites [21] Carter PJ, Taylor BJ, Williams SM, Taylor RW (2011) Longitudinal analysis of sleep in relation to BMI and body fat in children: the FLAME study. BMJ 342:d2712 sourceExperimental — accuracy not yet measured
The Introduction (page not supplied) reports a relatively consistent link between shorter sleep and childhood overweight, and the Discussion (page not supplied) reports greater fat-mass gain among children who slept less. The paper does not report that 22 of 28 longitudinal studies found this association across children and adults; its Introduction instead mentions eight recent prospective studies in the childhood literature. (LLM, conf=0.88)
- Not checked yetcites [38] Diethelm K, Bolzenius K, Cheng G, Remer T, Buyken AE (2011) Longitudinal associations between reported sleep duration in early childhood and the development of body mass index, fat mass index and fat free mass index until age 7. Int J Pediatr Obes 6:e114–e123 source
- Not checked yetcites [89] Landhuis CE, Poulton R, Welch D, Hancox RJ (2008) Childhood sleep time and long-term risk for obesity: a 32-year prospective birth cohort study. Pediatrics 122:955–960 source
- Not checked yetcites [94] Littman AJ et al (2007) Sleep, ghrelin, leptin and changes in body weight during a 1-year moderate-intensity physical activity intervention. Int J Obes 31:466–475 source
- Not checked yetcites [97] Lyytikainen P, Rahkonen O, Lahelma E, Lallukka T (2011) Association of sleep duration with weight and weight gain: a prospective follow-up study. J Sleep Res 20:298–302 source
- Not checked yetcites [101] Marshall NS et al (2010) Changes in sleep duration and changes in weight in obese patients: the Swedish obese subjects study. Sleep Biol Rhythms 8:63–71 source
- Partly supportedcites [105] Mozaffarian D, Hao T, Rimm EB, Willett WC, Hu FB (2011) Changes in diet and lifestyle and long-term weight gain in women and men. N Engl J Med 364:2392–2404 sourceExperimental — accuracy not yet measured
The Results and Discussion report an association between shorter sleep and greater weight gain, and the Discussion notes that some prospective studies support a link with obesity. Neither section reports a review of 28 longitudinal studies, a finding in 22 of them, or the claimed combined findings for children and adults. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Partly supportedcites [120] Nishiura C, Hashimoto H (2010) A 4-year study of the association between short sleep duration and change in body mass index in Japanese male workers. J Epidemiol 20:385–390 sourceExperimental — accuracy not yet measured
The Results and Discussion report an association between short sleep and relative BMI increase over four years in Japanese male workers. The paper does not report a tally of 28 longitudinal studies or say that 22 found increased weight gain, obesity, or fat mass in children and adults. (LLM, conf=0.84)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Two studies have demonstrated that poor sleep quality, independently of sleep duration, impairs glucose regulation in healthy young adults [167, 176].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Supportedcites [167] Stamatakis KA, Punjabi NM (2010) Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 137:95–101 source
The Discussion reports that two nights of fragmented sleep reduced measures of glucose regulation by 20%–25% while sleep duration was preserved. The study used healthy, younger volunteers (Discussion), and the paper also describes a second study reporting worsened insulin resistance after selective suppression of slow-wave sleep (Heart Rate Variability Analysis). (LLM, conf=0.91)
- Not checked yetcites [176] Tasali E, Leproult R, Ehrmann DA, Van Cauter E (2008) Slow-wave sleep and the risk of type 2 diabetes in humans. Proc Natl Acad Sci USA 105:1044–1049 source
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a study that assessed the 24-h leptin profiles after 6 days of 4-, 8-, and 12-h bedtimes in healthy lean young men under conditions of stable caloric intake and activity levels, all characteristics of the 24-h leptin profile (overall mean, nocturnal maximum, and amplitude) gradually increased from the 4- to the 12-h bedtime condition [161].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Partly supportedcites [161] Spiegel K et al (2004) Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metabol 89:5762–5771 sourceExperimental — accuracy not yet measured
The Leptin results report higher 24-hour mean, nocturnal peak, and amplitude with 12-h than with 4-h bedtimes despite similar caloric intake and activity. The Correlations section says the 8-h leptin data were intermediate, supporting the overall trend. However, the Experimental protocol says the 8-h profiles came from a separate study of nine subjects one year later, not from six days in an 8-h condition alongside the 4-h and 12-h conditions. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“a dose–response relationship between slow wave activity (SWA) and the amount of GH secreted has been evidenced in young and older men.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“conversely, total sleep deprivation leads to marked hyperphagia [133].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [133] Rechtschaffen A, Bergmann BM (1995) Sleep deprivation in the rat by the disk-over-water method. Behav Brain Res 69:55–63 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“SWS, which is particularly abundant at the beginning of the sleep period, has been shown to result in a 30–40% decrease in cerebral glucose metabolism relative to waking or rapid eye movement (REM) sleep [12].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [12] Boyle PJ et al (1994) Diminished brain glucose metabolism is a significant determinant for falling rates of systemic glucose utilization during sleep in normal humans. J Clin Invest 93:529–535 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Both nocturnal and daytime sleeps were associated with a marked decrease in glucose tolerance, reflected by increased glucose levels.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In rodents, food shortage or starvation results in decreased sleep [35]”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [35] Danguir J, Nicolaidis S (1979) Dependence of sleep on nutrients’ availability. Physiol Behav 22:735–740 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“As shown in Fig. 1b, this profile is only modestly affected by the presence or absence of sleep.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [151] Simon C, Brandenberger G, Follenius M (1987) Ultradian oscillations of plasma glucose, insulin, and C-peptide in man during continuous enteral nutrition. J Clin Endocrinol Metabol 64:669–674 source
- Not checked yetcites [152] Simon C, Brandenberger G, Saini J, Ehrhart J, Follenius M (1994) Slow oscillations of plasma glucose and insulin secretion rate are amplified during sleep in humans under continuous enteral nutrition. Sleep 17:333–338 source
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- It may state two separate claims as one. 44
- Probably not a substantial claim. 5
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Thus, of the three studies that assessed SI after a glucose load, two found reduced SI after sleep loss [5, 195] and one found reduced SI after recovery sleep [204].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
- Not checked yetcites [195] VanHelder T, Symons JD, Radomski MW (1993) Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 64:487–492
- Partly supportedcites [204] Wehrens SM, Hampton SM, Finn RE, Skene DJ (2010) Effect of total sleep deprivation on postprandial metabolic and insulin responses in shift workers and non-shift workers. J Endocrinol 206:205–215 sourceExperimental — accuracy not yet measured
The Discussion reports a larger postprandial insulin response after recovery sleep despite similar glucose levels, which the authors interpret as insulin insensitivity. However, they tested responses to a standard breakfast, not a glucose load, and inferred insulin sensitivity from those responses rather than directly measuring it. The other two studies in the citing sentence are attached to different citations. (LLM, conf=0.85)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In this latter study, however, the DI was not affected by the sleep fragmentation since an increase in insulin release was able to compensate the decrease in SI.”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Supportedcites [167] Stamatakis KA, Punjabi NM (2010) Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 137:95–101 source
The IVGTT results passage (indexed under Heart Rate Variability Analysis; page unavailable) reports that insulin sensitivity decreased and the acute insulin response increased after sleep fragmentation. It explicitly links those changes to a disposition index that was numerically lower but not statistically different from baseline (P = .37), supporting the claim in the statistical sense. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
In the paper
“in healthy young men, a major GH pulse that accounts for roughly 70% of the daily production occurs shortly after sleep onset [188], in association with the first phase of slow wave sleep (SWS).”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [188] Van Cauter E et al (1992) A quantitative estimation of growth hormone secretion in normal man: reproducibility and relation to sleep and time of day. J Clin Endocrinol Metabol 74:1441–1450 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“wake–sleep and sleep–wake transitions are associated with inhibition and stimulation of cortisol levels, respectively [59, 168, 186].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [59] Gronfier C, Brandenberger G (1998) Ultradian rhythms in pituitary and adrenal hormones: their relations to sleep. Sleep Med Rev 2:17–29 source
- Not checked yetcites [168] Steiger A (2003) Sleep and endocrinology. J Intern Med 254:13–22 source
- Not checked yetcites [186] Van Cauter E (2005) Endocrine physiology. In: Kryger M, Roth T, Dement WC (eds) Principles and practice of sleep medicine, 4th edn. Elsevier-Saunders, Philadelphia
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“A glucose and insulin elevation of roughly half the amplitude of the one observed during nocturnal sleep was apparent during the night of sleep deprivation, indicating that circadian-dependent processes also modulate glucose regulation.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“GH levels are increased during sleep, irrespective of the time at which sleep occurs, and they are markedly diminished during sleep deprivation.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [151] Simon C, Brandenberger G, Follenius M (1987) Ultradian oscillations of plasma glucose, insulin, and C-peptide in man during continuous enteral nutrition. J Clin Endocrinol Metabol 64:669–674 source
- Not checked yetcites [152] Simon C, Brandenberger G, Saini J, Ehrhart J, Follenius M (1994) Slow oscillations of plasma glucose and insulin secretion rate are amplified during sleep in humans under continuous enteral nutrition. Sleep 17:333–338 source
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the study by Benedict et al. [5], the decreased glucose tolerance in a state of sleep debt was the consequence of reduced SI combined to beta-cell dysfunction since insulin levels were not affected by the presence or absence of sleep.”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Glucose tolerance during this ivGTT was decreased by more than 40% when the subjects were in a state of sleep debt and reached values typical for older adults with impaired glucose tolerance [54].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [54] Garcia G et al (1997) Glucose metabolism in older adults: a study including subjects more than 80 years of age. J Am Geriatr Soc 45:813–817 source
plaindirectn = 11- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Short sleep duration (mostly ≤5and/or ≤6h) was found to predict a higher incidence of diabetes in seven of the nines studies, while poor sleep quality was associated with an increased risk of diabetes in five of the six studies [80].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Epidemiologic evidence
What the sources say
- Not checked yetcites [80] Knutson KL (2010) Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab 24:731–743 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Glucose tolerance was found to be altered in two studies, i.e., after 72–126 h of TSD [86] and after 24 h of TSD [5].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [86] Kuhn E, Brodan V, Brodanova M, Rysanek K (1969) Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 11:165–174
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased fasting glucose was reported after 120 h of TSD [200] but not after 72–126 h [86] or one single night of TSD [5, 143, 195, 204]”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [200] Vondra K et al (1981) Effects of sleep deprivation on the activity of selected metabolic enzymes in skeletal muscle. Eur J Appl Physiol Occup Physiol 47:41–46 source
- Not checked yetcites [86] Kuhn E, Brodan V, Brodanova M, Rysanek K (1969) Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 11:165–174
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
- Not checked yetcites [143] Schmid SM et al (2007) Sleep loss alters basal metabolic hormone secretion and modulates the dynamic counterregulatory response to hypoglycemia. J Clin Endocrinol Metabol 92:3044–3051 source
- Not checked yetcites [195] VanHelder T, Symons JD, Radomski MW (1993) Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 64:487–492
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“All [95, 166] but one [3] of the studies that have attempted to characterize the overnight profiles of acylated ghrelin in relation to unacylated ghrelin confirmed the increased nocturnal elevation in total ghrelin and demonstrated a concomitant increase in acylated ghrelin.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [95] Liu J et al (2008) Novel ghrelin assays provide evidence for independent regulation of ghrelin acylation and secretion in healthy young men. J Clin Endocrinol Metabol 93:1980–1987 source
- Not checked yetcites [166] Spiegel K, Tasali E, Leproult R, Scherberg N, Van Cauter E (2011) Twenty-four-hour profiles of acylated and total ghrelin: relationship with glucose levels and impact of time of day and sleep. J Clin Endocrinol Metabol 96:486–493 source
- Not checked yetcites [3] Avram AM, Jaffe CA, Symons KV, Barkan AL (2005) Endogenous circulating ghrelin does not mediate growth hormone rhythmicity or response to fasting. J Clin Endocrinol Metabol 90:2982–2987 source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“and an OR of 1.92 (95% CI, 1.15–3.2) in children with the shortest sleep duration, suggesting a dose–response relationship between sleep duration increased risk of obesity [23].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [23] Chen X, Beydoun MA, Wang Y (2008) Is sleep duration associated with childhood obesity? A systematic review and meta-analysis. Obesity (Silver Spring, Md) 16:265–274 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Studies in adults are less consistent and often show a U-shaped relationship between sleep duration and BMI.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“However, there were only five controlled studies among those published in literature, of which three yielded positive results, while the other two were unable to demonstrate a beneficial impact of CPAP on glucose homeostasis.”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The number of adults aged 25 years or older with diabetes has more than doubled over nearly three decades and is currently approaching 350 million [34].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [34] Danaei G et al (2011) National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet 378:31–40 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“glucose tolerance, the 24-h pattern of release of insulin, and the counterregulatory hormones growth hormone (GH) and cortisol, as well as of hormones involved in the regulation of appetite, such as leptin and ghrelin, are partly dependent on sleep timing, duration, and quality [59, 168, 186].”
§ Sleep and metabolic function > Introduction
What the sources say
- Not checked yetcites [59] Gronfier C, Brandenberger G (1998) Ultradian rhythms in pituitary and adrenal hormones: their relations to sleep. Sleep Med Rev 2:17–29 source
- Not checked yetcites [168] Steiger A (2003) Sleep and endocrinology. J Intern Med 254:13–22 source
- Not checked yetcites [186] Van Cauter E (2005) Endocrine physiology. In: Kryger M, Roth T, Dement WC (eds) Principles and practice of sleep medicine, 4th edn. Elsevier-Saunders, Philadelphia
plainconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Type 2 diabetes is a complex metabolic disorder that involves insulin resistance, impaired insulin secretion, and increased glucose production [37, 79].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [37] DeFronzo RA (2004) Pathogenesis of type 2 diabetes mellitus. Med Clin North Am 88:787–835, ix source
- Not checked yetcites [79] Kahn SE (2003) The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia 46:3–19 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Voluntary sleep curtailment has, indeed, become an increasingly common behavior in all age groups over the past several decades, most likely reflecting the demands and opportunities of modern society [75, 114].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [75] Institut National de Prévention et d’Education pour la Santé. Les français et leur sommeil. http://www.inpes.sante.fr/70000/dp/08/dp080310.pdf . 1–45.
- Not checked yetcites [114] National Sleep Foundation (2008) “Sleep in America” Poll. http://www.sleepfoundation.org./sites/default/files/2008%20POLL%20SOF.PDF . 1–45
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, glucose regulation is markedly influenced by circadian rhythmicity and sleep, and these effects could be partially mediated by cortisol and GH.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [56] Gasco V et al (2010) Endocrine and metabolic actions of ghrelin. Endocr Dev 17:86–95 source
- Not checked yetcites [58] Granata R, Baragli A, Settanni F, Scarlatti F, Ghigo E (2010) Unraveling the role of the ghrelin gene peptides in the endocrine pancreas. J Mol Endocrinol 45:107–118 source
- Not checked yetcites [92] Lim CT, Kola B, Korbonits M, Grossman AB (2010) Ghrelin’s role as a major regulator of appetite and its other functions in neuroendocrinology. Prog Brain Res 182:189–205 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“These findings support an inhibitory effect of sleep on ghrelin, consistent with the association between sleeping and fasting and, conversely, between feeding and arousal.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [166] Spiegel K, Tasali E, Leproult R, Scherberg N, Van Cauter E (2011) Twenty-four-hour profiles of acylated and total ghrelin: relationship with glucose levels and impact of time of day and sleep. J Clin Endocrinol Metabol 96:486–493 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Feeding and sleeping are mutually exclusive.
None of the sources cited for this claim have been checked yet.
In the paper
“Leptin inhibits hunger and food intake, increases EE, and promotes fat utilization [1, 193].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [1] Ahima RS, Saper CB, Flier JS, Elmquist JK (2000) Leptin regulation of neuroendocrine systems. Front Neuroendocrinol 21:263–307 source
- Not checked yetcites [193] van Dijk G (2001) The role of leptin in the regulation of energy balance and adiposity. J Neuroendocrinol 13:913–921 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“To note, one prospective study in adults reported a bidirectional relationship between short sleep and obesity; not only did short sleep predict weight gain a few years later [67], but body weight or obesity also predicted short sleep duration on a later occasion.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [67] Hasler G et al (2004) The association between short sleep duration and obesity in young adults: a 13-year prospective study. Sleep 27:661–666 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these results suggest the existence of a “vicious circle” where short sleep may initially promote weight gain, and the resulting excess adiposity would then induce sleep disturbances, with a further decrease in total sleep time.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, overall, the impact of reduced sleep duration on obesity risk is particularly clear in pediatric populations, probably because physiological and behavioral mechanisms responsible for this association are stronger in younger ages.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The physiological and behavioral mechanisms linking short sleep to obesity are stronger at younger ages.
None of the sources cited for this claim have been checked yet.
In the paper
“However, even modest increases in weight have been shown to have significant implications for long-term adiposity-related metabolic dysfunction, diabetes, cardiovascular disease, and cancer [28, 46, 135, 208].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [28] Colditz GA, Willett WC, Rotnitzky A, Manson JE (1995) Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med 122:481–486 source
- Not checked yetcites [46] Eliassen AH, Colditz GA, Rosner B, Willett WC, Hankinson SE (2006) Adult weight change and risk of postmenopausal breast cancer. JAMA 296:193–201 source
- Not checked yetcites [135] Rexrode KM et al (1997) A prospective study of body mass index, weight change, and risk of stroke in women. JAMA 277:1539–1545 source
- Not checked yetcites [208] Willett WC et al (1995) Weight, weight change, and coronary heart disease in women. Risk within the ‘normal’ weight range. JAMA 273:461–465 source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“U- or L-shaped associations were reported in some adult prospective studies (reviewed in [80]; additional studies: [97, 202]); hence, the relationship between longer sleep and BMI is conflicting in adults and inexistent in children.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [80] Knutson KL (2010) Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab 24:731–743 source
- Not checked yetcites [97] Lyytikainen P, Rahkonen O, Lahelma E, Lallukka T (2011) Association of sleep duration with weight and weight gain: a prospective follow-up study. J Sleep Res 20:298–302 source
- Not checked yetcites [202] Watanabe M, Kikuchi H, Tanaka K, Takahashi M (2010) Association of short sleep duration with weight gain and obesity at 1-year follow-up: a large-scale prospective study. Sleep 33:161–167 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It is possible that weight is not gained linearly over the course of the short sleeping period. As a consequence, “in order for short sleep to predict any physiological or behavioral change, the longitudinal time frame examined would need to start prior to or at the beginning of the short sleep transition for each participant” [98], which is less likely to be the case with older ages.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [98] Magee L, Hale L (2011) Longitudinal associations between sleep duration and subsequent weight gain: a systematic review. Sleep Med Rev. doi: 10.1016/j.smrv.2011.05.005 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- The authors state this as an assumption: Weight is not gained linearly over the course of a short sleeping period.
In the paper
“In the general population, the prevalence of OSA is around 17% [215].”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
What the sources say
- Not checked yetcites [215] Young T, Peppard PE, Taheri S (2005) Excess weight and sleep-disordered breathing. J Appl Physiol 99:1592–1599 source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“At the end of the 2 weeks of sleep curtailment, the proportion of weight lost as fat was decreased by 55%, and the loss of fat-free body mass was increased by 60%.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [117] Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD (2010) Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med 153:435–441 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Conversely, no impact of TSD was evidenced in another recent study that also reported reduced amplitude of the 24-h leptin diurnal variation due to increased daytime leptin levels [126].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [126] Pejovic S et al (2010) Leptin and hunger levels in young healthy adults after one night of sleep loss. J Sleep Res 19:552–558 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Of note, the study of St-Onge et al. reported an increase of ~300 kcal/day after 5 days of 4 h bedtimes, although there was no clear effect of sleep duration on subjective feelings of hunger and appetite on the previous day [11, 170], suggesting that subjective assessments are unreliable.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [11] Bosy-Westphal A et al (2008) Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Obes Facts 1:266–273 source
- Not checked yetcites [170] St-Onge MP et al (2011) Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals. Am J Clin Nutr 94:410–416 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“As leptin levels are enhanced by food intake and correlate with the degree of obesity [25], these latter results may be the expected consequence of the positive energy balance achieved by increased food intake [11, 116, 146] and weight gain [11, 116].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [25] Chin-Chance C, Polonsky KS, Schoeller DA (2000) Twenty-four-hour leptin levels respond to cumulative short-term energy imbalance and predict subsequent intake. J Clin Endocrinol Metabol 85:2685–2691 source
- Not checked yetcites [11] Bosy-Westphal A et al (2008) Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Obes Facts 1:266–273 source
- Not checked yetcites [116] Nedeltcheva AV et al (2009) Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr 89:126–133 source
- Not checked yetcites [146] Schmid SM et al (2009) Short-term sleep loss decreases physical activity under free-living conditions but does not increase food intake under time-deprived laboratory conditions in healthy men. Am J Clin Nutr 90:1476–1482 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Again, this unlimited availability of palatable food resulted in overeating (+60% regardless of the bedtime condition) and may have masked the impact of sleep loss on food consumption [146].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [146] Schmid SM et al (2009) Short-term sleep loss decreases physical activity under free-living conditions but does not increase food intake under time-deprived laboratory conditions in healthy men. Am J Clin Nutr 90:1476–1482 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One pathway that may link short sleep to excess weight is increased caloric intake in short sleepers.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“For example, in the study that submitted the subjects to caloric restriction, leptin levels declined in parallel with the loss of weight and adiposity without a significant independent effect of sleep loss: The negative energy balance most likely overrode the impact of sleep duration [117].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [117] Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD (2010) Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med 153:435–441 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“By contrast, Nedeltcheva et al. observed similar weight at the end of each 14-day period of sleep extension or sleep restriction in overweight men and women exposed to unlimited palatable food in a laboratory setting. Consistent with the fact that overeating usually occurs when unlimited palatable food is available [132], the subjects overate and gained ~2 kg in each sleep condition [116].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [116] Nedeltcheva AV et al (2009) Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr 89:126–133 source
- Not checked yetcites [132] Raynor HA, Wing RR (2007) Package unit size and amount of food: do both influence intake? Obesity (Silver Spring Md) 15:2311–2319 source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Leptin decreased by 18%, while ghrelin increased by 28%, and the ghrelin/leptin ratio increased by more than 70% when sleep was restricted (Fig. 3).”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [162] Spiegel K, Tasali E, Penev P, Van Cauter E (2004) Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 141:846–850 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Accordingly, in the study by Benedict et al., ghrelin was higher in the second half of the night compared to a night of normal sleep, whereas nighttime leptin levels were unchanged.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Importantly, in the latter two studies, EE measured with the gold standard doubly labeled water method did not differ between study conditions, therefore suggesting that the increase in food consumption most often associated with sleep loss is not related to a comparable rise in energy needs and would eventually result in a positive energy balance.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In overweight middle-aged adults, increased consumption of calories from snacks with higher carbohydrate content was observed after 2 weeks of sleep restriction (−1.5 h/night) in comparison to after 2 weeks of sleep extension (+1.5 h/night), while energy intake from meal and total energy intake were unaffected by bedtime condition [116].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [116] Nedeltcheva AV et al (2009) Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr 89:126–133 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, increased ghrelin levels and elevated hunger scores were observed in the sleep restriction condition, suggesting that, in contrast to what was observed with leptin, sleep loss was able to exacerbate the upregulation of ghrelin and hunger triggered by a negative energy balance.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The state of sleep loss also resulted in a 23% increase in hunger and in a 33% increase in appetite for nutrients with high carbohydrate content.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [162] Spiegel K, Tasali E, Penev P, Van Cauter E (2004) Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 141:846–850 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“By comparison, 3 days of underfeeding by approximately 900 cal/day in healthy lean volunteers resulted in a 22% decrease of leptin levels [25]; these results highlight the functional significance of the decrease in leptin observed with sleep loss.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [25] Chin-Chance C, Polonsky KS, Schoeller DA (2000) Twenty-four-hour leptin levels respond to cumulative short-term energy imbalance and predict subsequent intake. J Clin Endocrinol Metabol 85:2685–2691 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Methodological differences may also account for the variability of results obtained: four positive studies relied on the hyperinsulinemic–euglycemic clamp technique to assess SI [15, 65, 66, 142], which is considered the gold standard to evaluate SI; another two used continuous glucose monitoring (CGMS) [4, 205], which provides 288 readings of interstitial glucose levels per 24 h (every 5 min) and”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
What the sources say
- Not checked yetcites [15] Brooks B et al (1994) Obstructive sleep apnea in obese noninsulin-dependent diabetic patients: effects of continuous positive airway pressure treatment on insulin responsiveness. J Clin Endocrinol Metabol 79:1681–1685 source
- Not checked yetcites [65] Harsch IA et al (2004) Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome. Am J Respir Crit Care Med 169:156–162 source
- Not checked yetcites [66] Harsch IA et al (2004) The effect of continuous positive airway pressure treatment on insulin sensitivity in patients with obstructive sleep apnoea syndrome and type 2 diabetes. Respiration 71:252–259 source
- Not checked yetcites [142] Schahin SP et al (2008) Long-term improvement of insulin sensitivity during CPAP therapy in the obstructive sleep apnoea syndrome. Med Sci Mon 14:CR117–CR121
- Not checked yetcites [4] Babu AR, Herdegen J, Fogelfeld L, Shott S, Mazzone T (2005) Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med 165:447–452 source
- Not checked yetcites [205] Wei CY et al (2009) Effects of continuous positive airway pressure upon 24 h changes of blood glucose level in patients with obstructive sleep apnea hypopnea syndrome and type 2 diabetes. Zonghua Yi Xue Yi Chuan Xue Za Zi 89:2686–2689
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“HOMA-IR has been found to correlate reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance in several studies of distinct populations. However, it is a measure of basal insulin sensitivity/resistance and does not provide information about dynamic conditions [201].”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
What the sources say
- Not checked yetcites [201] Wallace TM, Levy JC, Matthews DR (2004) Use and abuse of HOMA modeling. Diabetes Care 27:1487 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: HOMA-IR correlates reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance.
The paper relies on this without support.
Feeding and sleeping are mutually exclusive.
“Feeding and sleeping are mutually exclusive: They are both time-consuming and occur in cyclic patterns.”
The paper relies on this without support.
In healthy subjects, insulin resistance is accompanied by compensatory hyperinsulinemia that maintains a constant disposition index.
“In healthy subjects, insulin resistance is accompanied by compensatory hyperinsulinemia, which in turn maintains a constant DI.”
The paper relies on this without support.
Sympathetic activation inhibits insulin release and parasympathetic activation stimulates it.
“Sympathetic activation inhibits and para-sympathetic activation stimulates insulin release”
The paper relies on this without support.
Aging and obstructive sleep apnea are recognized risk factors for decreased glucose tolerance and increased diabetes risk.
“Both aging and OSA are recognized risk factors for decreased glucose tolerance and increased diabetes risk.”
The paper relies on this without support.
PYY inhibits appetite.
“In contrast to ghrelin, PYY inhibits appetite.”
The paper relies on this without support.
Modern lifestyle of physical inactivity and increased food intake contributes to the growing prevalence of type 2 diabetes worldwide.
“If it is obvious that our modern lifestyle of physical inactivity and increased food intake is involved in the growing prevalence of type 2 diabetes worldwide”
The paper relies on this without support.
The prevalence of sleep disorders, particularly obstructive sleep apnea, has greatly increased, although they often remain undiagnosed.
“In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has greatly increased, although they often remain undiagnosed.”
The paper relies on this without support.
The physiological and behavioral mechanisms linking short sleep to obesity are stronger at younger ages.
“probably because physiological and behavioral mechanisms responsible for this association are stronger in younger ages”
The authors state this as an assumption.
Weight is not gained linearly over the course of a short sleeping period.
“It is possible that weight is not gained linearly over the course of the short sleeping period.”
The paper relies on this without support.
Obesity and obstructive sleep apnea alter leptin and ghrelin regulation and leptin action.
“Obesity is associated with hypoghrelinemia, hyperleptinemia, and leptin resistance, while OSA is associated with hyperghrelinemia, hyperleptinemia, and leptin resistance.”
The paper relies on this without support.
HOMA-IR correlates reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance.
“HOMA-IR has been found to correlate reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance in several studies of distinct populations.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [24]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Both self-reported short and long sleep duration have been associated with elevated risk of obesity in both children and adults[1-7]”
From Habitual sleep duration associated with self-reported and objectively determined cardiometabolic risk factors (2014) · cites this paper as [4]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Many studies have found associations between sleep duration and adiposity and obesity.39–41”
From Sleep, Health, and Society (2017) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“diabetes[4, 11, 12]”
From Habitual sleep duration associated with self-reported and objectively determined cardiometabolic risk factors (2014) · cites this paper as [4]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Because the hypothalamic-pituitary-adrenal (HPA) axis regulates a wide range of physiologic processes and is affected by experimental sleep restriction, it is a putative key mediator of the adverse health effects of insufficient sleep (3–11).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
Experimental — accuracy not yet measured
In the citing paper
“Because the hypothalamic-pituitary-adrenal (HPA) axis regulates a wide range of physiologic processes and is affected by experimental sleep restriction, it is a putative key mediator of the adverse health effects of insufficient sleep (3–11).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
In the citing paper
“Habitual short sleep, usually 6 hours or less, has been linked in epidemiological studies to increased mortality and increased prevalence and incidence of numerous pathological conditions including obesity, diabetes, cardiovascular diseases, vulnerability to infection, depression, and anxiety (3–10).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
In the citing paper
“Because the hypothalamic-pituitary-adrenal (HPA) axis regulates a wide range of physiologic processes and is affected by experimental sleep restriction, it is a putative key mediator of the adverse health effects of insufficient sleep (3–11).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
In the citing paper
“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 [24]
In the citing paper
“Sleep deprivation alters glucose homeostasis, leading to insulin resistance and risk of diabetes(17, 18, 24, 59-61).”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [24]
Citations
Cites
(1992) · Applied Ergonomics · doi:10.1016/0003-6870(92)90318-p · Cited by 5,774
Principles and Practice of Sleep Medicine
Kryger, M. H., Roth, T. G., & Dement, W. C. (2011) · Elsevier eBooks · doi:10.1016/c2009-0-59875-3 · Cited by 5,118
Use and Abuse of HOMA Modeling
Wallace, T. M., Levy, J. C., & Matthews, D. R. (2004) · Diabetes Care · doi:10.2337/diacare.27.6.1487 · Cited by 5,114 · cited 1×
“However, it is a measure of basal insulin sensitivity/resistance and does not provide information about dynamic conditions [201].”
Impact of sleep debt on metabolic and endocrine function
Spiegel, K., Leproult, R., & Van Cauter, E. (1999) · The Lancet · doi:10.1016/s0140-6736(99)01376-8 · Cited by 3,668 · cited 6×
“The two left panels illustrate the effects of reduced sleep duration (adapted from [16, 159]).”
InfluentialSelf-citationDanaei, G., Finucane, M. M., Lu, Y., Singh, G. M., Cowan, M. J., Paciorek, C. J., Lin, J. K., Farzadfar, F., Khang, Y.-H., Stevens, G. A., et al. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60679-x · Cited by 3,568 · cited 1×
“The prevalence of type 2 diabetes is increasing worldwide, reaching pandemic proportions: The number of adults aged 25 years or older with diabetes has more than doubled over nearly three decades and is currently approaching 350 million [34].”
A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans
Cummings, D. E., Purnell, J. Q., Frayo, R. S., Schmidova, K., Wisse, B. E., & Weigle, D. S. (2001) · Diabetes · doi:10.2337/diabetes.50.8.1714 · Cited by 2,940 · cited 1×
“As early as 2001 [32], studies involving frequent sampling across the 24h cycle observed a nocturnal elevation of total ghrelin levels with peak values during the sleep period and declining levels toward the morning.”
Sympathetic neural mechanisms in obstructive sleep apnea.
Somers, V. K., Dyken, M. E., Clary, M. P., & Abboud, F. M. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118235 · Cited by 2,527
Changes in diet and lifestyle and long-term weight gain in women and men
Mozaffarian, D., Hao, T., Rimm, E. B., Willett, W. C., & Hu, F. B. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1014296 · Cited by 2,527 · cited 1×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
Taheri, S., Lin, L., Austin, D., Young, T., & Mignot, E. (2004) · PLoS Medicine · doi:10.1371/journal.pmed.0010062 · Cited by 2,477 · cited 4×
“These findings are in agreement with the role of leptin in signaling long-term nutritional status, while ghrelin is more involved in acute hunger [174].”
InfluentialSpiegel, K., Tasali, E., Penev, P., & Cauter, E. V. (2004) · Annals of Internal Medicine · doi:10.7326/0003-4819-141-11-200412070-00008 · Cited by 2,459 · cited 10×
“Results regarding subjective feelings of hunger seem less consistent, as only five studies [14, 99, 117, 144, 162] of the 11 [11, 14, 99, 117, 122, 144–146, 162, 170, 194] that examined the effect of reduced sleep duration on hunger reported positive effects.”
InfluentialSelf-citation
Research works printed but not linked: 1
- Spiegel K et al (2005) The 24-hour profile of plasma PYY levels in normal adults: relationships with sleep, meal intake and ghrelin levels. In: The Endocrine Society’s 87th Annual Meeting Abstract number OR8-3, San Diego, CA, USA, June 2005, pp. 82–83
Cited by
Sorted by citations
The effects of physical activity on sleep: A meta-analytic review
Kredlow, M. A., Capozzoli, M. C., Hearon, B. A., Calkins, A. W., & Otto, M. W. (2015) · Journal of Behavioral Medicine · doi:10.1007/s10865-015-9617-6 · Cited by 1,333
“…temperature changes (McGinty & Szymusiak, 1990), cytokine concentration changes (Santos et al., 2007), increased energy consumption/metabolic rate (Morselli et al., 2012), CNS fatigue (Uchida et al., 2012), changes in mood/anxiety symptoms (Buman & King, 2010; Uchida et al., 2012), changes in…”
BackgroundSt-Onge, M.-P., Grandner, M. A., Brown, D., Conroy, M. B., Jean-Louis, G., Coons, M., & Bhatt, D. L. (2016) · Circulation · doi:10.1161/cir.0000000000000444 · Cited by 1,044
Sleep and exercise: A reciprocal issue?
Chennaoui, M., Arnal, P. J., Sauvet, F., & Léger, D. (2014) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2014.06.008 · Cited by 770
Grandner, M. A. (2017) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2016.10.012 · Cited by 720
Fatima, Y., Doi, S. A. R., & Mamun, A. A. (2015) · Obesity Reviews · doi:10.1111/obr.12245 · Cited by 577
Sleep disparity, race/ethnicity, and socioeconomic position
Grandner, M. A., Williams, N. J., Knutson, K. L., Roberts, D., & Jean-Louis, G. (2016) · Sleep Medicine · doi:10.1016/j.sleep.2015.01.020 · Cited by 481
“laboratory studies, has been associated with weight gain and obesity [14], hypertension [15–17], hyperlipidemia [15,16], inflammation [18], diabetes [15,19–21], stroke [16,22], heart attack [16,23], and mortality [24–28].”
The metabolic burden of sleep loss
Schmid, S. M., Hallschmid, M., & Schultes, B. (2015) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(14)70012-9 · Cited by 328
Reutrakul, S., & Van Cauter, E. (2014) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12355 · Cited by 321
The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms
Briançon‐Marjollet, A., Weiszenstein, M., Henri, M., Thomas, A., Godin‐Ribuot, D., & Polak, J. (2015) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-015-0018-3 · Cited by 338
“Appetite regulation Prospective and cross-sectional studies have also identified short sleep duration as an independent risk factor for weight gain and abdominal fat accumulation (as reviewed in [109,110]).”
BackgroundGrandner, M. A., Chakravorty, S., Perlis, M. L., Oliver, L., & Gurubhagavatula, I. (2014) · Sleep Medicine · doi:10.1016/j.sleep.2013.09.012 · Cited by 300
“Both self-reported short and long sleep duration have been associated with elevated risk for obesity in children and adults [1–7], as well as cardiovascular disease [8–10], diabetes mellitus (DM) [4,11,12], hypertension [2,13,14], and other negative health outcomes [2,15–17] (i.”
Exercise effects on sleep physiology
Uchida, S., Shioda, K., Morita, Y., Kubota, C., Ganeko, M., & Takeda, N. (2012) · Frontiers in Neurology · doi:10.3389/fneur.2012.00048 · Cited by 277
“EXERCISE EFFECTS ON METABOLIC FUNCTIONS DURING SLEEP There has been increasing interest in the relationships between sleep and metabolic functioning (Morselli et al., 2012), following epidemiological investigations detailing the relationships between sleep loss, obesity, and diabetes (e.”
BackgroundSleep duration versus sleep insufficiency as predictors of cardiometabolic health outcomes
Altman, N. G., Izci-Balserak, B., Schopfer, E., Jackson, N., Rattanaumpawan, P., Gehrman, P. R., Patel, N. P., & Grandner, M. A. (2012) · Sleep Medicine · doi:10.1016/j.sleep.2012.08.005 · Cited by 229
Dietary Intake Following Experimentally Restricted Sleep in Adolescents
Beebe, D. W., Simon, S., Summer, S., Hemmer, S., Strotman, D., & Dolan, L. M. (2013) · Sleep · doi:10.5665/sleep.2704 · Cited by 232
Sedentary Behavior and Sleep Problems: a Systematic Review and Meta-Analysis
Yan, Y., Shin, J. C., Li, D., & An, R. (2016) · International Journal of Behavioral Medicine · doi:10.1007/s12529-016-9609-0 · Cited by 255
Sleep Duration and Diabetes Risk: Population Trends and Potential Mechanisms
Grandner, M. A., Seixas, A. A., Shetty, S., & Shenoy, S. (2016) · Current Diabetes Reports · doi:10.1007/s11892-016-0805-8 · Cited by 201
Grandner, M. A. (2022) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2022.03.001 · Cited by 188
Sleep: important considerations for the prevention of cardiovascular disease
Grandner, M. A., Alfonso-Miller, P., Fernandez-Mendoza, J., Shetty, S., Shenoy, S., & Combs, D. (2016) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000324 · Cited by 166
Grandner, M. A. (2020) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2020.02.017 · Cited by 143
Effects of Acute Sleep Loss on Physical Performance: A Systematic and Meta-Analytical Review
Craven, J., McCartney, D., Desbrow, B., Sabapathy, S., Bellinger, P., Roberts, L. A., & Irwin, C. G. (2022) · Sports Medicine · doi:10.1007/s40279-022-01706-y · Cited by 162
“It has been shown to promote memory [1], regulate emotions [2], enhance metabolic functions [3], improve energy balance, and moderate the immune system [4], and may play a pivotal role in the stress–recovery balance, via its influence on the activity of the hypothalamic–pituitary–adrenal axis [5].”
BackgroundSleep Disorders and the Development of Insulin Resistance and Obesity
Mesarwi, O. A., Polak, J., Jun, J. C., & Polotsky, V. Y. (2013) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2013.05.001 · Cited by 150
“Indeed, cross-sectional and prospective studies have linked short sleep with weight gain and abdominal fat accumulation.(142,143) Interestingly, short sleep was associated with lower fat loss during caloric restriction in overweight subjects.”
Mendelson, M., Borowik, A., Michallet, A. ‐., Perrin, C., Monneret, D., Faure, P., Levy, P. A., Pépin, J., Wuyam, B., & Flore, P. (2015) · Pediatric Obesity · doi:10.1111/ijpo.12015 · Cited by 129
“A large body of evidence suggests that short sleep duration may contribute to weight gain (16,17) and a potential mechanism for this relation is a hormonal and metabolic shift (18).”
BackgroundGuyon, A., Balbo, M., Morselli, L. L., Tasali, E., Leproult, R., L'Hermite-Balériaux, M., Van Cauter, E., & Spiegel, K. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2013-4254 · Cited by 127
Self-citationLajoie, P., Aronson, K. J., Day, A. G., & Tranmer, J. E. (2015) · BMJ Open · doi:10.1136/bmjopen-2014-007327 · Cited by 126
“Moreover, sleep has a regulatory effect on glucose metabolism and hormones regulating appetite, and therefore disturbances in sleep may promote weight gain among shift workers.(11) In the population-based Wisconsin Sleep Cohort Study, those with 5 h of sleep”
BackgroundFaraut, B., Nakib, S., Drogou, C., Elbaz, M., Sauvet, F., Bandt, J. P. D., & Léger, D. (2015) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2014-2566 · Cited by 124
Al‐Rashed, F., Sindhu, S. T. A. K., Madhoun, A. S. A., Alghaith, A., Azim, R., Al‐Mulla, F., & Ahmad, R. (2021) · Nature and Science of Sleep · doi:10.2147/nss.s311415 · Cited by 124
The genetics of insomnia – Evidence for epigenetic mechanisms?
Palagini, L., Biber, K. P. H., & Riemann, D. W. (2013) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2013.05.002 · Cited by 122
Shift work and sleep: medical implications and management
McFarlane, S. I. (2017) · Sleep Medicine and Disorders International Journal · doi:10.15406/smdij.2017.01.00008 · Cited by 97
“Sleep duration and quality are strongly related to the metabolic functioning of the body, and disturbed sleep slows metabolism, which could lead to weight gain and impaired glucose metabolism [92].”
BackgroundSleep deprivation lowers reactive aggression and testosterone in men
Côté, K. A., McCormick, C. M., Geniole, S. N., Renn, R. P., & MacAulay, S. D. (2012) · Biological Psychology · doi:10.1016/j.biopsycho.2012.09.011 · Cited by 91
Brindle, R. C., Yu, L., Buysse, D. J., & Hall, M. H. (2019) · SLEEP · doi:10.1093/sleep/zsz116 · Cited by 90
“eating) that are consistent with disturbed sleep playing a causal role in the development of cardiometabolic disorders [32, 33].”
BackgroundComplex physiology and clinical implications of time-restricted eating
Petersen, M. C., Gallop, M. R., Ramos, S. F., Zarrinpar, A., Broussard, J. L., Chondronikola, M., Chaix, A., & Klein, S. (2022) · Physiological Reviews · doi:10.1152/physrev.00006.2022 · Cited by 94
Addressing sleep disturbances: an opportunity to prevent cardiometabolic disease?
Grandner, M. A. (2014) · International Review of Psychiatry · doi:10.3109/09540261.2014.911148 · Cited by 88
“…factors associated with sleep-disordered breathing and sleep apnoea (Butt et al., 2010; Fava et al., 2011; Golbidi et al., 2012; Kent et al., 2011; Loke et al., 2012; Lurie, 2011; Monahan & Redline, 2011; Morselli et al., 2012; Pak et al., 2014; Phillips et al., 2013; Primhak & Kingshott, 2012).”
BackgroundSleep in the intensive care unit
Beltrami, F. G., Nguyên, X.-L., Pichereau, C., Maury, É., Fleury, B., & Fagondes, S. C. (2015) · Jornal Brasileiro de Pneumologia · doi:10.1590/s1806-37562015000000056 · Cited by 88
“(51,52) Such findings, however, are primarily based on epidemiological cohort studies evaluating chronic sleep deprivation or on models of sleep fragmentation in individuals with OSAS, which does not allow extrapolation of the findings to the acute setting of critically ill patients.(51,52)”
BackgroundSleep restriction is not associated with a positive energy balance in adolescent boys
Klingenberg, L., Chaput, J., Holmbäck, U. C., Jennum, P., Astrup, A. V., & Sjödin, A. M. (2012) · American Journal of Clinical Nutrition · doi:10.3945/ajcn.112.038638 · Cited by 87
Insufficient Sleep as a Contributor to Weight Gain: An Update
Chaput, J., & Tremblay, A. (2012) · Current Obesity Reports · doi:10.1007/s13679-012-0026-7 · Cited by 89
The impact of exercise on sleep and sleep disorders
Korkutata, A., Korkutata, M., & Lazarus, M. (2025) · npj Biological Timing and Sleep · doi:10.1038/s44323-024-00018-w · Cited by 101
Olea, E., Agapito, M. T., Gallego‐Martin, T., Rocher, A., Gómez-Niño, Á., Obeso, A., González, C., & Yubero, S. (2014) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00454.2014 · Cited by 83
“Repetitive awakenings fragment sleep and lead to diurnal somnolence and anxiety that contribute to sympathetic hyperactivity (52).”
BackgroundChronomedicine and type 2 diabetes: shining some light on melatonin
Forrestel, A. C., Miedlich, S. U., Yurcheshen, M. E., Wittlin, S. D., & Sellix, M. T. (2016) · Diabetologia · doi:10.1007/s00125-016-4175-1 · Cited by 82
“The most salient rhythm regulated by the internal timing system inmammals is the sleep/wake cycle [80, 81].”
BackgroundAn integrative review of sleep for nutrition professionals
Golem, D. L., Martin-Biggers, J. T., Koenings, M. M., Davis, K. F., & Byrd-Bredbenner, C. (2014) · Advances in Nutrition · doi:10.3945/an.114.006809 · Cited by 77
Aiding sleep in type 2 diabetes: therapeutic considerations
Tan, X., van Egmond, L., Chapman, C. D., Cedernaes, J., & Benedict, C. (2018) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(17)30233-4 · Cited by 72
Longitudinal associations of sleep curtailment with metabolic risk in mid-childhood
Feliciano, E. M. C., Rifas‐Shiman, S. L., Redline, S. S., Gillman, M. W., Peña, M.-M., & Taveras, E. M. (2014) · Obesity · doi:10.1002/oby.20894 · Cited by 71
“Independent of obesity, inadequate sleep may contribute to metabolic dysfunction: in adults, experimental evidence supports a role for shorter sleep in decreased insulin sensitivity (4), disrupted glucose homeostasis and appetite regulation (5) as well as cardiac risk factors such as hypertension (6) and incident diab…”
BackgroundPatterson, R. E., Emond, J. A., Natarajan, L., Wesseling-Perry, K., Kolonel, L. N., Jardack, P., Ancoli-Israel, S., & Arab, L. (2014) · The Journal of Nutrition · doi:10.3945/jn.113.186890 · Cited by 62
“In particular, sleep modulates the 24-h pattern of secretion of 2 key hormones involved in appetite and energy regulation: leptin and ghrelin (61).”
BackgroundEarly‐life influences on obesity: from preconception to adolescence
Wahlqvist, M. L., Krawetz, S. A., Rizzo, N., Domínguez-Bello, M. G., Szymanski, L. M., Barkin, S. L., Yatkine, A., Waterland, R. A., Mennella, J. A., Desai, M., et al. (2015) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12778 · Cited by 59
Obstructive sleep apnoea and metabolic syndrome: put CPAP efficacy in a more realistic perspective
Pépin, J., Tamisier, R., & Levy, P. A. (2012) · Thorax · doi:10.1136/thoraxjnl-2012-202807 · Cited by 64
The Effects of Music Intervention on Sleep Quality in Community-Dwelling Elderly
Wang, Q., Chair, S. Y., Wong, E. M. L., & Li, X. (2016) · The Journal of Alternative and Complementary Medicine · doi:10.1089/acm.2015.0304 · Cited by 55
Ferreira, M. B., de Almeida, F., Soro, J. C., Herter, M. M., Pinto, D. C., & Silva, C. S. (2021) · Frontiers in Psychology · doi:10.3389/fpsyg.2021.591875 · Cited by 61
Xiao, D. W., Shi, D., Yang, D., et al. (2012) · Biochemical Pharmacology · doi:10.1016/j.bcp.2012.11.026 · Cited by 51
Grandner, M. A. (2017) · Sleep Health · doi:10.1016/j.sleh.2017.07.014 · Cited by 50
Jeong, S. H., Jang, B. N., Kim, S. H., Kim, G. R., Park, E., & Jang, S. (2021) · BMC Public Health · doi:10.1186/s12889-021-12388-y · Cited by 42
Association between sleeping difficulty and type 2 diabetes in women
Li, Y., Gao, X., Winkelman, J. W., Feliciano, E. M. C., Jackson, C. L., Walters, A. S., Schernhammer, E. S., Redline, S. S., & Hu, F. B. (2016) · Diabetologia · doi:10.1007/s00125-015-3860-9 · Cited by 45
“Sleep continuity is considered to be important for normal metabolic function by modulating or controlling daily patterns in human physiology [27–29].”
Age protects from harmful effects produced by chronic intermittent hypoxia
Quintero, M., Olea, E., Conde, S. V., Obeso, A., Gallego‐Martin, T., González, C., Monserrat, J. M., Gómez-Niño, Á., Yubero, S., & Agapito, T. (2016) · The Journal of Physiology · doi:10.1113/jp270878 · Cited by 41
Zhang, Z., Sousa‐Sá, E., Pereira, J. R., Chaput, J., Okely, A. D., Feng, X., & Santos, R. (2018) · Sleep Medicine · doi:10.1016/j.sleep.2018.08.035 · Cited by 40
Endocrine Physiology in Relation to Sleep and Sleep Disturbances
Cauter, E. V., & Tasali, E. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4160-6645-3.00026-8 · Cited by 38
Przybylko, G., Morton, D. P., Kent, L. M., Morton, J. K., Hinze, J. S., Beamish, P., & Renfrew, M. E. (2021) · BMC Psychology · doi:10.1186/s40359-021-00577-8 · Cited by 40
“The causal relationship between insomnia and depression [34] is well established; and quality sleep is known to be paramount to good physical and mental health [35, 36].”
BackgroundSatoh, A., Brace, C. S., Rensing, N., & Imai, S. (2014) · Aging Cell · doi:10.1111/acel.12299 · Cited by 36
“Because sleep quality and metabolism are highly associated (Morselli et al., 2012), poor sleep quality by knockdown of Prdm13 in the DMH might cause increased body weight secondarily.”
BackgroundLi, A., Luo, H., Zhu, Y., Zhang, Z., Liu, B., Kan, H., Jia, H., Wu, Z., Guo, Y., & Chen, R. (2025) · Nature Communications · doi:10.1038/s41467-025-57781-y · Cited by 44
Over-indebtedness and its association with sleep and sleep medication use
Warth, J., Puth, M., Tillmann, J., Porz, J., Zier, U., Weckbecker, K., & Münster, E. (2019) · BMC Public Health · doi:10.1186/s12889-019-7231-1 · Cited by 37
Lee, G.-J., Kim, K., Kim, S.-Y., Kim, J., Suh, C., Son, B.-C., Lee, C. K., & Choi, J. (2016) · Annals of Occupational and Environmental Medicine · doi:10.1186/s40557-016-0148-6 · Cited by 33
“, eating and exercise habits) and weight gain [20, 21].”
BackgroundMetabolic Risk Factors and Posttraumatic Stress Disorder
Talbot, L. S., Rao, M. N., Cohen, B. E., Richards, A. L., Inslicht, S. S., O’Donovan, A., Maguen, S., Metzler, T. J., & Neylan, T. C. (2015) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000176 · Cited by 31
Maddahi, N. S., Yarizadeh, H., Setayesh, L., Nasir, Y., Alizadeh, S., & Mirzaei, K. (2020) · BMC Research Notes · doi:10.1186/s13104-020-05025-1 · Cited by 30
“Mechanistically, sleep modulates the pattern of secretion of two key hormones involved in appetite and energy regulation: ghrelin and leptin [48].”
BackgroundChen, L., Tiong, C., Tsai, C., Liao, W., Yang, S., Youn, S., Mai, F., & Chang, H. (2014) · Brain Structure and Function · doi:10.1007/s00429-014-0716-x · Cited by 30
Distinct Associations between Hypertension and Obstructive Sleep Apnea in Male and Female Patients
Yu, Q., Yin, G., Zhāng, P., Song, Z., Chen, Y., Zhang, D., & Hu, W. (2014) · PLoS ONE · doi:10.1371/journal.pone.0113076 · Cited by 29
“Normal sleep is a basic physiological process to maintain health by decreasing the body’s metabolic rate, sympathetic nervous activity, blood pressure, and heart rate and increasing cardiac vagal tone [7].”
BackgroundPositionspapier „Schlafmedizin in der Kardiologie“
Oldenburg, O., Arzt, M. E., Bitter, T., Bonnemeier, H., Edelmann, F., Fietze, I., Podszus, T., Schäfer, T., Schöbel, C., Skobel, E. C., et al. (2015) · Der Kardiologe · doi:10.1007/s12181-015-0654-8 · Cited by 30
Dong, Y., & Zhang, X. (2021) · Building and Environment · doi:10.1016/j.buildenv.2021.108060 · Cited by 28
Lin, J., Zhao, H., Shen, J., & Jiao, F. (2017) · The Journal of Pediatrics · doi:10.1016/j.jpeds.2017.08.039 · Cited by 25
Marfuah, D., Hadi, H., & Huriyati, E. (2016) · Jurnal Gizi dan Dietetik Indonesia (Indonesian Journal of Nutrition and Dietetics) · doi:10.21927/ijnd.2013.1(2).93-101 · Cited by 25
Optimizing Sleep in Older Adults: Where Does High-Intensity Interval Training Fit?
Bullock, A., Kovacevic, A., Kuhn, T., & Heisz, J. J. (2020) · Frontiers in Psychology · doi:10.3389/fpsyg.2020.576316 · Cited by 23
Xiang, S., Dong, J., Li, X., & Li, L. (2021) · BioMed Research International · doi:10.1155/2021/5585678 · Cited by 26
“Previous reports have already shown that insufficient sleep duration can increase the risk of many diseases, such as cardiovascular and metabolic disease risk [17, 18], neurocognitive dysfunction [19], and mental health [20].”
BackgroundImpact of menstrual cycle phase on endocrine effects of partial sleep restriction in healthy women
LeRoux, A., Wright, L., Perrot, T. S., & Rusak, B. (2014) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2014.06.002 · Cited by 24
Nonlinear Dynamics Forecasting of Obstructive Sleep Apnea Onsets
Le, T., & Bukkapatnam, S. (2016) · PLoS ONE · doi:10.1371/journal.pone.0164406 · Cited by 23
Sleep Deficiency and Cardiometabolic Disease
Killick, R., Stranks, L., & Hoyos, C. M. (2022) · Clinics in Chest Medicine · doi:10.1016/j.ccm.2022.02.011 · Cited by 23
Hart, C. N., Hawley, N. L., & Wing, R. R. (2016) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2016.08.002 · Cited by 22
Aerenhouts, D., Ickmans, K., Clarys, P., et al. (2014) · Disability and Rehabilitation · doi:10.3109/09638288.2014.993093 · Cited by 22
“Sleep plays a major role in maintaining metabolic health [2].”
BackgroundSleep disturbances and risk of sick leave: systematic review and meta-analysis
Amiri, S., & Behnezhad, S. (2020) · Sleep and Biological Rhythms · doi:10.1007/s41105-020-00270-0 · Cited by 19
Wirth, J., Hillesheim, E., & Brennan, L. (2022) · Nutrition Reviews · doi:10.1093/nutrit/nuac061 · Cited by 21
McWhorter, K. L., Park, Y., Gaston, S. A., Fang, K., Sandler, D. P., & Jackson, C. L. (2019) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2019-000652 · Cited by 21
“of sleep can lead to upregulation of the hunger-inducing ghrelin hormone and downregulation of the leptin hormone, which is associated with satiety.(15) 16 Dysregulation of these hormones may lead to overeating and eventually obesity—a strong risk factor for type 2 diabetes.”
BackgroundLu, Y., Liu, Y., & Li, Y. (2013) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2013.12.006 · Cited by 21
Rozanski, A. (2016) · Cardiovascular Innovations and Applications · doi:10.15212/cvia.2016.0033 · Cited by 22
Olfactory Insights into Sleep-Dependent Learning and Memory
Shanahan, L. K., & Gottfried, J. A. (2014) · Progress in brain research · doi:10.1016/b978-0-444-63350-7.00012-7 · Cited by 25
Byrne, E. M., Gehrman, P., Trzaskowski, M., Tiemeier, H. W., & Pack, A. I. (2016) · SLEEP · doi:10.5665/sleep.6168 · Cited by 19
A Scientometric Review of Obstructive Sleep Apnea and Obesity
Neoh, M. J. Y., Carollo, A., Lim, M., Dimitriou, D., & Esposito, G. (2023) · Applied Sciences · doi:10.3390/app13020753 · Cited by 20
Effects of Sleep Deficiency on Hormones, Cytokines, and Metabolism
Buxton, O. M., Broussard, J. L., Zahl, A. K., & Hall, M. H. (2013) · Springer eBooks · doi:10.1007/978-1-4614-9527-7_2 · Cited by 22
Assessing the effect of physical activity and exercise on nurses’ well-being
Owusu-Sekyere, F. (2020) · Nursing Standard · doi:10.7748/ns.2020.e11533 · Cited by 20
van den Ende, E. S., Merten, H., der Roest, L. V., Toussaint, B., van Rijn, Q., Keesenberg, M., Lodders, A. M., van Veldhuizen, K. D. I., Vos, I. E., Hoekstra, S., et al. (2022) · JAMA Network Open · doi:10.1001/jamanetworkopen.2022.32623 · Cited by 19
“of awakenings Actigraphy 12 (9-18) 13 (8-19) 1 .”
InfluentialIwagami, M., Seol, J., Hiei, T., Tani, A., Chiba, S., Kanbayashi, T., Kondo, H., Tanaka, T., & Yanagisawa, M. (2023) · Scientific Reports · doi:10.1038/s41598-023-47979-9 · Cited by 15
“These findings suggest that certain EEG-based sleep characteristics are not only associated with blood pressure, but also with metabolic functions and inflammation, in line with previous results 25–27 .”
ResultTaji, W., Pierson-Bartel, R., & Ujma, P. P. (2023) · PLoS ONE · doi:10.1371/journal.pone.0288909 · Cited by 13
Hart, C. N., Hawley, N. L., & Wing, R. R. (2016) · Pediatric Clinics of North America · doi:10.1016/j.pcl.2016.02.007 · Cited by 14
Cha, E., Talman, M. S., Massey, A. H., Yan, F., & Rogers, A. E. (2018) · Biological Research For Nursing · doi:10.1177/1099800418791047 · Cited by 14
Unacylated ghrelin, leptin, and appetite display diurnal rhythmicity in lean adults
Templeman, I., Smith, H., Walhin, J., Middleton, B., Gonzalez, J. T., Karagounis, L. G., Johnston, J. D., & Betts, J. A. (2021) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00920.2020 · Cited by 17
“365 Sleep also plays an important role in the nocturnal peak in leptin, which is thought to 366 facilitate prolonged fasting overnight (33, 47).”
BackgroundBadia, P., Hickey, V., Flesch, L., Byerly, M., Sensibaugh, C., Potts, K., Michel, C., Drozd, A., Curd, F. M., Crosby, L. E., et al. (2019) · Transplantation and Cellular Therapy · doi:10.1016/j.bbmt.2019.05.001 · Cited by 13
Zhu, D., Kang, W., Zhang, S., Qiao, X., Liu, J., Liu, C., & Lu, H. (2020) · Scientific Reports · doi:10.1038/s41598-020-70238-0 · Cited by 12
Positionspapier „Schlafmedizin in der Kardiologie“, Update 2021
Fox, H., Arzt, M. E., Bergmann, M. W., Bitter, T., Linz, D., Oldenburg, O., Penzel, T., Rillig, A., Schöbel, C., Sinha, A. M., et al. (2021) · Der Kardiologe · doi:10.1007/s12181-021-00506-4 · Cited by 12
Gu, H., Ru, Y., Wang, W., Cai, G., Gu, L., Ye, J., Zhang, W., & Wang, L. (2022) · Drug Design Development and Therapy · doi:10.2147/dddt.s363286 · Cited by 12
“cardiovascular diseases, neurocognitive dysfunction, metabolic disturbances, and the condition can also result in sudden death.(2) Chronic intermittent hypoxia (CIH), a typical pathophysiological hallmark of obstructive sleep apnea, is”
BackgroundYano, Y., Hayakawa, M., Kuroki, K., Ueno, H., Yamagishi, S., Takeuchi, M., Eto, T., Nagata, N., Nakazato, M., Shimada, K., et al. (2013) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2012.12.006 · Cited by 11
Li, P. W. C., Yu, D. S. F., Chong, S. O. K., & Lin, R. S. Y. (2020) · The Journal of Cardiovascular Nursing · doi:10.1097/jcn.0000000000000662 · Cited by 12
Sleep Deficiency and Cardiometabolic Disease
Killick, R., Stranks, L., & Hoyos, C. M. (2023) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2023.05.012 · Cited by 12
Lin, C., Lin, K., Hsueh, M., & Liao, Y. (2023) · Journal of the Formosan Medical Association · doi:10.1016/j.jfma.2023.08.001 · Cited by 11
Recommendations for psychologists in Stage III pediatric obesity program
Cadieux, A. M., Testa, E. G., Baughcum, A. E., Shaffer, L. A., Santos, M., Gaffka, B. J. S., Gray, J. S., Burton, E. T., & Ward, W. L. (2015) · Children s Health Care · doi:10.1080/02739615.2014.979919 · Cited by 11
Endocrine Physiology in Relation to Sleep and Sleep Disturbances
Cauter, E. V., & Tasali, E. (2016) · Elsevier eBooks · doi:10.1016/b978-0-323-24288-2.00020-9 · Cited by 10
Pépin, J., Tamisier, R., Godin‐Ribuot, D., & Levy, P. A. (2014) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2014.12.004 · Cited by 11
Sleep chart of biological ageing clocks in middle and late life
O’Toole, C. K., Song, Z., Anagnostakis, F., Yang, Z., Tian, Y., Duggan, M. R., Zou, C., Leng, Y., Cai, Y., Bai, W., et al. (2026) · Nature · doi:10.1038/s41586-026-10524-5 · Cited by 21
Metadata
- Authors
- Morselli, L. L., Guyon, A., & Spiegel, K.
- Affiliations
- University of Chicago (US)
- Lyon 1 Université (FR)
- Corresponding author
- Spiegel, Karine
- Venue
- Pflügers Archiv - European Journal of Physiology
- Published
- 2011-11-19
- Volume
- 463
- Issue
- 1
- Pages
- 139-160
- ISSN
- 0031-6768 (ISSN-L)
- 1432-2013
- PMC
- PMC3289068
- OpenAlex
- W1966891298
- Semantic Scholar
- 28ae604abbcdd449c303e162c78fe2dd56e66a64
- Cited by
- 199
- References
- 230
- Citations by year
- 2026: 8 · 2025: 13 · 2024: 9 · 2023: 11 · 2022: 13 · 2021: 15 · 2020: 13 · 2019: 10 · 2018: 6 · 2017: 10 · 2016: 24 · 2015: 21 · 2014: 23 · 2013: 10 · 2012: 12
- FWCI
- 1.91
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Pflügers Archiv - European Journal of Physiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute on Aging (P01-AG11412., P01AG011412)
- National Heart, Lung, and Blood Institute (R01HL075079, R01HL075025)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK-071960, P60DK20595, P60DK020595)
- National Center for Research Resources (M01RR000055)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Health Sciences › Medicine › Physiology (medical) › Obstructive Sleep Apnea Research
- Keywords
- sleep, metabolic function, glucose homeostasis, appetite regulation, sleep duration, sleep quality, obesity, diabetes mellitus, obstructive sleep apnea, intermittent hypoxemia, continuous positive airway pressure, endocrine function
- MeSH terms
- Animals, Appetite Regulation, Diabetes Mellitus, Glucose, Humans, Metabolism, Obesity, Sleep, Sleep Apnea, Obstructive
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