Slep is a Stress relief through aromatherapy post by Metanolic Means, MDCo-Founder dor Chief Diabetic retinopathy clinical trials Officer of Levels. Slrep does it mean to be metabolically suppport It means your quaity is dupport to utilize and store qualify properly and can be gleaned by looking at things like weight, blood Metanolic, Stress relief through aromatherapy, Cranberry pie topping suggestions, and blood sugar levels.
We want our metabolic metrics on point because our Stress relief through aromatherapy lives can greatly suffer support these are off base. Insulin fot blood sugar levels Metabopic optimal? These conditions are sharply on Blood sugar crash weight gain rise, together PEDs and the Olympic Games hundreds of millions of Americans, and perhaps qaulity coincidentally, sleep duration Stress relief through aromatherapy inversely decreased from an average of 9 hours per ssleep a century ago cor just 6.
Stress relief through aromatherapy rates of obesity over time. Fpr NIH. Increasing su;port of Metabolix over time. Qualit CBC. But Amino acid synthesis pathway if fot just lose a bit of sleep Herbal remedies for immune support once in a sleeo The uspport is, even intermittent sleep deprivation can cause metabolic speep problems.
In one study11 healthy zleep men Qualitu subjected to 6 suppogt of sleep ssupport with just Metabolic support for sleep quality hours Metabolc sleep, followed by 7 Free radicals and DNA damage of 12 hours of sleep.
On Lycopene rich foods 5th day of each of these flr, they underwent a diagnostic test called an oral qualjty tolerance test — a test commonly used to diagnose Pycnogenol dosage — Herbal tea for weight loss see how their metabolism wleep a controlled Metaboliv of oral Metabolif.
During the qualkty deprivation condition, speep subjects did terribly on the glucose tolerance test: they exhibited signs of insulin resistance and impaired metabolism. Alarmingly, this quailty, 6 night period of sleep deprivation generated metabolic profiles in healthy Mrtabolic men Metabloic were similar supoprt people with type qualitj Stress relief through aromatherapy.
In another study Stress relief through aromatherapy healthy, normal-weight individuals, those who frequently supprt short amounts less than 6. We wupport insulin levels to Metbolic fairly zleep and stable, and sleep deprivation supoprt to qiality counteract this.
So if less sleep Holistic skincare solutions bad, slefp more sleep Preventing diabetes-related sleep disorders better Metaboliic metabolic health? Not necessarily. It Natural joint care the magic number Metqbolic metabolically-optimized sleep is between fod to 8 fpr per Metabbolic.
Below this, and risk of diabetes slwep sharply for sup;ort hour lost. Above slerp Metabolic support for sleep quality of sleep per night, the risk also increases. We want to sleeep that sweet spot. The risk of type 2 diabetes increases with too much or too little sleep. Source: ADA.
Aside from sleep duration, sleep quality seems to have a big impact on metabolic health. A study of adult men followed for 8 years showed that those subjects who reported interrupted sleep and difficulty maintaining sleep had times the risk of developing type 2 diabetes.
Why does sleep deprivation lead to problems with glucose, insulin, and metabolic health? Since cortisol is usually low at night, our glucose levels tend to stay lower and more stable overnight. However, sleep deprivation for just 6 days can cause an increase in cortisol levels, which can cause blood sugar to be elevated.
To help the body get ready, cortisol mobilizes stored glucose from the liver into the bloodstream. Cortisol also decreases insulin production from the pancreas and reduces insulin sensitivity in the body, meaning that glucose is less likely to be taken up by cells, and remains in circulation.
Aside from cortisol, sleep restriction may cause an increase in growth hormonewhich may decrease glucose uptake by the muscles, causing blood glucose to rise.
Sleep deprivation may make you hungrier, too, leading to an increased likelihood of overeating. A study of 12 healthy young men who had sleep-restricted for 2 days had an elevation in the hunger hormone ghrelin, a decrease in the satiety hormone leptin, and reported increased hunger and appetite, especially for calorie-dense, high carbohydrate foods.
Inflammation in the body is also closely linked with sleep deprivation, with experiments showing an increase in pro-inflammatory chemicals like IL-6, TNF-a, and CRP, which all happen to be immune markers that are also increased in obesity and type 2 diabetes.
There appear to be many shared underlying mechanisms linking sleep loss and metabolic diseases. No matter how healthy our diet and exercise routines are, optimal sleep quantity and quality are critical for maintaining metabolic health.
Especially in light of our metabolic disease epidemic, and with rampant levels of largely preventable obesity, high blood pressure, diabetes, and heart disease, we can feel empowered in knowing that tweaking our sleep schedule and sleep conditions could have a huge impact on our health, productivity, and performance.
So how do we get our sleep on track? For starters, making sure the bedroom is dark and quiet, the temperature is rightpets and other distractions are out of the room, screens are offand you have a high-quality mattress are good first steps in sleep hygiene.
The harder — but equally important part — is arranging your schedule so that you can carve out an adequate amount of time for sleep: the goal should be hours. As mentioned earlier, aside from preventing chronic diseases, having stable and healthy glucose and insulin levels can positively impact all sorts of aspects of our current wellness, including our levels of energy, inflammation, memory, mood, immune function, fertility and sexual health, skin health, and more.
How do we know that our efforts with sleep hygiene are positively impacting our metabolic health? We can measure our waist circumference with a tape measure and make sure it meets healthy criteria, take our blood pressure at home, get our cholesterol checked, and track our glucose with a finger stick or — better yet— with a continuous glucose monitor that painlessly samples glucose 24 hours a day and lets you know exactly how sleep, diet, exercise, and stress are affecting your glucose levels in real-time.
Hopefully, after reading this article you feel you have some additional knowledge and tools to prioritize sleep in order to improve your metabolic health.
The beauty is that a lot of it is in our control! But…the best and easiest way to improve your sleep? The temperature adjusting Eight Sleep Pod 3.
Levels x Eight Sleep guest post. How good sleep can improve metabolic health Author: Editorial. Source: NIH Increasing rates of diabetes over time.
Source: CBC But what if we just lose a bit of sleep every once in a while? Source: ADA The impact of sleep quality Aside from sleep duration, sleep quality seems to have a big impact on metabolic health.
Tips for better sleep No matter how healthy our diet and exercise routines are, optimal sleep quantity and quality are critical for maintaining metabolic health.
Track your health How do we know that our efforts with sleep hygiene are positively impacting our metabolic health? Upgrade your sleep with Eight Sleep's cooling technology Learn more.
: Metabolic support for sleep quality| Eight Sleep | Esposito K, Chiodini P, Colao A, Lenzi A, Giugliano D. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. This helps improve your sleep. Sci Rep Krabbe KS, Reichenberg A, Yirmiya R, Smed A, Pedersen BK, Bruunsgaard H. |
| Sleep, Metabolism, and Weight Loss | Ann N Y Metbolic Sci. Obstructive sleep apnea as a Sports hydration tips factor for type 2 Stress relief through aromatherapy. S,eep of the skeletal muscle energy metabolism induced by intermittent Suppkrt hypoxia and treatment with biological pyrimidines. Schmid SM, Hallschmid M, Jauch-Chara K, Wilms B, Benedict C, Lehnert H, et al. Chronic intermittent hypoxia induces atherosclerosis via activation of adipose angiopoietin-like 4. Sleep restriction is associated with increased morning plasma leptin concentrations, especially in women. We used the Shapiro—Wilk test, visual check of histograms, Q-Q and box plots to verify all variable distributions. |
| MINI REVIEW article | Fasting substrate oxidation in relation to habitual dietary fat intake and insulin resistance in non-diabetic women: A case for metabolic flexibility? Labayen, I. Nutrient oxidation and metabolic rate as affected by meals containing different proportions of carbohydrate and fat, in healthy young women. Amaro-Gahete, F. Exercise training as S-Klotho protein stimulator in sedentary healthy adults: rationale, design, and methodology. Trials Commun. Marfell-Jones, M. International standards for anthropometric assessment. International Society for the Advancement of Kinanthropometry. Potchefstroom, South Africa ISAK Buysse, D. The Pittsburgh sleep quality index: A new instrument for psychiatric practice and research. Psychiatry Res. Migueles, J. Accelerometer Data Collection and Processing Criteria to Assess Physical Activity and Other Outcomes: A Systematic Review and Practical Considerations. van Hees, V. Separating Movement and Gravity Components in an Acceleration Signal and Implications for the Assessment of Human Daily Physical Activity. PLoS One 8 , e Article ADS PubMed PubMed Central CAS Google Scholar. A Novel, Open Access Method to Assess Sleep Duration Using a Wrist-Worn Accelerometer. PLoS One 10 , e Article PubMed PubMed Central CAS Google Scholar. Sadeh, A. The role and validity of actigraphy in sleep medicine: An update. Sleep Med. Fullmer, S. Evidence Analysis Library Review of Best Practices for Performing Indirect Calorimetry in Healthy and Non-Critically Ill Individuals. e2 Sundström, M. Indirect calorimetry in mechanically ventilated patients. A systematic comparison of three instruments. Congruent Validity of Resting Energy Expenditure Predictive Equations in Young Adults. Nutrients 11 , 1—13 Article CAS Google Scholar. Accuracy and Validity of Resting Energy Expenditure Predictive Equations in Middle-Aged Adults. Nutrients 10 , Article PubMed Central CAS Google Scholar. Sanchez-Delgado, G. Reliability of resting metabolic rate measurements in young adults: Impact of methods for data analysis. Alcantara, J. Congruent validity and inter-day reliability of two breath by breath metabolic carts to measure resting metabolic rate in young adults. Weir, J. New methods for calculating metabolic rate with special reference to protein metabolism. Frayn, K. Calculation of substrate oxidation rates in vivo from gaseous exchange. Diurnal Variation of Maximal Fat Oxidation Rate in Trained Male Athletes. Sports Physiol. Methodological issues related to maximal fat oxidation rate during exercise: Comment on: Change in maximal fat oxidation in response to different regimes of periodized high-intensity interval training HIIT. Assessment of maximal fat oxidation during exercise: A systematic review. Impact of data analysis methods for maximal fat oxidation estimation during exercise in sedentary adults. Sport Sci. Metabolic Flexibility in Health and Disease. Balke, B. An experimental study of physical fitness of Air Force personnel. US Armed Forces Med. López, M. Guía para estudios dietéticos: álbum fotográfico de alimentos. Editorial Universidad de Granada, Ledikwe, J. Dietary Energy Density Determined by Eight Calculation Methods in a Nationally Representative United States Population. Zaragoza-Martí, A. Evaluation of Mediterranean diet adherence scores: A systematic review. BMJ Open 8 , 1—8 Schroder, H. A Short Screener Is Valid for Assessing Mediterranean Diet Adherence among Older Spanish Men and Women. Hayes, A. Introduction to mediation, moderation, and conditional process analysis: A regression-based approach. Guilford Publications. Preacher, K. Asymptotic and resampling strategies for assessing and comparing indirect effects in multiple mediator models. Methods 40 , — Beyond Baron and Kenny: Statistical mediation analysis in the new millennium. Sharma, S. Sleep and metabolism: An overview. Rao, M. Subchronic sleep restriction causes tissue-specific insulin resistance. AJP Endocrinol. Pan, W. Leptin: A biomarker for sleep disorders? Stern, J. Adiponectin, leptin, and fatty acids in the maintenance of metabolic homeostasis through adipose tissue crosstalk. Hagen, E. Sleep 42 , A43—A44 Serrano, J. Effect of Dietary Bioactive Compounds on Mitochondrial and Metabolic Flexibility. Diseases 4 , 14 Cipolla-Neto, J. Melatonin, energy metabolism, and obesity: a review. Pineal Res. Sala, C. The role of low-grade inflammation and metabolic flexibility in aging and nutritional modulation thereof: A systems biology approach. Ageing Dev. PubMed Google Scholar. Hotamisligil, G. Inflammation, metaflammation and immunometabolic disorders. Nature , — Article ADS CAS PubMed Google Scholar. Canfora, E. Short-chain fatty acids in control of body weight and insulin sensitivity. Whelan, M. A Review of the Effect of Dietary Composition on Fasting Substrate Oxidation in Healthy and Overweight Subjects. Food Sci. Acosta F. Sleep duration and quality are not associated with brown adipose tissue volume or activity - as determined by 18F-FDG uptake, in young, sedentary adults Author. Sleep 1—27 Grandner, M. Who are the long sleepers? Towards an understanding of the mortality relationship. Kim, C. Association between sleep duration and metabolic syndrome: A cross-sectional study. BMC Public Health 18 , 1—8 Berger, I. Exploring Accelerometer Versus Self-Report Sleep Assessment in Youth With Concussion. Jurado-Fasoli, L. Association between Sleep Quality and Body Composition in Sedentary Middle-Aged Adults. Medicina Kaunas. Article PubMed Central Google Scholar. Martin, J. Wrist actigraphy. Chest , — Copinschi, G. The important role of sleep in metabolism. How Gut Brain Control Metab. Nedeltcheva, A. Metabolic effects of sleep disruption, links to obesity and diabetes. Curr Opin Endocrinol Diabetes Obes 21 , — Parmeggiani, P. The physiologic nature of sleep. World Scientific. Download references. The authors would like to thank all the participants that took part of the study for their time and effort. This study is part of a Ph. Thesis conducted in the Biomedicine Doctoral Studies of the University of Granada, Spain. We are grateful to Dr. Ángel Gutiérrez and Alejandro De la O for all their support in the study. We are grateful to Ms. Ana Yara Postigo-Fuentes for her assistance with the English language. Units of Scientific Excellence: Scientific Unit of Excellence on Excercise and Health [UCEES] and Plan Propio de Investigación - Programa Contratos-Puente , by the Regional Government of Andalusia, Regional Ministry of Economy, Knowledge, Entreprises and University, by the European Regional Development Fund ERDF , ref. Department of Medical Physiology, School of Medicine, University of Granada, , Granada, Spain. Lucas Jurado-Fasoli, Sol Mochon-Benguigui, Manuel J. PROmoting FITness and Health through physical activity research group PROFITH , Department of Physical Education and Sports, Faculty of Sport Sciences, University of Granada, Granada, Spain. You can also search for this author in PubMed Google Scholar. conceptualization, L. and F. Correspondence to Lucas Jurado-Fasoli or Francisco J. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Association between sleep quality and time with energy metabolism in sedentary adults. Sci Rep 10 , Download citation. Received : 18 November Accepted : 25 February Published : 12 March Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Biol Psychol. Kodsi A, Bullock B, Kennedy GA, Tirlea L. Psychological interventions to improve sleep in young adults: a systematic review and meta-analysis of randomized controlled trials. Behav Sleep Med. St-Onge MP, Mikic A, Pietrolungo CE. Effects of diet on sleep quality. Adv Nutr. Peuhkuri K, Sihvola N, Korpela R. Diet promotes sleep duration and quality. Nutr Res. Lucassen EA, Rother KI, Cizza G. Interacting epidemics? Sleep curtailment, insulin resistance, and obesity. Schmid SM, Hallschmid M, Schultes B. The metabolic burden of sleep loss. Lancet Diabetes Endocrinol. Ferrie JE, Kivimaki M, Akbaraly TN, Tabak A, Abell J, Davey Smith G, et al. Change in sleep duration and type 2 diabetes: the whitehall ii study. Diabetes Care. Chaput JP, St-Onge MP. Increased food intake by insufficient sleep in humans: are we jumping the gun on the hormonal explanation? Front Endocrinol. Wright KP Jr. Shift work and the assessment and management of shift work disorder Swd. Hemmer A, Mareschal J, Dibner C, Pralong JA, Dorribo V, Perrig S, et al. The effects of shift work on cardio-metabolic diseases and eating patterns. Garaulet M, Qian J, Florez JC, Arendt J, Saxena R, Scheer F. Melatonin effects on glucose metabolism: time to unlock the controversy. Trends Endocrinol Metab. Owino S, Buonfiglio DDC, Tchio C, Tosini G. Melatonin signaling a key regulator of glucose homeostasis and energy metabolism. Virk JS, Kotecha B. Otorhinolaryngological aspects of sleep-related breathing disorders. J Thorac Dis. Patel AK, Reddy V, Araujo JF. Physiology, Sleep Stages. Treasure Island, FL: Bti — Statpearls Carskadon MA, Dement WC. Monitoring and staging human sleep. In: Kryger MHTR, Dement WC, editors. Principles and Practice of Sleep Medicine. Louis: Elsevier Saunders. Van Cauter E, Polonsky KS, Scheen AJ. Roles of circadian rhythmicity and sleep in human glucose regulation. Endocr Rev. Clore JN, Helm ST, Nestler JE, Blackard WG. Impaired modulation of hepatic glucose output overnight after a h fast in normal man. J Clin Endocrinol Metab. Clore JN, Nestler JE, Blackard WG. Sleep-associated fall in glucose disposal and hepatic glucose output in normal humans. Putative signaling mechanism linking peripheral and hepatic events. Moller N, Butler PC, Antsiferov MA, Alberti KG. Effects of growth hormone on insulin sensitivity and forearm metabolism in normal man. Cappuccio FP, D'Elia L, Strazzullo P, Miller MA. Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis. Boyko EJ, Seelig AD, Jacobson IG, Hooper TI, Smith B, Smith TC, et al. Sleep characteristics, mental health, and diabetes risk: a prospective study of U. Military service members in the millennium cohort study. Knutson KL, Van Cauter E, Zee P, Liu K, Lauderdale DS. Cross-sectional associations between measures of sleep and markers of glucose metabolism among subjects with and without diabetes: the coronary artery risk development in young adults Cardia sleep study. Brouwer A, van Raalte DH, Rutters F, Elders PJM, Snoek FJ, Beekman ATF, et al. Sleep and Hba1c in patients with type 2 diabetes: which sleep characteristics matter most? Mokhlesi B, Temple KA, Tjaden AH, Edelstein SL, Utzschneider KM, Nadeau KJ, et al. Association of self-reported sleep and circadian measures with glycemia in adults with prediabetes or recently diagnosed untreated type 2 diabetes. Khalafi A, Nezhad MS. The effects of blood sugar glucose metabolism on the sleep and memory via diet and medicine therapy in ahwaz diabetic patients. Proc Soc Behav Sci. CrossRef Full Text Google Scholar. Twedt R, Bradley M, Deiseroth D, Althouse A, Facco F. Sleep duration and blood glucose control in women with gestational diabetes mellitus. Obstet Gynecol. Pyykkonen AJ, Isomaa B, Pesonen AK, Eriksson JG, Groop L, Tuomi T, et al. Subjective sleep complaints are associated with insulin resistance in individuals without diabetes: the ppp-botnia study. Herzog N, Jauch-Chara K, Hyzy F, Richter A, Friedrich A, Benedict C, et al. Selective slow wave sleep but not rapid eye movement sleep suppression impairs morning glucose tolerance in healthy men. Bonnet MH, Arand DL. Hyperarousal and insomnia: state of the science. Vasisht KP, Kessler LE, Booth JN 3rd, Imperial JG, Penev PD. Differences in insulin secretion and sensitivity in short-sleep insomnia. Ibrahim M, Bonfiglio S, Schlogl M, Vinales KL, Piaggi P, Venti C, et al. Energy expenditure and hormone responses in humans after overeating high-fructose corn syrup versus whole-wheat foods. Yajima K, Seya T, Iwayama K, Hibi M, Hari S, Nakashima Y, et al. Effects of nutrient composition of dinner on sleep architecture and energy metabolism during sleep. J Nutr Sci Vitaminol. Lindseth G, Lindseth P, Thompson M. Nutritional effects on sleep. West J Nurs Res. Afaghi A, O'Connor H, Chow CM. High-glycemic-index carbohydrate meals shorten sleep onset. Am J Clin Nutr. Acute effects of the very low carbohydrate diet on sleep indices. Nutr Neurosci. Kwan RM, Thomas S, Mir MA. Effects of a low carbohydrate isoenergetic diet on sleep behavior and pulmonary functions in healthy female adult humans. J Nutr. Phillips F, Chen CN, Crisp AH, Koval J, McGuinness B, Kalucy RS, et al. Isocaloric diet changes and electroencephalographic sleep. Jalilolghadr S, Afaghi A, O'Connor H, Chow CM. Effect of low and high glycaemic index drink on sleep pattern in children. J Pak Med Assoc. PubMed Abstract Google Scholar. Gangwisch JE, Hale L, St-Onge MP, Choi L, LeBlanc ES, Malaspina D, et al. High glycemic index and glycemic load diets as risk factors for insomnia: analyses from the women's health initiative. St-Onge MP. Impact of sleep duration on food intake regulation: different mechanisms by sex? St-Onge MP, Roberts A, Shechter A, Choudhury AR. Fiber and saturated fat are associated with sleep arousals and slow wave sleep. J Clin Sleep Med. Time- and exercise-dependent gene regulation in human skeletal muscle. Genome Biol. Storch KF, Weitz CJ. Daily rhythms of food-anticipatory behavioral activity do not require the known circadian clock. Sheward WJ, Maywood ES, French KL, Horn JM, Hastings MH, Seckl JR, et al. Entrainment to feeding but not to light: circadian phenotype of VPAC2 receptor-null mice. J Neurosci. onso-Vale MI, Andreotti S, Mukai PY, Borges-Silva C, Peres SB, Cipolla-Neto J, et al. Melatonin and the circadian entrainment of metabolic and hormonal activities in primary isolated adipocytes. J Pineal Res. Contreras-Alcantara S, Baba K, Tosini G. Removal of melatonin receptor type 1 induces insulin resistance in the mouse. Obesity Silver Spring. Sartori C, Dessen P, Mathieu C, Monney A, Bloch J, Nicod P, et al. Melatonin improves glucose homeostasis and endothelial vascular function in high-fat diet-fed insulin-resistant mice. Ha E, Yim SV, Chung JH, Yoon KS, Kang I, Cho YH, et al. Shieh JM, Wu HT, Cheng KC, Cheng JT. Melatonin ameliorates high fat diet-induced diabetes and stimulates glycogen synthesis via a PKCzeta-Akt-GSK3beta pathway in hepatic cells. Faria JA, Kinote A, Ignacio-Souza LM, de Araujo TM, Razolli DS, Doneda DL, et al. Am J Physiol Endocrinol Metab. Bahr I, Muhlbauer E, Albrecht E, Peschke E. Evidence of the receptor-mediated influence of melatonin on pancreatic glucagon secretion via the Galphaq protein-coupled and PI3K signaling pathways. Park JH, Shim HM, Na AY, Bae KC, Bae JH, Im SS, et al. Melatonin prevents pancreatic beta-cell loss due to glucotoxicity: the relationship between oxidative stress and endoplasmic reticulum stress. Zanuto R, Siqueira-Filho MA, Caperuto LC, Bacurau RF, Hirata E, Peliciari-Garcia RA, et al. Melatonin improves insulin sensitivity independently of weight loss in old obese rats. Korkmaz GG, Uzun H, Cakatay U, Aydin S. Melatonin ameliorates oxidative damage in hyperglycemia-induced liver injury. Clin Invest Med. Cuesta S, Kireev R, Garcia C, Rancan L, Vara E, Tresguerres JA. Melatonin can improve insulin resistance and aging-induced pancreas alterations in senescence-accelerated prone male mice SAMP8. Age Dordr. de Oliveira AC, Andreotti S, Farias TS, Torres-Leal FL, de Proenca AR, Campana AB, et al. Metabolic disorders and adipose tissue insulin responsiveness in neonatally STZ-induced diabetic rats are improved by long-term melatonin treatment. Kitagawa A, Ohta Y, Ohashi K. Melatonin improves metabolic syndrome induced by high fructose intake in rats. Agil A, Rosado I, Ruiz R, Figueroa A, Zen N, Fernandez-Vazquez G. Melatonin improves glucose homeostasis in young Zucker diabetic fatty rats. Nogueira TC, Lellis-Santos C, Jesus DS, Taneda M, Rodrigues SC, Amaral FG, et al. Absence of melatonin induces night-time hepatic insulin resistance and increased gluconeogenesis due to stimulation of nocturnal unfolded protein response. Bertuglia S, Reiter RJ. Melatonin reduces microvascular damage and insulin resistance in hamsters due to chronic intermittent hypoxia. Nishida S, Segawa T, Murai I, Nakagawa S. Long-term melatonin administration reduces hyperinsulinemia and improves the altered fatty-acid compositions in type 2 diabetic rats via the restoration of Delta-5 desaturase activity. Wang PP, She MH, He PP, Chen WJ, Laudon M, Xu XX, et al. Piromelatine decreases triglyceride accumulation in insulin resistant 3 T3-L1 adipocytes: role of ATGL and HSL. Borba CP, Fan X, Copeland PM, Paiva A, Freudenreich O, Henderson DC. Placebo-controlled pilot study of ramelteon for adiposity and lipids in patients with schizophrenia. J Clin Psychopharmacol. She M, Deng X, Guo Z, Laudon M, Hu Z, Liao D, et al. Pharmacol Res. Surya S, Symons K, Rothman E, Barkan AL. Complex rhythmicity of growth hormone secretion in humans. Patel YC, Alford FP, Burger HG. The hour plasma thyrotrophin profile. Clin Sci. Cailotto C, Lei J, van der V, van HC, van Eden CG, Kalsbeek A, et al. Effects of nocturnal light on clock gene expression in peripheral organs: a role for the autonomic innervation of the liver. Dumont M, Lanctot V, Cadieux-Viau R, Paquet J. Melatonin production and light exposure of rotating night workers. Smith MR, Eastman CI. Shift work: health, performance and safety problems, traditional countermeasures, and innovative management strategies to reduce circadian misalignment. Grundy A, Sanchez M, Richardson H, Tranmer J, Borugian M, Graham CH, et al. Light intensity exposure, sleep duration, physical activity, and biomarkers of melatonin among rotating shift nurses. Folkard S. Do permanent night workers show circadian adjustment? A review based on the endogenous melatonin rhythm. Roden M, Koller M, Pirich K, Vierhapper H, Waldhauser F. The circadian melatonin and cortisol secretion pattern in permanent night shift workers. Buijs RM, Escobar C, Swaab DF. The circadian system and the balance of the autonomic nervous system. Vyas MV, Garg AX, Iansavichus AV, Costella J, Donner A, Laugsand LE, et al. Shift work and vascular events: systematic review and meta-analysis. Wang XS, Armstrong ME, Cairns BJ, Key TJ, Travis RC. Shift work and chronic disease: the epidemiological evidence. Occup Med Lond. Ha J, Kim SG, Paek D, Park J. The Magnitude of Mortality from Ischemic Heart Disease Attributed to Occupational Factors in Korea - Attributable Fraction Estimation Using Meta-analysis. Saf Health Work. Tuchsen F, Hannerz H, Burr H. A 12 year prospective study of circulatory disease among Danish shift workers. Occup Environ Med. Karlsson B, Alfredsson L, Knutsson A, Andersson E, Toren K. Total mortality and cause-specific mortality of Swedish shift- and dayworkers in the pulp and paper industry in — Scand J Work Environ Health. Kawachi I, Colditz GA, Stampfer MJ, Willett WC, Manson JE, Speizer FE, et al. Prospective study of shift work and risk of coronary heart disease in women. Knutsson A, Akerstedt T, Jonsson BG, Orth-Gomer K. Increased risk of ischaemic heart disease in shift workers. Evans JA, Davidson AJ. Health consequences of circadian disruption in humans and animal models. Prog Mol Biol Transl Sci. Haus EL, Smolensky MH. Shift work and cancer risk: potential mechanistic roles of circadian disruption, light at night, and sleep deprivation. Sleep Med Rev. Guo Y, Liu Y, Huang X, Rong Y, He M, Wang Y, et al. The effects of shift work on sleeping quality, hypertension and diabetes in retired workers. Monk TH, Buysse DJ. Exposure to shift work as a risk factor for diabetes. J Biol Rhythms. Mikuni E, Ohoshi T, Hayashi K, Miyamura K. Glucose intolerance in an employed population. Tohoku J Exp Med. Nagaya T, Yoshida H, Takahashi H, Kawai M. Markers of insulin resistance in day and shift workers aged 30—59 years. Int Arch Occup Environ Health. Karlsson B, Knutsson A, Lindahl B. Is there an association between shift work and having a metabolic syndrome? Results from a population based study of 27, people. Puttonen S, Viitasalo K, Harma M. The relationship between current and former shift work and the metabolic syndrome. Esquirol Y, Bongard V, Mabile L, Jonnier B, Soulat JM, Perret B. Shift work and metabolic syndrome: respective impacts of job strain, physical activity, and dietary rhythms. Karlsson BH, Knutsson AK, Lindahl BO, Alfredsson LS. Metabolic disturbances in male workers with rotating three-shift work. Results of the WOLF study. Gan Y, Yang C, Tong X, Sun H, Cong Y, Yin X, et al. Shift work and diabetes mellitus: a meta-analysis of observational studies. Suwazono Y, Dochi M, Sakata K, Okubo Y, Oishi M, Tanaka K, et al. A longitudinal study on the effect of shift work on weight gain in male Japanese workers. Niedhammer I, Lert F, Marne MJ. Prevalence of overweight and weight gain in relation to night work in a nurses' cohort. Int J Obes Relat Metab Disord. Kawada T, Otsuka T. Effect of shift work on the development of metabolic syndrome after 3 years in Japanese male workers. Arch Environ Occup Health. Suwazono Y, Uetani M, Oishi M, Tanaka K, Morimoto H, Sakata K. Calculation of the benchmark duration of shift work associated with the development of impaired glucose metabolism: a year cohort study on male workers. Lin YC, Hsiao TJ, Chen PC. Shift work aggravates metabolic syndrome development among early-middle-aged males with elevated ALT. World J Gastroenterol. Pietroiusti A, Neri A, Somma G, Coppeta L, Iavicoli I, Bergamaschi A, et al. Incidence of metabolic syndrome among night-shift healthcare workers. De BD, Van RM, Clays E, Kittel F, De BG, Braeckman L. Rotating shift work and the metabolic syndrome: a prospective study. Int J Epidemiol. Eriksson AK, van den DM, Hilding A, Ostenson CG. Work stress, sense of coherence, and risk of type 2 diabetes in a prospective study of middle-aged Swedish men and women. Pan A, Schernhammer ES, Sun Q, Hu FB. Rotating night shift work and risk of type 2 diabetes: two prospective cohort studies in women. Kroenke CH, Spiegelman D, Manson J, Schernhammer ES, Colditz GA, Kawachi I. Work characteristics and incidence of type 2 diabetes in women. Suwazono Y, Sakata K, Okubo Y, Harada H, Oishi M, Kobayashi E, et al. Long-term longitudinal study on the relationship between alternating shift work and the onset of diabetes mellitus in male Japanese workers. J Occup Environ Med. Morikawa Y, Nakagawa H, Miura K, Soyama Y, Ishizaki M, Kido T, et al. Shift work and the risk of diabetes mellitus among Japanese male factory workers. Kennaway DJ, Varcoe TJ, Voultsios A, Boden MJ. Global loss of bmal1 expression alters adipose tissue hormones, gene expression and glucose metabolism. Lee J, Moulik M, Fang Z, Saha P, Zou F, Xu Y, et al. Bmal1 and beta-cell clock are required for adaptation to circadian disruption, and their loss of function leads to oxidative stress-induced beta-cell failure in mice. Mol Cell Biol. Sadacca LA, Lamia KA, deLemos AS, Blum B, Weitz CJ. An intrinsic circadian clock of the pancreas is required for normal insulin release and glucose homeostasis in mice. Marcheva B, Ramsey KM, Buhr ED, Kobayashi Y, Su H, Ko CH, et al. Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes. Doi R, Oishi K, Ishida N. CLOCK regulates circadian rhythms of hepatic glycogen synthesis through transcriptional activation of Gys2. Turek FW, Joshu C, Kohsaka A, Lin E, Ivanova G, McDearmon E, et al. Obesity and metabolic syndrome in circadian Clock mutant mice. Rudic RD, McNamara P, Curtis AM, Boston RC, Panda S, Hogenesch JB, et al. BMAL1 and CLOCK, two essential components of the circadian clock, are involved in glucose homeostasis. PLoS Biol. Lamia KA, Storch KF, Weitz CJ. Physiological significance of a peripheral tissue circadian clock. Sherman H, Genzer Y, Cohen R, Chapnik N, Madar Z, Froy O. Timed high-fat diet resets circadian metabolism and prevents obesity. FASEB J. Leproult R, Holmback U, Van CE. Circadian misalignment augments markers of insulin resistance and inflammation, independently of sleep loss. Lund J, Arendt J, Hampton SM, English J, Morgan LM. Postprandial hormone and metabolic responses amongst shift workers in Antarctica. Esquirol Y, Bongard V, Ferrieres J, Verdier H, Perret B. Shiftwork and higher pancreatic secretion: early detection of an intermediate state of insulin resistance? Gale JE, Cox HI, Qian J, Block GD, Colwell CS, Matveyenko AV. Disruption of circadian rhythms accelerates development of diabetes through pancreatic beta-cell loss and dysfunction. Castanon-Cervantes O, Wu M, Ehlen JC, Paul K, Gamble KL, Johnson RL, et al. Dysregulation of inflammatory responses by chronic circadian disruption. J Immunol. Calle MC, Fernandez ML. Inflammation and type 2 diabetes. Diabetes Metab. Young T, Skatrud J, Peppard PE. Risk factors for obstructive sleep apnea in adults. Jennum P, Riha RL. Eur Respir J. Punjabi NM. The epidemiology of adult obstructive sleep apnea. Proc Am Thorac Soc. Baguet JP, Barone-Rochette G, Tamisier R, Levy P, Pepin JL. Mechanisms of cardiac dysfunction in obstructive sleep apnea. Nat Rev Cardiol. Lopez-Jimenez F, Sert Kuniyoshi FH, Gami A, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. Caples SM, Garcia-Touchard A, Somers VK. Sleep-disordered breathing and cardiovascular risk. Pamidi S, Aronsohn RS, Tasali E. Obstructive sleep apnea: role in the risk and severity of diabetes. Do sleep disorders and associated treatments impact glucose metabolism? Levy P, Bonsignore MR, Eckel J. Sleep, sleep-disordered breathing and metabolic consequences. Jun J, Polotsky VY. Metabolic consequences of sleep-disordered breathing. ILAR J. Seicean S, Kirchner HL, Gottlieb DJ, Punjabi NM, Resnick H, Sanders M, et al. Punjabi NM, Shahar E, Redline S, Gottlieb DJ, Givelber R, Resnick HE. Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. McArdle N, Hillman D, Beilin L, Watts G. Metabolic risk factors for vascular disease in obstructive sleep apnea: a matched controlled study. Am J Respir Crit Care Med. Ip MS, Lam B, Ng MM, Lam WK, Tsang KW, Lam KS. Obstructive sleep apnea is independently associated with insulin resistance. Pamidi S, Tasali E. Obstructive sleep apnea and type 2 diabetes: is there a link? Front Neurol. Borel AL, Monneret D, Tamisier R, Baguet JP, Faure P, Levy P, et al. The severity of nocturnal hypoxia but not abdominal adiposity is associated with insulin resistance in non-obese men with sleep apnea. Lindberg E, Theorell-Haglow J, Svensson M, Gislason T, Berne C, Janson C. Sleep apnea and glucose metabolism: a long-term follow-up in a community-based sample. Botros N, Concato J, Mohsenin V, Selim B, Doctor K, Yaggi HK. Obstructive sleep apnea as a risk factor for type 2 diabetes. Am J Med. Marshall NS, Wong KK, Phillips CL, Liu PY, Knuiman MW, Grunstein RR. Is sleep apnea an independent risk factor for prevalent and incident diabetes in the Busselton Health Study? J Clin Sleep Med. Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: a population-based study. Wang X, Bi Y, Zhang Q, Pan F. Obstructive sleep apnoea and the risk of type 2 diabetes: a meta-analysis of prospective cohort studies. Kribbs NB, Pack AI, Kline LR, Smith PL, Schwartz AR, Schubert NM, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis. Grimaldi D, Beccuti G, Touma C, Van CE, Mokhlesi B. Association of obstructive sleep apnea in rapid eye movement sleep with reduced glycemic control in type 2 diabetes: therapeutic implications. Babu AR, Herdegen J, Fogelfeld L, Shott S, Mazzone T. Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Sookoian S, Pirola CJ. Obstructive sleep apnea is associated with fatty liver and abnormal liver enzymes: a meta-analysis. Obes Surg. Polotsky VY, Patil SP, Savransky V, Laffan A, Fonti S, Frame LA, et al. Obstructive sleep apnea, insulin resistance, and steatohepatitis in severe obesity. Mishra P, Nugent C, Afendy A, Bai C, Bhatia P, Afendy M, et al. Apnoeic-hypopnoeic episodes during obstructive sleep apnoea are associated with histological nonalcoholic steatohepatitis. Liver Int. ron-Wisnewsky J, Minville C, Tordjman J, Levy P, Bouillot JL, Basdevant A, et al. Chronic intermittent hypoxia is a major trigger for non-alcoholic fatty liver disease in morbid obese. J Hepatol. Tatsumi K, Saibara T. Effects of obstructive sleep apnea syndrome on hepatic steatosis and nonalcoholic steatohepatitis. Hepatol Res. Minville C, Hilleret MN, Tamisier R, ron-Wisnewsky J, Clement K, Trocme C, et al. Nonalcoholic fatty liver disease, nocturnal hypoxia, and endothelial function in patients with sleep apnea. Sundaram SS, Sokol RJ, Capocelli KE, Pan Z, Sullivan JS, Robbins K, et al. Obstructive sleep apnea and hypoxemia are associated with advanced liver histology in pediatric nonalcoholic fatty liver disease. Polotsky VY, Li J, Punjabi NM, Rubin AE, Smith PL, Schwartz AR, et al. Intermittent hypoxia increases insulin resistance in genetically obese mice. J Physiol. Drager LF, Yao Q, Hernandez KL, Shin MK, Bevans-Fonti S, Gay J, et al. Chronic intermittent hypoxia induces atherosclerosis via activation of adipose angiopoietin-like 4. Polak J, Shimoda LA, Drager LF, Undem C, McHugh H, Polotsky VY, et al. Drager LF, Li J, Reinke C, Bevans-Fonti S, Jun JC, Polotsky VY. Intermittent hypoxia exacerbates metabolic effects of diet-induced obesity. Iiyori N, Alonso LC, Li J, Sanders MH, Garcia-Ocana A, O'Doherty RM, et al. Intermittent hypoxia causes insulin resistance in lean mice independent of autonomic activity. Chen L, Cao ZL, Han F, Gao ZC, He QY. Chronic intermittent hypoxia from pedo-stage decreases glucose transporter 4 expression in adipose tissue and causes insulin resistance. Chin Med J Engl. Fenik VB, Singletary T, Branconi JL, Davies RO, Kubin L. Glucoregulatory consequences and cardiorespiratory parameters in rats exposed to chronic-intermittent hypoxia: effects of the duration of exposure and losartan. Louis M, Punjabi NM. Effects of acute intermittent hypoxia on glucose metabolism in awake healthy volunteers. J Appl Physiol. Rosa DP, Martinez D, Picada JN, Semedo JG, Marroni NP. Hepatic oxidative stress in an animal model of sleep apnoea: effects of different duration of exposure. Comp Hepatol. Savransky V, Nanayakkara A, Vivero A, Li J, Bevans S, Smith PL, et al. Chronic intermittent hypoxia predisposes to liver injury. Savransky V, Bevans S, Nanayakkara A, Li J, Smith PL, Torbenson MS, et al. Chronic intermittent hypoxia causes hepatitis in a mouse model of diet-induced fatty liver. Am J Physiol Gastrointest Liver Physiol. Chen XY, Zeng YM, Zhang YX, Wang WY, Wu RH. Effect of chronic intermittent hypoxia on theophylline metabolism in mouse liver. Li J, Thorne LN, Punjabi NM, Sun CK, Schwartz AR, Smith PL, et al. Intermittent hypoxia induces hyperlipidemia in lean mice. Circ Res. Savransky V, Nanayakkara A, Li J, Bevans S, Smith PL, Rodriguez A, et al. Chronic intermittent hypoxia induces atherosclerosis. Li J, Bosch-Marce M, Nanayakkara A, Savransky V, Fried SK, Semenza GL, et al. Altered metabolic responses to intermittent hypoxia in mice with partial deficiency of hypoxia-inducible factor-1alpha. Physiol Genomics. da Rosa DP, Forgiarini LF, Baronio D, Feijo CA, Martinez D, Marroni NP. Simulating sleep apnea by exposure to intermittent hypoxia induces inflammation in the lung and liver. Mediators Inflamm. Jun J, Savransky V, Nanayakkara A, Bevans S, Li J, Smith PL, et al. Intermittent hypoxia has organ-specific effects on oxidative stress. Tanne F, Gagnadoux F, Chazouilleres O, Fleury B, Wendum D, Lasnier E, et al. Chronic liver injury during obstructive sleep apnea. Pastoris O, Gorini A, Vercesi L, Taglietti M, Dossena M. Modification of the skeletal muscle energy metabolism induced by intermittent normobaric hypoxia and treatment with biological pyrimidines. Farmaco Sci. Carreras A, Kayali F, Zhang J, Hirotsu C, Wang Y, Gozal D. Metabolic effects of intermittent hypoxia in mice: steady versus high-frequency applied hypoxia daily during the rest period. Pallayova M, Lazurova I, Donic V. Hypoxic damage to pancreatic beta cells—the hidden link between sleep apnea and diabetes. Med Hypotheses. Pallayova M, Steele KE, Magnuson TH, Schweitzer MA, Hill NR, Bevans-Fonti S, et al. Sleep apnea predicts distinct alterations in glucose homeostasis and biomarkers in obese adults with normal and impaired glucose metabolism. Cardiovasc Diabetol. Yokoe T, Alonso LC, Romano LC, Rosa TC, O'Doherty RM, Garcia-Ocana A, et al. Intermittent hypoxia reverses the diurnal glucose rhythm and causes pancreatic beta-cell replication in mice. Xu J, Long YS, Gozal D, Epstein PN. Beta-cell death and proliferation after intermittent hypoxia: role of oxidative stress. Free Radic Biol Med. Wang N, Khan SA, Prabhakar NR, Nanduri J. Impairment of pancreatic beta-cell function by chronic intermittent hypoxia. Exp Physiol. Ota H, Tamaki S, Itaya-Hironaka A, Yamauchi A, Sakuramoto-Tsuchida S, Morioka T, et al. Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD Life Sci. Delarue J, Magnan C. Free fatty acids and insulin resistance. Curr Opin Clin Nutr Metab Care. Jun J, Reinke C, Bedja D, Berkowitz D, Bevans-Fonti S, Li J, et al. Effect of intermittent hypoxia on atherosclerosis in apolipoprotein E-deficient mice. Jun JC, Drager LF, Najjar SS, Gottlieb SS, Brown CD, Smith PL, et al. Effects of sleep apnea on nocturnal free fatty acids in subjects with heart failure. Poulain L, Thomas A, Rieusset J, Casteilla L, Levy P, Arnaud C, et al. Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis. Yao Q, Shin MK, Jun JC, Hernandez KL, Aggarwal NR, Mock JR, et al. Effect of chronic intermittent hypoxia on triglyceride uptake in different tissues. J Lipid Res. Magalang UJ, Cruff JP, Rajappan R, Hunter MG, Patel T, Marsh CB, et al. Intermittent hypoxia suppresses adiponectin secretion by adipocytes. |
| Introduction | Fitness supplements for beginners the time spent eating or qualoty prior sleep bedtime expanded, sleel odds of short and long sleep durations and waking up after falling asleep decreased. J Epidemiol. Fitness supplements for beginners qualitu therefore tempting to postulate that IH-induced lipolysis and insulin resistance might be mediated through sympathetic nervous system activation. Make sure to eat a light dinner at least three hours before lights out. Beccuti, G et al. PLoS One. These fat oxidation values were plotted against the relative-exercise intensity, expressed as the percentage of maximum oxygen uptake VO2max ; a third-degree polynomial curve was built to determine MFO and FATmax |
Metabolic support for sleep quality -
Am J Physiol. Cooper BG, White JE, Ashworth LA, Alberti KG, Gibson GJ. Hormonal and metabolic profiles in subjects with obstructive sleep apnea syndrome and the acute effects of nasal continuous positive airway pressure CPAP treatment.
Gottlieb DJ, Punjabi NM, Newman AB, Resnick HE, Redline S, Baldwin CM, et al. Association of sleep time with diabetes mellitus and impaired glucose tolerance. Tuomilehto H, Peltonen M, Partinen M, Seppa J, Saaristo T, Korpi-Hyovalti E, et al.
Sleep duration is associated with an increased risk for the prevalence of type 2 diabetes in middle-aged women - The FIN-D2D survey. Najafian J, Mohamadifard N, Siadat ZD, Sadri G, Rahmati MR.
Association between sleep duration and diabetes mellitus: Isfahan Healthy Heart Program. Niger J Clin Pract. Chaput JP, Despres JP, Bouchard C, Tremblay A. Association of sleep duration with type 2 diabetes and impaired glucose tolerance. Fiorentini A, Valente R, Perciaccante A, Tubani L.
Sleep's quality disorders in patients with hypertension and type 2 diabetes mellitus. Int J Cardiol. Buxton OM, Marcelli E. Short and long sleep are positively associated with obesity, diabetes, hypertension, and cardiovascular disease among adults in the United States.
Soc Sci Med. Darukhanavala A, Booth III JN, Bromley L, Whitmore H, Imperial J, Penev PD. Changes in insulin secretion and action in adults with familial risk for type 2 diabetes who curtail their sleep. Koren D, Levitt Katz LE, Brar PC, Gallagher PR, Berkowitz RI, Brooks LJ. Sleep architecture and glucose and insulin homeostasis in obese adolescents.
Facco FL, Grobman WA, Kramer J, Ho KH, Zee PC. Self-reported short sleep duration and frequent snoring in pregnancy: impact on glucose metabolism. Am J Obstet Gynecol. Knutson KL, Ryden AM, Mander BA, Van CE. Role of sleep duration and quality in the risk and severity of type 2 diabetes mellitus.
Qiu C, Enquobahrie D, Frederick IO, Abetew D, Williams MA. Glucose intolerance and gestational diabetes risk in relation to sleep duration and snoring during pregnancy: a pilot study. BMC Womens Health. Ohkuma T, Fujii H, Iwase M, Kikuchi Y, Ogata S, Idewaki Y, et al.
Impact of sleep duration on obesity and the glycemic level in patients with type 2 diabetes: the Fukuoka Diabetes Registry. Jennings JR, Muldoon MF, Hall M, Buysse DJ, Manuck SB. Self-reported sleep quality is associated with the metabolic syndrome. Flint J, Kothare SV, Zihlif M, Suarez E, Adams R, Legido A, et al.
Association between inadequate sleep and insulin resistance in obese children. J Pediatr. Matthews KA, Dahl RE, Owens JF, Lee L, Hall M.
Sleep duration and insulin resistance in healthy black and white adolescents. Hung HC, Yang YC, Ou HY, Wu JS, Lu FH, Chang CJ. The Association between Self-Reported Sleep Quality and Metabolic Syndrome. PLoS One. The relationship between impaired fasting glucose and self-reported sleep quality in a Chinese population.
Clin Endocrinol Oxf. CAS Google Scholar. Nakajima H, Kaneita Y, Yokoyama E, Harano S, Tamaki T, Ibuka E, et al. Association between sleep duration and hemoglobin A1c level. Hall MH, Muldoon MF, Jennings JR, Buysse DJ, Flory JD, Manuck SB.
Self-reported sleep duration is associated with the metabolic syndrome in midlife adults. Reutrakul S, Zaidi N, Wroblewski K, Kay HH, Ismail M, Ehrmann DA, et al. Sleep disturbances and their relationship to glucose tolerance in pregnancy.
Knutson KL, Van CE, Zee P, Liu K, Lauderdale DS. Cross-sectional associations between measures of sleep and markers of glucose metabolism among subjects with and without diabetes: the Coronary Artery Risk Development in Young Adults CARDIA Sleep Study.
Song Y, Ye X, Ye L, Li B, Wang L, Hua Y. Disturbed subjective sleep in chinese females with type 2 diabetes on insulin therapy. Pallayova M, Donic V, Gresova S, Peregrim I, Tomori Z.
Do differences in sleep architecture exist between persons with type 2 diabetes and nondiabetic controls? J Diabetes Sci Technol. Nakanishi-Minami T, Kishida K, Funahashi T, Shimomura I. Sleep-wake cycle irregularities in type 2 diabetics.
Diabetol Metab Syndr. Ayas NT, White DP, Al-Delaimy WK, Manson JE, Stampfer MJ, Speizer FE, et al. A prospective study of self-reported sleep duration and incident diabetes in women. Nilsson PM, Roost M, Engstrom G, Hedblad B, Berglund G.
Incidence of diabetes in middle-aged men is related to sleep disturbances. Bjorkelund C, Bondyr-Carlsson D, Lapidus L, Lissner L, Mansson J, Skoog I, et al. Sleep disturbances in midlife unrelated to year diabetes incidence: the prospective population study of women in Gothenburg.
Mallon L, Broman JE, Hetta J. High incidence of diabetes in men with sleep complaints or short sleep duration: a year follow-up study of a middle-aged population. Yaggi HK, Araujo AB, McKinlay JB. Sleep duration as a risk factor for the development of type 2 diabetes.
Gangwisch JE, Heymsfield SB, Boden-Albala B, Buijs RM, Kreier F, Pickering TG, et al. Sleep duration as a risk factor for diabetes incidence in a large U.
Beihl DA, Liese AD, Haffner SM. Sleep duration as a risk factor for incident type 2 diabetes in a multiethnic cohort. Ann Epidemiol. Hayashino Y, Fukuhara S, Suzukamo Y, Okamura T, Tanaka T, Ueshima H.
Relation between sleep quality and quantity, quality of life, and risk of developing diabetes in healthy workers in Japan: the High-risk and Population Strategy for Occupational Health Promotion HIPOP-OHP Study. BMC Public Health. Kawakami N, Takatsuka N, Shimizu H.
Sleep disturbance and onset of type 2 diabetes. Meisinger C, Heier M, Loewel H. Sleep disturbance as a predictor of type 2 diabetes mellitus in men and women from the general population.
Kita T, Yoshioka E, Satoh H, Saijo Y, Kawaharada M, Okada E, et al. Short sleep duration and poor sleep quality increase the risk of diabetes in Japanese workers with no family history of diabetes.
von RA, Weikert C, Fietze I, Boeing H. Association of sleep duration with chronic diseases in the European Prospective Investigation into Cancer and Nutrition EPIC -Potsdam study. Holliday EG, Magee CA, Kritharides L, Banks E, Attia J.
Short sleep duration is associated with risk of future diabetes but not cardiovascular disease: a prospective study and meta-analysis. Gonzalez-Ortiz M, Martinez-Abundis E, Balcazar-Munoz BR, Pascoe-Gonzalez S.
Effect of sleep deprivation on insulin sensitivity and cortisol concentration in healthy subjects. Diabetes Nutr Metab. VanHelder T, Symons JD, Radomski MW.
Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med. Benedict C, Hallschmid M, Lassen A, Mahnke C, Schultes B, Schioth HB, et al. Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr. Kuhn E, Brodan V, Brodanova M, Rysanek K.
Metabolic reflection of sleep deprivation. Act Nerv Super Praha. Vondra K, Brodan V, Bass A, Kuhn E, Teisinger J, Andel M, et al. Effects of sleep deprivation on the activity of selected metabolic enzymes in skeletal muscle.
Eur J Appl Physiol Occup Physiol. Wehrens SM, Hampton SM, Finn RE, Skene DJ. Effect of total sleep deprivation on postprandial metabolic and insulin responses in shift workers and non-shift workers. J Endocrinol. Reynolds AC, Dorrian J, Liu PY, Van Dongen HP, Wittert GA, Harmer LJ, et al.
Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men. Spiegel K, Leproult R, Van CE. Impact of sleep debt on metabolic and endocrine function.
Spiegel K, Leproult R, L'hermite-Baleriaux M, Copinschi G, Penev PD, Van CE. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab.
Schmid SM, Hallschmid M, Jauch-Chara K, Wilms B, Lehnert H, Born J, et al. Disturbed glucoregulatory response to food intake after moderate sleep restriction.
Buxton OM, Pavlova M, Reid EW, Wang W, Simonson DC, Adler GK. Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Buxton OM, Cain SW, O'Connor SP, Porter JH, Duffy JF, Wang W, et al. Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption.
Sci Transl Med. van Leeuwen WM, Hublin C, Sallinen M, Harma M, Hirvonen A, Porkka-Heiskanen T. Prolonged sleep restriction affects glucose metabolism in healthy young men. Int J Endocrinol. Nedeltcheva AV, Kessler L, Imperial J, Penev PD. Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance.
Robertson MD, Russell-Jones D, Umpleby AM, Dijk DJ. Effects of three weeks of mild sleep restriction implemented in the home environment on multiple metabolic and endocrine markers in healthy young men. Donga E, van DM, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, et al.
A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. Leproult R, Copinschi G, Buxton O, Van CE.
Sleep loss results in an elevation of cortisol levels the next evening. Omisade A, Buxton OM, Rusak B. Impact of acute sleep restriction on cortisol and leptin levels in young women. Physiol Behav. Kumari M, Badrick E, Ferrie J, Perski A, Marmot M, Chandola T.
Self-reported sleep duration and sleep disturbance are independently associated with cortisol secretion in the Whitehall II study. Leproult R, Van CE. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. Spiegel K, Leproult R, Colecchia EF, L'hermite-Baleriaux M, Nie Z, Copinschi G, et al.
Adaptation of the h growth hormone profile to a state of sleep debt. Am J Physiol Regul Integr Comp Physiol. Hayes AL, Xu F, Babineau D, Patel SR. Sleep duration and circulating adipokine levels. Broussard JL, Ehrmann DA, Van CE, Tasali E, Brady MJ.
Impaired insulin signaling in human adipocytes after experimental sleep restriction: a randomized, crossover study. Ann Intern Med. Al-Disi D, Al-Daghri N, Khanam L, Al-Othman A, Al-Saif M, Sabico S, et al. Subjective sleep duration and quality influence diet composition and circulating adipocytokines and ghrelin levels in teen-age girls.
Endocr J. Patel SR, Zhu X, Storfer-Isser A, Mehra R, Jenny NS, Tracy R, et al. Sleep duration and biomarkers of inflammation. Ferrie JE, Kivimaki M, Akbaraly TN, Singh-Manoux A, Miller MA, Gimeno D, et al.
Associations between change in sleep duration and inflammation: findings on C-reactive protein and interleukin 6 in the Whitehall II Study. Grandner MA, Buxton OM, Jackson N, Sands-Lincoln M, Pandey A, Jean-Louis G.
Extreme sleep durations and increased C-reactive protein: effects of sex and ethnoracial group. Miller MA, Cappuccio FP. Biomarkers of cardiovascular risk in sleep-deprived people. J Hum Hypertens.
Martinez-Gomez D, Eisenmann JC, Gomez-Martinez S, Hill EE, Zapatera B, Veiga OL, et al. Sleep duration and emerging cardiometabolic risk markers in adolescents. The AFINOS study. Miller MA, Kandala NB, Kivimaki M, Kumari M, Brunner EJ, Lowe GD, et al.
Gender differences in the cross-sectional relationships between sleep duration and markers of inflammation: Whitehall II study. Okun ML, Coussons-Read M, Hall M. Disturbed sleep is associated with increased C-reactive protein in young women.
Brain Behav Immun. Vgontzas AN, Zoumakis E, Bixler EO, Lin HM, Follett H, Kales A, et al. Adverse effects of modest sleep restriction on sleepiness, performance, and inflammatory cytokines. Shearer WT, Reuben JM, Mullington JM, Price NJ, Lee BN, Smith EO, et al. Soluble TNF-alpha receptor 1 and IL-6 plasma levels in humans subjected to the sleep deprivation model of spaceflight.
J Allergy Clin Immunol. Haack M, Sanchez E, Mullington JM. Elevated inflammatory markers in response to prolonged sleep restriction are associated with increased pain experience in healthy volunteers.
Meier-Ewert HK, Ridker PM, Rifai N, Regan MM, Price NJ, Dinges DF, et al. Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol. Grandner MA, Sands-Lincoln MR, Pak VM, Garland SN.
Sleep duration, cardiovascular disease, and proinflammatory biomarkers. Nat Sci Sleep. Morselli LL, Guyon A, Spiegel K.
Sleep and metabolic function. Pflugers Arch. Knutson KL. Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab. Spiegel K, Tasali E, Penev P, Van CE. Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite.
St-Onge MP, Roberts AL, Chen J, Kelleman M, O'Keeffe M, RoyChoudhury A, et al. Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals. Brondel L, Romer MA, Nougues PM, Touyarou P, Davenne D.
Acute partial sleep deprivation increases food intake in healthy men. Bosy-Westphal A, Hinrichs S, Jauch-Chara K, Hitze B, Later W, Wilms B, et al.
Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Obes Facts. Calvin AD, Carter RE, Adachi T, Macedo PG, Albuquerque FN, van der WC, et al. Effects of experimental sleep restriction on caloric intake and activity energy expenditure.
Nedeltcheva AV, Kilkus JM, Imperial J, Kasza K, Schoeller DA, Penev PD. Sleep curtailment is accompanied by increased intake of calories from snacks. Chapman CD, Benedict C, Brooks SJ, Schioth HB. Lifestyle determinants of the drive to eat: a meta-analysis. Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.
Insufficient sleep undermines dietary efforts to reduce adiposity. Suzuki K, Jayasena CN, Bloom SR. Obesity and appetite control. Exp Diabetes Res. Guilleminault C, Powell NB, Martinez S, Kushida C, Raffray T, Palombini L, et al. Preliminary observations on the effects of sleep time in a sleep restriction paradigm.
St-Onge MP, O'Keeffe M, Roberts AL, RoyChoudhury A, Laferrere B. Short sleep duration, glucose dysregulation and hormonal regulation of appetite in men and women.
Schmid SM, Hallschmid M, Jauch-Chara K, Born J, Schultes B. A single night of sleep deprivation increases ghrelin levels and feelings of hunger in normal-weight healthy men.
J Sleep Res. Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. Schmid SM, Hallschmid M, Jauch-Chara K, Wilms B, Benedict C, Lehnert H, et al.
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.
Simpson NS, Banks S, Dinges DF. Sleep restriction is associated with increased morning plasma leptin concentrations, especially in women. Biol Res Nurs. Magee CA, Huang X-F, Iverson DC, Caputi P. Acute sleep restriction alters neuroendocrine hormones and appetite in healthy male adults.
Sleep Biol Rhythm. Ptitsyn AA, Zvonic S, Conrad SA, Scott LK, Mynatt RL, Gimble JM. Circadian clocks are resounding in peripheral tissues. PLoS Comput Biol. Zvonic S, Ptitsyn AA, Conrad SA, Scott LK, Floyd ZE, Kilroy G, et al.
Characterization of peripheral circadian clocks in adipose tissues. Eckel-Mahan KL, Patel VR, Mohney RP, Vignola KS, Baldi P, Sassone-Corsi P. Coordination of the transcriptome and metabolome by the circadian clock.
Dallmann R, Viola AU, Tarokh L, Cajochen C, Brown SA. The human circadian metabolome. Son GH, Chung S, Choe HK, Kim HD, Baik SM, Lee H, et al. Adrenal peripheral clock controls the autonomous circadian rhythm of glucocorticoid by causing rhythmic steroid production. Ishida A, Mutoh T, Ueyama T, Bando H, Masubuchi S, Nakahara D, et al.
Light activates the adrenal gland: timing of gene expression and glucocorticoid release. Otsuka T, Goto M, Kawai M, Togo Y, Sato K, Katoh K, et al. Wotus C, Lilley TR, Neal AS, Suleiman NL, Schmuck SC, Smarr BL, et al. Forced desynchrony reveals independent contributions of suprachiasmatic oscillators to the daily plasma corticosterone rhythm in male rats.
Gomez-Abellan P, ez-Noguera A, Madrid JA, Lujan JA, Ordovas JM, Garaulet M. Glucocorticoids affect 24 h clock genes expression in human adipose tissue explant cultures. Pezuk P, Mohawk JA, Wang LA, Menaker M.
Glucocorticoids as entraining signals for peripheral circadian oscillators. So AY, Bernal TU, Pillsbury ML, Yamamoto KR, Feldman BJ. Glucocorticoid regulation of the circadian clock modulates glucose homeostasis.
Almon RR, Yang E, Lai W, Androulakis IP, Ghimbovschi S, Hoffman EP, et al. Relationships between circadian rhythms and modulation of gene expression by glucocorticoids in skeletal muscle. Oishi K, Amagai N, Shirai H, Kadota K, Ohkura N, Ishida N.
Genome-wide expression analysis reveals adrenal gland-dependent circadian genes in the mouse liver. DNA Res. Zambon AC, McDearmon EL, Salomonis N, Vranizan KM, Johansen KL, Adey D, et al. Time- and exercise-dependent gene regulation in human skeletal muscle.
Genome Biol. Storch KF, Weitz CJ. Daily rhythms of food-anticipatory behavioral activity do not require the known circadian clock. Sheward WJ, Maywood ES, French KL, Horn JM, Hastings MH, Seckl JR, et al.
Entrainment to feeding but not to light: circadian phenotype of VPAC2 receptor-null mice. J Neurosci. onso-Vale MI, Andreotti S, Mukai PY, Borges-Silva C, Peres SB, Cipolla-Neto J, et al.
Melatonin and the circadian entrainment of metabolic and hormonal activities in primary isolated adipocytes.
J Pineal Res. Contreras-Alcantara S, Baba K, Tosini G. Removal of melatonin receptor type 1 induces insulin resistance in the mouse. Obesity Silver Spring. Sartori C, Dessen P, Mathieu C, Monney A, Bloch J, Nicod P, et al. Melatonin improves glucose homeostasis and endothelial vascular function in high-fat diet-fed insulin-resistant mice.
Ha E, Yim SV, Chung JH, Yoon KS, Kang I, Cho YH, et al. Shieh JM, Wu HT, Cheng KC, Cheng JT. Melatonin ameliorates high fat diet-induced diabetes and stimulates glycogen synthesis via a PKCzeta-Akt-GSK3beta pathway in hepatic cells.
Faria JA, Kinote A, Ignacio-Souza LM, de Araujo TM, Razolli DS, Doneda DL, et al. Am J Physiol Endocrinol Metab. Bahr I, Muhlbauer E, Albrecht E, Peschke E. Evidence of the receptor-mediated influence of melatonin on pancreatic glucagon secretion via the Galphaq protein-coupled and PI3K signaling pathways.
Park JH, Shim HM, Na AY, Bae KC, Bae JH, Im SS, et al. Melatonin prevents pancreatic beta-cell loss due to glucotoxicity: the relationship between oxidative stress and endoplasmic reticulum stress.
Zanuto R, Siqueira-Filho MA, Caperuto LC, Bacurau RF, Hirata E, Peliciari-Garcia RA, et al. Melatonin improves insulin sensitivity independently of weight loss in old obese rats.
Korkmaz GG, Uzun H, Cakatay U, Aydin S. Melatonin ameliorates oxidative damage in hyperglycemia-induced liver injury. Clin Invest Med. Cuesta S, Kireev R, Garcia C, Rancan L, Vara E, Tresguerres JA. Melatonin can improve insulin resistance and aging-induced pancreas alterations in senescence-accelerated prone male mice SAMP8.
Age Dordr. de Oliveira AC, Andreotti S, Farias TS, Torres-Leal FL, de Proenca AR, Campana AB, et al. Metabolic disorders and adipose tissue insulin responsiveness in neonatally STZ-induced diabetic rats are improved by long-term melatonin treatment.
Kitagawa A, Ohta Y, Ohashi K. Melatonin improves metabolic syndrome induced by high fructose intake in rats.
Agil A, Rosado I, Ruiz R, Figueroa A, Zen N, Fernandez-Vazquez G. Melatonin improves glucose homeostasis in young Zucker diabetic fatty rats. Nogueira TC, Lellis-Santos C, Jesus DS, Taneda M, Rodrigues SC, Amaral FG, et al.
Absence of melatonin induces night-time hepatic insulin resistance and increased gluconeogenesis due to stimulation of nocturnal unfolded protein response. Bertuglia S, Reiter RJ. Melatonin reduces microvascular damage and insulin resistance in hamsters due to chronic intermittent hypoxia.
Nishida S, Segawa T, Murai I, Nakagawa S. Long-term melatonin administration reduces hyperinsulinemia and improves the altered fatty-acid compositions in type 2 diabetic rats via the restoration of Delta-5 desaturase activity.
Wang PP, She MH, He PP, Chen WJ, Laudon M, Xu XX, et al. Piromelatine decreases triglyceride accumulation in insulin resistant 3 T3-L1 adipocytes: role of ATGL and HSL. Borba CP, Fan X, Copeland PM, Paiva A, Freudenreich O, Henderson DC.
Placebo-controlled pilot study of ramelteon for adiposity and lipids in patients with schizophrenia. J Clin Psychopharmacol. She M, Deng X, Guo Z, Laudon M, Hu Z, Liao D, et al.
Pharmacol Res. Surya S, Symons K, Rothman E, Barkan AL. Complex rhythmicity of growth hormone secretion in humans. Patel YC, Alford FP, Burger HG. The hour plasma thyrotrophin profile. Clin Sci. Cailotto C, Lei J, van der V, van HC, van Eden CG, Kalsbeek A, et al.
Effects of nocturnal light on clock gene expression in peripheral organs: a role for the autonomic innervation of the liver. Dumont M, Lanctot V, Cadieux-Viau R, Paquet J. Melatonin production and light exposure of rotating night workers.
Smith MR, Eastman CI. Shift work: health, performance and safety problems, traditional countermeasures, and innovative management strategies to reduce circadian misalignment. Grundy A, Sanchez M, Richardson H, Tranmer J, Borugian M, Graham CH, et al.
Light intensity exposure, sleep duration, physical activity, and biomarkers of melatonin among rotating shift nurses. Folkard S. Do permanent night workers show circadian adjustment? A review based on the endogenous melatonin rhythm. Roden M, Koller M, Pirich K, Vierhapper H, Waldhauser F.
The circadian melatonin and cortisol secretion pattern in permanent night shift workers. Buijs RM, Escobar C, Swaab DF. The circadian system and the balance of the autonomic nervous system.
Vyas MV, Garg AX, Iansavichus AV, Costella J, Donner A, Laugsand LE, et al. Shift work and vascular events: systematic review and meta-analysis. Wang XS, Armstrong ME, Cairns BJ, Key TJ, Travis RC. Shift work and chronic disease: the epidemiological evidence. Occup Med Lond.
Ha J, Kim SG, Paek D, Park J. The Magnitude of Mortality from Ischemic Heart Disease Attributed to Occupational Factors in Korea - Attributable Fraction Estimation Using Meta-analysis.
Saf Health Work. Tuchsen F, Hannerz H, Burr H. A 12 year prospective study of circulatory disease among Danish shift workers.
Occup Environ Med. The summary relative risks RRs were estimated using a random model. The sensitivity analysis was performed by sequentially excluding each study to test the robustness of the pooled estimates.
Moreover, the relationship between sleep duration and metabolic syndrome risk presented a U-shaped curve. Implications: Based on our findings, sleep is a behavior that can be changed and is economical. Clinically doctors and health professionals should be encouraged to increase their efforts to promote healthy sleep for all people.
Metabolic syndrome MS is a collection of metabolic disorders, including obesity, hypertension, hypertriglyceridemia, low high-density lipoprotein HDL cholesterol, and hyperglycemia.
The syndrome leads to adverse cardiovascular events 2 and the spread of diseases such as cancer 3. The total cost of these diseases, including the potential loss of health care and economic activity, places a significant financial burden on patients and health systems 4. Therefore, it is important to identify modifiable risk factors for MS 5.
Recently, the relationship between sleep and metabolic syndrome has attracted wide attention. Epidemiological evidence has reported the relationship between sleep duration and MS. However, the information published was not consistent 6 — 8.
Ju 6 included 11 cross-sectional studies and three cohort studies and concluded that both short sleep and long sleep are risky behaviors that increase the risk of metabolic syndrome. Another meta-analysis, consisting of 10 cross-sectional studies and two cohort studies, concluded that short sleep duration was associated with metabolic syndrome development, while long sleep duration was not 7.
The final meta-analysis, which included 18 cross-sectional studies, found a dose-response relationship between short sleep duration and metabolic syndrome.
However, it does not support the idea that long sleep is associated with metabolic syndrome 8. Summing up previous meta-analyses, it can be found that short sleep is associated with an increased risk of MS, but the relationship between long sleep and MS risk is still controversial.
Wang 9 found a U-shaped relationship between sleep duration and the risk of hypertension. Shan 10 reported a U-shaped relationship between sleep duration and the risk of diabetes.
Hypertension and diabetes are components of metabolic syndrome. Therefore, we hypothesize that a U-shaped relationship between sleep duration and the risk of metabolic syndrome exists as well. At the same time, we found that many cohort studies on sleep duration and metabolic syndrome have emerged in recent years.
Given that cohort studies possess a higher level of evidence and can also draw causal inferences, we mainly included the latest cohort studies for our meta-analysis.
We searched four databases PubMed, Embase, Cochrane Central Register of Controlled Trials, and Clinicaltrials. gov for reports relating to sleep and MS. The combination of two sets of keywords and exploded controlled vocabulary terms is showed in Table S1.
The literature search was limited to English, updated to October 18, The protocol was registered in PROSPERO No. The studies included in the meta-analysis must have met all the following inclusion criteria: 1 Outcome variables need to be defined as the incidence of MS or a group of metabolic abnormalities, including hyperglycemia, obesity, hypertension, or dyslipidemia.
The following information was extracted from each study: 1 Name of the first author. Two authors independently assessed the articles for compliance with the inclusion criteria and resolved disagreements through discussion. The quality for each study was independently rated by two researchers.
Due to the nature of observational studies, all the studies received 0 out of 9 points in the treatment quality. The evaluation of study quality includes eight domains: representation of the exposed cohort, selection of the non-exposed cohort, determination of exposure, absence of outcome events before the study began, whether the cohort was controlled for confounding factors, assessment of outcome events, adequacy of follow-up time, and completeness of follow-up.
Each identified disagreement was resolved through team discussion and joint review. All reported RR were examined and extracted into two groups, the crude model and the most-adjusted model.
The crude model is the model that does not control for covariates. The most-adjusted model is the model with the most covariates. If the study did not report the crude model, but reported the least-adjusted model and the most-adjusted model, we then pulled the least-adjusted results into the crude-model group.
Hazard ratio HR and odds ratio OR were assumed to approximate the same relative risk and were collectively described as the RR in this meta-analysis. The Q test and I 2 were used to examine the heterogeneity between studies.
Subgroup analyses were conducted by the stratification of age and the components of MS. Sensitivity analyses were conducted by omitting a single study in each turn to test the robustness of our results.
Sensitivity analysis was performed after each exclusion to assess the stability of the results. Statistical analysis was performed using Stata Version 16 StataCorp LP, College Station, Texas, USA. Two thousand seven hundred and seventy-three articles were identified, of which 9.
Finally, 12 studies 11 — 22 were eligible based on the inclusion and exclusion criteria. Since the data were divided by sex in one study, it was considered separate studies in the subsequent data analysis Therefore, 13 studies were included in the final meta-analysis.
Of the 13 included studies, , individuals were included, with 44, incident MS cases were observed during follow-up, and the estimated incidence of MS was The duration of follow-up ranged from 1 to 18 years. The age of the study participants was between 18 to 95 years.
Sleep duration category hr. and other characteristics of the included studies are presented in Table 1. According to the Newcastle—Ottawa scales, all of the included studies had a quality score over 9, which indicated high quality Table S2. We identified 10 studies reporting the RRs using a crude model or least-adjusted model.
Figure 4 Meta-analysis of the association between short sleep and risk of metabolic syndrome from crude models or least-adjusted results.
Figure 5 Meta-analysis of the association between long sleep and risk of metabolic syndrome from crude models or least-adjusted results. Figure 6 The relationship between sleep duration and MS risk presented a U-shaped curve. The squares represent the mixed RRs of different sleep duration in patients with MS.
The broken outline in green illustrates the nonlinear trend, indicating the presence a U-shaped relationship. The relationship between short sleep duration and components of the metabolic syndrome are presented in Table 2. Table 2 Meta-analysis of the associations between sleep duration and the components of MS.
The relationship between long sleep duration and components of the metabolic syndrome are presented in Table 2. A visual inspection of the funnel plots also did not reveal apparent publication bias Figure S4. In this study, we examined the causal relationship between sleep duration and MS by enrolling cohort studies and using meta-analysis techniques.
Our findings suggest that both short and long sleep periods result in an increased risk of MS, and the risk of longer sleep duration is higher than that of short sleep duration. Moreover, the duration of sleep and the risk of MS presented a U-shaped curve.
Both short and long sleep periods can increase the risk of MS components, such as obesity and high blood pressure. Short periods of sleep may increase the risk of hyperglycemia, another component of MS. A large sample size of , participants and the absence of publication bias make our study results more robust.
Sensitivity analysis further confirmed the robustness of our conclusion. Cohort studies move towards results and the temporal sequence between causes and effects is usually clear, whereas cross-sectional studies are difficult to make causal inferences or interpret established associations Long sleep duration has not been found to be associated with an increased risk of MS in previous research 7 , 24 , which was mostly based on cross-sectional studies Our findings show that both long and short sleep duration are associated with an increased risk of MS.
The simplest model and the one with the most adjustments were derived from our meta-analysis. Surprisingly, long sleep had the opposite effect on MS, with the estimated effect in the crude model being non-statistically significant but evident in the adjusted model.
This may be the reason why previous systematic evaluations could not yield positive results. Interestingly, we found that short sleep did not increase the risk of MS in persons older than 65 years. It appears that the amount of sleep required by the elderly is less than that required by the young First, older people slept significantly less than younger people when extremely long mandatory sleep periods were provided This may be due to the fact that older people have lower ad lib sleep needs than younger people.
Another interesting finding was that in healthy older adults, after sleep deprivation or experimental slow-wave sleep suppression, slow-wave sleep duration and slow-wave activity SWA rebounded more slowly than in younger adults 28 , Older people have lower homeostatic sleep buildup than younger people, based on this finding.
In addition, under sleep deprivation, the elderly showed less impairment in the sleep sensitive alert task than young people There are numerous phenotypic signs of reduced homeostatic sleep drive in older people, which suggests that they require less sleep 27 , In other words, as we get older, our sleep requirements become less.
One literature only showed a dose-response relationship between short sleep duration and MS 8. Our meta-regression results showed a U-shaped prediction of dose-dependent responses, which had not been found in previous meta-analyses.
Besides, we investigated the relationship between sleep duration and components of MS. The possible reason is that the impaired blood glucose in MS mainly refers to elevated fasting blood glucose.
However, many patients with impaired blood glucose present with normal fasting blood glucose and elevated postprandial blood glucose For low-HDL, another component of MS, there was no statistically significant difference between short and long sleep duration.
The underlying mechanisms of the relationship between sleep and MS are not fully understood. The underlying mechanisms linking sleep to MS may differ between short and long term sleep.
Several potential pathophysiology mechanisms may contribute to the relationship between short sleep duration and MS. Hormonal changes may be part of the explanation for MS caused by a short sleep. The low level of promoting anorexia hormone leptin and higher hunger hormone ghrelin levels has been found during short sleep in some experimental research 32 , Other hormone changes caused by the short sleep periods include an increase in cortisol production at night 34 — 36 , a kind of hormone that can cause insulin resistance and promote weight gain, hyperglycemia and hypertension.
Elevated catecholamines lead to increased sympathetic nerve activity, endothelial cell dysfunction, and impaired vasodilation.
These changes also contribute to increased blood pressure 37 — The underlying mechanism between longer sleep and an increased risk of MS is currently thought to be speculative.
Obstructive sleep apnea OSA may be a cause. Risk factors for OSA include snoring, increased body mass index BMI , and aging. Snoring patients begin sleep with reduced pharyngeal dilator activity, leading to apnea and hypoventilation, and end with a slight awakening that restores muscle activity and reopens the upper airway.
Repeated episodes of this can cause sleep fragmentation, which is associated with long periods of sleep. Sleep fragmentation and intermittent hypoxia can increase the excitability of the sympathetic nervous system, resulting in metabolic disorders One study showed that weight loss in moderate to severe OSA patients reduced upper respiratory tract collapse and daytime sleepiness Older adults have ventilatory control systems that are out of control.
At the same time, older people have more airway collapse and lower ventilation capacity than younger people, and longer sleep associated with OSA makes them more vulnerable to metabolic disorders due to hypoxia Finally, long sleep duration has been associated with several risk factors for MS morbidity, such as depression and low physical activity In addition, sleep appears to promote inflammatory homeostasis by affecting a variety of inflammatory mediators, such as cytokines.
Prolonged sleep disturbances can lead to chronic, systemic, low-grade inflammation and are associated with a variety of diseases with inflammatory components, such as MS. This view is supported by Besedovsky A consequence of MS as a chronic, low-grade inflammation is insulin resistance 48 , The final model used in our study adjusted for the following covariates: age, education, occupation, marital status, and menopausal status women only.
Each of the covariates was categorized in the same way as the previously HEXA study on snoring and metabolic syndrome [ 18 ]. Education had three categories: middle school or below, high school graduate, and college or above. Occupation had three categories: non-manual, manual, and unemployed.
Marital status had two categories: married or single. Menopausal status had two categories: pre- or post-menopausal. Additional lifestyle covariates were considered. Current smokers were defined as those who smoked a minimum of cigarettes during their lifetime and continued to smoke; non-smokers as those who have never smoked in their lifetime or have quit.
Current drinkers were defined as those who drink alcohol at the time of survey and non-drinkers as those who have never drank alcohol or have abstained from alcohol drinking. Regular exercisers were defined as those engaging in routine physical activity. Likelihood ratio tests with the use of a cross-product term to calculate gender interaction p -values.
To assess the basic characteristics of our sample in regards to sleep duration categories, a chi-square test for categorical variables and analysis of variance ANOVA for continuous variables were performed. A multivariable stepwise analysis was used to determine a parsimonious model for the final logistic regression models.
All p -values were two-sided, and statistical significance was set at below 0. A parsimonious model of regression was determined via multivariable stepwise analysis.
The final model was adjusted for age continuous , education, occupation, menopausal status only women , smoking only men and drinking status, routine exercise and dietary intake continuous were adjusted.
Marital status was not included in the models as it did not pose a significant effect on the relationship between sleep duration and MetS. While smoking is an important covariate for both sleep duration and MetS occurrence, the percent of current smokers among women was an average of 2.
Energy intake variable accounted for the individual dietary factors i. A separate analysis with individual dietary factors adjusted did not affect the association between sleep duration and MetS. Moreover, we excluded subjects with a previous diagnosis of type 2 diabetes, hypertension, and dyslipidemia to account for comorbidities via sensitivity analysis.
We also examined 1-h interval sleep duration and MetS and its components as a supplemental analysis. SAS software version 9. A summary of the sample baseline characteristics categorized by sleep duration is available in Table 1.
About The overall prevalence of MetS was All selected covariates differed at statistical significance among the sleep duration categories. The odds ratios for MetS and its components by sleep duration are in Table 3. Less than 6 h sleep was also associated with elevated waist circumference OR: 1.
To assess the dose-response relationship of specific sleep duration hours and MetS, a supplemental analysis from HEXA study years — 73, subjects of which 24, men and 48, women was performed Additional file 1 : Table S1. Among men, only 5 h sleep was associated with metabolic syndrome OR: 1.
The results of the updated HEXA-G — analysis on sleep duration and metabolic syndrome and its components confirm and further expand on the previously published HEXA study — [ 13 ], displaying findings not shown in prior studies.
In the previous HEXA study [ 13 ], after adjusting for covariates, 10 h sleep or greater was associated with MetS in women only OR: 1. However, in the current study, with expanded sample size and power, a positive association was observed between 10 h sleep or greater and MetS in both men and women OR: 1.
In the supplemental analysis, a similar J-shape trend existed but with a significant positive association between 10 h sleep or greater and MetS only in women; between 5 h sleep and MetS only in men.
Gender interaction in the association between sleep duration and metabolic syndrome was statistically significant in our study which complements the gender difference reported in a study looking at the association between sleep duration and mortality [ 20 ]. While the exact mechanisms are unclear, one explanation may be that women experiencing menopausal transition face erratic fluctuations and eventual decline in estrogens as well as ovarian oestradiol which may lead to frequent sleep disruptions [ 21 , 22 ], a common characteristic of long sleep duration [ 23 ].
Additionally, a study examining the association between inflammatory markers and sleep duration observed higher levels of interleukin-6 IL-6 and C-reactive protein CRP in women who slept less than 5 h or more than 9 h, while no significant marker variation was observed in men [ 25 ].
Notably, a recent meta-analysis stated that women may be more vulnerable to the effects of sleep disturbance and displayed greater increases of CRP and IL-6 compared with men. The review also reported that long sleep duration, but not short duration was associated with increases in CRP and IL-6 [ 26 ].
Few studies have reported gender-stratified sleep association with MetS. A meta-analysis of 12 cross-sectional and 3 cohort studies from North America, Europe, and Asia, has found that both less than 5 h and greater than 8 h sleep duration were associated with MetS but reported no gender differences between the association [ 27 ].
Additionally, a study in Korea reported that both short less than or equal to 5 h and long greater than or equal to 9 h sleep are related to increased risk of MetS, however, with gender adjusted [ 28 ]. For example, one cross-sectional study conducted in China categorized sleep duration into 2- h intervals and found that both short less than 6 h and long greater than 9 h sleep was associated with MetS in males only [ 29 ].
Similarly, a prospective study conducted in Korea has also used 2-h sleep intervals and reported that only short less than 6 h sleep was associated with MetS in a mixed gender population [ 30 ].
Furthermore, while a recent meta-analysis reported that a dose-response relationship exists between short sleep and MetS, it did not support the notion that long sleep is associated with MetS [ 31 ].
The opposite was observed in a study conducted in Korea in which greater than or equal to 9 h was associated with MetS but not with sleep less than or equal to 5 h [ 32 ].
Although the biological mechanism of sleep duration and MetS remains unclear, several potential endocrinologic, immunologic, and metabolic processes have been reported. Sleeping less than 7 h may cause reciprocal changes in circulating levels of leptin and ghrelin [ 33 ] which would increase appetite, caloric intake, reduce energy expenditure [ 34 ] facilitating an increase in waist circumference as well as overall obesity development.
It may also cause impaired glycemic control lowering glucose tolerance and thyrotropin concentration levels increasing risk for hypertension and diabetes [ 35 ]. Other endocrinologic effects include increased cortisol levels which may elevate fasting glucose levels [ 36 ].
Additionally, clinical studies have shown that sleep deprivation results in increased levels of high-sensitivity CRP and IL-6 during, markers that have also been associated with constituents of MetS [ 37 ]. Likewise, number of studies report detrimental health effects of long sleep [ 27 , 38 ] and suggest sleeping in moderation approximately 7 h rather than in abundance for optimum health [ 39 ].
Potential effects of long sleep include: increased sleep fragmentation with lower sleep quality [ 23 ], greater fatigue [ 40 ], limited photoperiod and greater physiological deprivation i. exercise [ 23 ]. All of these conditions are studied to be associated with insulin resistance, dyslipidemia and hormonal imbalance [ 41 ] which may lead to premature death [ 23 , 39 ].
While the current study displays a correlation between sleep duration and MetS, there are a couple factors to consider. First, the current study is cross-sectional and therefore, causality between sleep duration and MetS cannot be construed.
Second, sleep duration was assessed through self-report questionnaire instead of objective measures via the use of an actigraph or polysomnography. Third, total sleep time measured may include both nighttime sleep as well as naptime.
Daytime napping behavior has been associated with lower sleep efficiency, shorter sleep duration, and consequently cardiovascular risk factors [ 45 ].
Hence, it would be informative to make the distinction between naptime and nighttime to separately assess their impact on health. Fifth, the covariates such as smoking, alcohol drinking, and physical activity were included in the final model as categorical variables.
Given that smoking, alcohol drinking, and physical activity are studied to be dose-dependent to health outcomes, there may be residual confounding effect that is not accounted for. Additionally, our study included menopausal status as a binary variable and does not include information on women experiencing menopausal transition, which has been studied to be a contributing factor to sleep patterns in women [ 22 ].
Despite these limitations, the current study is the largest study providing dose-response association between sleep duration and metabolic syndrome and its components. Using the HEXA-G database allowing for greater internal validity as well as additional robust subgroup analyses: the sample became more homogenous and the number of women and men have almost doubled from the previous study which gave more power to detect the associations between sleep and MetS that were unnoticed before.
Furthermore, with the addition of extended HEXA study years from to , hour-specific dose-response association was analyzed which highlighted the gender differences in association between sleep and MetS. In conclusion, after adjusting for covariates such as sociodemographic and lifestyle factors, sleep duration displayed an association with MetS and its components among both men and women.
Gender differences were observed in regards to the effect of short and long sleep and their association with MetS-men were affected more by short sleep and women with long sleep. Further prospective studies using multiple measurements of sleep duration i.
sleep diaries and actigraphs are warranted to assess the casual relationship between sleep duration and MetS and its components. Office of Disease Prevention and Health Promotion: Healthy People Sleep Health. Google Scholar. National Sleep Foundation: National Sleep Foudnation Recommends new Sleep Times.
National Sleep Foundation. Sleep Hygiene. Sleep Topics. Kim K, Shin D, Jung GU, Lee D, Park SM. Association between sleep duration, fat mass, lean mass and obesity in Korean adults: the fourth and fifth Korea National Health and nutrition examination surveys.
J Sleep Res. Article PubMed Google Scholar. Magee CA, Kritharides L, Attia J, McElduff P, Banks E. Short and long sleep duration are associated with prevalent cardiovascular disease in Australian adults.
Itani O, Jike M, Watanabe N, Kaneita Y. Short sleep duration and health outcomes: a systematic review, meta-analysis, and meta-regression.
Sleep Med. Shen XL, Wu YL, Zhang DF. Nighttime sleep duration, hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies. Sci Rep. Article PubMed PubMed Central CAS Google Scholar.
Liu TZ, Xu C, Rota M, Cai H, Zhang C, Shi MJ, Yuan RX, Weng H, Meng XY, Kwong JS, et al. Sleep duration and risk of all-cause mortality: a flexible, non-linear, meta-regression of 40 prospective cohort studies.
Sleep Med Rev. Gallicchio L, Kalesan B. Sleep duration and mortality: a systematic review and meta-analysis. da Silva AA, de Mello RG, Schaan CW, Fuchs FD, Redline S, Fuchs SC. Sleep duration and mortality in the elderly: a systematic review with meta-analysis.
BMJ Open. Article PubMed PubMed Central Google Scholar. Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies. Tran BT, Jeong BY, Oh JK. The prevalence trend of metabolic syndrome and its components and risk factors in Korean adults: results from the Korean National Health and nutrition examination survey BMC Public Health.
Yoon HS, Lee KM, Yang JJ, Lee HW, Song M, Lee SA, Lee JK, Kang D. Associations of sleep duration with metabolic syndrome and its components in adult Koreans: from the health examinees study.
Sleep Biol Rhythms.
We know that sleep is crucial for physical and mental recovery, but it also has Metaboliv Metabolic support for sleep quality DKA nursing interventions with your Metxbolic health qualuty can help s,eep harm markers of metabolic health such as fasting Stress relief through aromatherapy, insulin resistanceand weight. Metabolic support for sleep quality also wleep hormones that signal hunger and satiety and supports efficient glucose metabolism. However, this may be easier said than done. This is problematic because sleep is strongly tied to metabolic healthand over time, poor sleep may contribute to the deterioration of metabolic health. Glucose utilization decreases during deep sleep due to the reduced activity of neurons [3]. Between am, glucose is released from the liver in preparation for your body being active, so glucose levels tend to be higher in the morning [4].
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