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Cited by 199Sleep and related disordersSleep and Wakefulness ResearchObstructive Sleep Apnea Research

Sleep and metabolic function

Open access
Morselli, Lisa L., Guyon, Aurore, Spiegel, Karine·2012·Pflügers Archiv - European Journal of Physiology
DOI 10.1007/s00424-011-1053-zPMC PMC3289068
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Abstract

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.

AI snapshot

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.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1007/s00424-011-1053-z

Cites

227 of 227 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 197 cited sources checked · 0 supported · 0 flagged

  • Findingnone given

    A dose-response relationship exists between slow wave activity and the amount of growth hormone secreted in young and older men.

    “a dose–response relationship between slow wave activity (SWA) and the amount of GH secreted has been evidenced in young and older men.”
    Quote in the paperSubstantial claim
  • Findingcitation

    Total sleep deprivation leads to marked hyperphagia in rodents.

    “conversely, total sleep deprivation leads to marked hyperphagia [133].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [133] Rechtschaffen A, Bergmann BM (1995) Sleep deprivation in the rat by the disk-over-water method. Behav Brain Res 69:55–63 source

      Not checked in the free run.

  • Findingcitation

    Slow wave sleep results in a 30-40% decrease in cerebral glucose metabolism relative to waking or REM sleep.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [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

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  • Findingcitation

    Both nocturnal and daytime sleep are associated with a marked decrease in glucose tolerance, reflected by increased glucose levels.

    “Both nocturnal and daytime sleeps were associated with a marked decrease in glucose tolerance, reflected by increased glucose levels.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

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  • Findingcitation

    In rodents, food shortage or starvation results in decreased sleep.

    “In rodents, food shortage or starvation results in decreased sleep [35]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [35] Danguir J, Nicolaidis S (1979) Dependence of sleep on nutrients’ availability. Physiol Behav 22:735–740 source

      Not checked in the free run.

  • May combine two claims. 44
  • Classified as probably not a substantial claim. 5

  • May combine two claims.

    Findingcitation

    In healthy young men, a major growth hormone pulse accounting for about 70% of daily production occurs shortly after sleep onset, associated with the first phase of slow wave sleep.

    “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).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

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    Findingcitation

    Wake-sleep transitions inhibit cortisol levels, and sleep-wake transitions stimulate them.

    “wake–sleep and sleep–wake transitions are associated with inhibition and stimulation of cortisol levels, respectively [59, 168, 186].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [59] Gronfier C, Brandenberger G (1998) Ultradian rhythms in pituitary and adrenal hormones: their relations to sleep. Sleep Med Rev 2:17–29 source

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    • cites [168] Steiger A (2003) Sleep and endocrinology. J Intern Med 254:13–22 source

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    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    During sleep deprivation, glucose and insulin elevations are about half the amplitude of those during nocturnal sleep, indicating that circadian-dependent processes also modulate glucose regulation.

    “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.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    Growth hormone levels increase during sleep regardless of when sleep occurs and are markedly reduced during sleep deprivation.

    “GH levels are increased during sleep, irrespective of the time at which sleep occurs, and they are markedly diminished during sleep deprivation.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [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 in the free run.

    • cites [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

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    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    In Benedict et al., decreased glucose tolerance during sleep debt resulted from reduced insulin sensitivity combined with beta-cell dysfunction, since insulin levels were not affected by sleep.

    “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.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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 in the free run.

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    Findingcitation

    Of three studies assessing insulin sensitivity after a glucose load, two found reduced insulin sensitivity after sleep loss and one found reduced insulin sensitivity after recovery sleep.

    “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].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source

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    • cites [195] VanHelder T, Symons JD, Radomski MW (1993) Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 64:487–492

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    • cites [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 source

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    Findingcitation

    During ivGTT, glucose tolerance was decreased by more than 40% in sleep debt and reached values typical for older adults with impaired glucose tolerance.

    “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].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    Short sleep duration predicted a higher incidence of diabetes in seven of nine prospective studies, while poor sleep quality was associated with increased risk in five of six studies.

    “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].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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 in the free run.

  • May combine two claims.

    Findingcitation

    Glucose tolerance was altered after 72-126 hours of total sleep deprivation and after 24 hours of total sleep deprivation.

    “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].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [86] Kuhn E, Brodan V, Brodanova M, Rysanek K (1969) Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 11:165–174

      Not checked in the free run.

    • cites [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 in the free run.

  • May combine two claims.

    Findingcitation

    Increased fasting glucose was reported after 120 hours of total sleep deprivation but not after 72-126 hours or one night of total sleep deprivation.

    “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]”
    Quote in the paperSubstantial claim0 of 5 sources checked
    • cites [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 in the free run.

    • cites [86] Kuhn E, Brodan V, Brodanova M, Rysanek K (1969) Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 11:165–174

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    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [195] VanHelder T, Symons JD, Radomski MW (1993) Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 64:487–492

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    All but one of the studies characterizing overnight acylated ghrelin profiles confirmed increased nocturnal total ghrelin and demonstrated a concomitant increase in acylated ghrelin.

    “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.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    In the sleep fragmentation study, the disposition index was not affected because an increase in insulin release compensated for the decrease in insulin sensitivity.

    “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.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [167] Stamatakis KA, Punjabi NM (2010) Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 137:95–101 source

      Not checked in the free run.

  • May combine two claims.

    Findingcitation

    The same meta-analysis reported an odds ratio of 1.92 in children with the shortest sleep duration, suggesting a dose-response relationship between sleep duration and increased risk of obesity.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Findingnone given

    In adults, studies are less consistent and often show a U-shaped relationship between sleep duration and BMI.

    “Studies in adults are less consistent and often show a U-shaped relationship between sleep duration and BMI.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingreasoning

    Among the published studies, only five were controlled; three found a positive effect of CPAP on glucose homeostasis and two did not.

    “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.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    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.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Sleep timing, duration, and quality partly determine glucose tolerance, the 24-hour insulin release pattern, growth hormone and cortisol, and the appetite hormones leptin and ghrelin.

    “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].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [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 in the free run.

    • cites [168] Steiger A (2003) Sleep and endocrinology. J Intern Med 254:13–22 source

      Not checked in the free run.

    • cites [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

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Type 2 diabetes involves insulin resistance, impaired insulin secretion, and increased glucose production.

    “Type 2 diabetes is a complex metabolic disorder that involves insulin resistance, impaired insulin secretion, and increased glucose production [37, 79].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [37] DeFronzo RA (2004) Pathogenesis of type 2 diabetes mellitus. Med Clin North Am 88:787–835, ix source

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    • cites [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

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  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Voluntary sleep curtailment has become increasingly common in all age groups over the past several decades.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [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.

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    • cites [114] National Sleep Foundation (2008) “Sleep in America” Poll. http://www.sleepfoundation.org./sites/default/files/2008%20POLL%20SOF.PDF . 1–45

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  • May combine two claims.

    Interpretationreasoning

    Glucose regulation is markedly influenced by circadian rhythmicity and sleep, and these effects could be partially mediated by cortisol and growth hormone.

    “Thus, glucose regulation is markedly influenced by circadian rhythmicity and sleep, and these effects could be partially mediated by cortisol and GH.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Ghrelin stimulates hunger and food intake, reduces energy expenditure, and promotes fat retention.

    “In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [56] Gasco V et al (2010) Endocrine and metabolic actions of ghrelin. Endocr Dev 17:86–95 source

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    • cites [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

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    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    Findings support an inhibitory effect of sleep on ghrelin, consistent with the association between sleeping and fasting and between feeding and arousal.

    “These findings support an inhibitory effect of sleep on ghrelin, consistent with the association between sleeping and fasting and, conversely, between feeding and arousal.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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 in the free run.

    • Rests on an assumption: Feeding and sleeping are mutually exclusive.

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    Premisecitation

    Leptin inhibits hunger and food intake, increases energy expenditure, and promotes fat utilization.

    “Leptin inhibits hunger and food intake, increases EE, and promotes fat utilization [1, 193].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [1] Ahima RS, Saper CB, Flier JS, Elmquist JK (2000) Leptin regulation of neuroendocrine systems. Front Neuroendocrinol 21:263–307 source

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    • cites [193] van Dijk G (2001) The role of leptin in the regulation of energy balance and adiposity. J Neuroendocrinol 13:913–921 source

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  • May combine two claims.

    Premisecitation

    One adult prospective study found a bidirectional relationship: short sleep predicted later weight gain, and body weight or obesity predicted later short sleep.

    “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.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    The findings suggest a vicious circle in which short sleep initially promotes weight gain, excess adiposity then induces sleep disturbances, and total sleep time falls further.

    “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.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    The effect of reduced sleep duration on obesity risk is especially clear in children, probably because the relevant physiological and behavioral mechanisms are stronger at younger ages.

    “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.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The physiological and behavioral mechanisms linking short sleep to obesity are stronger at younger ages.

  • May combine two claims.

    Premisecitation

    Even modest weight increases have significant long-term implications for adiposity-related metabolic dysfunction, diabetes, cardiovascular disease, and cancer.

    “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].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [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

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    • cites [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

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    • cites [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

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    • cites [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

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  • May combine two claims.

    Premisecitation

    Some adult prospective studies report U- or L-shaped associations, so the link between longer sleep and BMI is conflicting in adults and absent in children.

    “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.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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

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  • May combine two claims.

    Interpretationcitation

    Weight may not increase linearly during a period of short sleep, so a longitudinal study must begin before or at the start of the short-sleep transition to detect effects, which is less likely in older people.

    “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.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

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    • The authors state this as an assumption: Weight is not gained linearly over the course of a short sleeping period.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    In the general population, the prevalence of obstructive sleep apnea is around 17%.

    “In the general population, the prevalence of OSA is around 17% [215].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [215] Young T, Peppard PE, Taheri S (2005) Excess weight and sleep-disordered breathing. J Appl Physiol 99:1592–1599 source

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    Premisecitation

    In overweight and obese middle-aged adults on moderate caloric restriction, 14 nights of 5.5 h versus 8.5 h sleep opportunity decreased the proportion of weight lost as fat by 55% and increased fat-free mass loss by 60%.

    “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%.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

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    Premisecitation

    Another study found no effect of total sleep deprivation but reported reduced 24-hour leptin diurnal amplitude due to higher daytime leptin.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [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

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  • May combine two claims.

    Interpretationcitation

    St-Onge et al. found an increase of about 300 kcal/day after five days of 4 h bedtimes despite no clear effect on subjective hunger and appetite, suggesting that subjective assessments are unreliable.

    “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.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [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 in the free run.

    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Because leptin is increased by food intake and correlates with obesity, the unchanged or increased leptin levels may be the expected consequence of the positive energy balance from greater food intake and weight gain.

    “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].”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    The sole study finding no change in caloric intake after sleep loss provided highly palatable food ad libitum 1 h after awakening; overeating of 60% regardless of condition may have masked the effect of sleep loss on food consumption.

    “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].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    One pathway that may link short sleep to excess weight is increased caloric intake in short sleepers.

    “One pathway that may link short sleep to excess weight is increased caloric intake in short sleepers.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationcitation

    In the caloric-restriction study, leptin declined with weight and adiposity loss without a significant independent effect of sleep loss, so negative energy balance most likely overrode the effect of sleep duration.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Nedeltcheva et al. observed similar weight at the end of each 14-day sleep extension or restriction period in overweight men and women with unlimited palatable food; subjects overate and gained about 2 kg in each condition.

    “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].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [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 in the free run.

    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In a randomized crossover study of young normal-weight men, two nights of 4 h in bed versus 10 h decreased leptin by 18%, increased ghrelin by 28%, and raised the ghrelin/leptin ratio by more than 70%.

    “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).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In Benedict et al., ghrelin was higher in the second half of the night after total sleep deprivation than during normal sleep, while nighttime leptin was unchanged.

    “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.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    In the latter two studies, energy expenditure measured by doubly labeled water did not differ between conditions, suggesting that the increased food consumption with sleep loss is not due to a comparable rise in energy needs and would eventually produce a positive energy balance.

    “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.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    In overweight middle-aged adults, two weeks of sleep restriction by 1.5 h/night versus extension by 1.5 h/night increased calories from high-carbohydrate snacks, while meal and total energy intake were unchanged.

    “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].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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 in the free run.

  • May combine two claims.

    Interpretationreasoning

    In the sleep-restriction condition with negative energy balance, ghrelin and hunger increased, suggesting that sleep loss can exacerbate the upregulation of ghrelin and hunger triggered by negative energy balance.

    “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.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    The same sleep-restriction study found a 23% increase in hunger and a 33% increase in appetite for high-carbohydrate nutrients.

    “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.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Three days of underfeeding by about 900 cal/day in healthy lean volunteers decreased leptin levels by 22%, highlighting the functional significance of the leptin decrease seen with sleep loss.

    “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.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [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 in the free run.

  • May combine two claims.

    Premisecitation

    Four positive studies used the hyperinsulinemic-euglycemic clamp, two used continuous glucose monitoring, and one used the minimal model estimate from an intravenous glucose tolerance test.

    “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”
    Quote in the paperSubstantial claim0 of 6 sources checked
    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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 in the free run.

    • cites [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

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    HOMA-IR correlates reasonably well with clamp and minimal model estimates of insulin sensitivity/resistance, but it measures basal insulin sensitivity/resistance and does not provide information about dynamic conditions.

    “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].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [201] Wallace TM, Levy JC, Matthews DR (2004) Use and abuse of HOMA modeling. Diabetes Care 27:1487 source

      Not checked in the free run.

    • Rests on an assumption: HOMA-IR correlates reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance.
47 of 47

  • 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.”
11 of 11

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 hypothalamic-pituitary-adrenal axis is a putative key mediator of the adverse health effects of insufficient sleep.

    “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]

  • Habitual short sleep, usually 6 hours or less, is 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.

    “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]

  • The hypothalamic-pituitary-adrenal axis regulates a wide range of physiologic processes.

    “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]

  • The hypothalamic-pituitary-adrenal axis is affected by experimental sleep restriction.

    “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]

  • Insufficient sleep duration is associated with weight gain and obesity.

    “short sleep duration (6 hours or less), and especially very short sleep duration (less than 5 hours) is associated with increased cardiometabolic morbidity and mortality, including weight gain and obesity, hypertension, hyperlipidemia, and diabetes.”

    From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [24]

Cites

Flagged first, then by citations

3 of the 230 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  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

Related

Authors
Morselli, L. L., Guyon, A., & Spiegel, K.
Affiliations
  • University of Chicago (US)
  • Lyon 1 Université (FR)
Corresponding author
Spiegel, Karine
ORCID
Venue
Pflügers Archiv - European Journal of Physiology
Publisher
Springer Science and Business Media LLC
Published
2011-11-19
Volume
463
Issue
1
Pages
139-160
ISSN
  • 0031-6768 (ISSN-L)
  • 1432-2013
DOI
10.1007/s00424-011-1053-z
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
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 › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-09.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-09.

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