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Gomes, S.; Ramalhete, C.; Ferreira, I.; Bicho, M.; Valente, A. Noncommunicable Diseases. Encyclopedia. Available online: https://encyclopedia.pub/entry/45299 (accessed on 27 July 2024).
Gomes S, Ramalhete C, Ferreira I, Bicho M, Valente A. Noncommunicable Diseases. Encyclopedia. Available at: https://encyclopedia.pub/entry/45299. Accessed July 27, 2024.
Gomes, Sofia, Cátia Ramalhete, Isabel Ferreira, Manuel Bicho, Ana Valente. "Noncommunicable Diseases" Encyclopedia, https://encyclopedia.pub/entry/45299 (accessed July 27, 2024).
Gomes, S., Ramalhete, C., Ferreira, I., Bicho, M., & Valente, A. (2023, June 07). Noncommunicable Diseases. In Encyclopedia. https://encyclopedia.pub/entry/45299
Gomes, Sofia, et al. "Noncommunicable Diseases." Encyclopedia. Web. 07 June, 2023.
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This entry is adapted from the peer-reviewed paper 10.3390/nu15112462

Sleep is extremely important for the homeostasis of the organism. In recent years, various studies have been carried out to address factors related to sleep patterns and their influence on food choices, as well as on the onset of chronic noncommunicable diseases.

sleep patterns metabolism hormones appetite

1. Factors That Affect Sleep

Homeostatic and circadian processes control the quality of sleep, and awake periods [1]. The main role of the circadian clock is to promote awakening during the internal biological day and to favor sleep during the internal biological night [1]. However, today, due to unlimited access to artificial light, people exhibit undesirable behaviors regarding their endogenous circadian rhythm [2]. This temporal misalignment, called circadian misalignment, occurs when the internal circadian system is not correctly aligned with the external environment [3] and can lead to chronic sleep deprivation, very common in modern societies [4]. This deprivation can be attributed to quantitative factors, such as insufficient sleep duration, or to qualitative factors, such as fragmented sleep periods [5]. Circadian misalignment is often associated with numerous health problems [2]. One of the effects of circadian misalignment is a reduction in total sleep time, which may also affect sleep architecture since human sleep is composed of rapid eye movement (REM) sleep and non-REM sleep [1][6]. Several factors are responsible for circadian misalignment: the increase in the number of individuals who work in shifts or at night, the increase in the number of working hours, commute times, jet lag, psychosocial stress and engagement with television, radio, and the Internet [1][3][5][7]. Shift work is an essential system in society, being very present in industry as well as in medical institutions [8]. However, shift work is associated with adverse health outcomes, including gastrointestinal disorders, metabolic syndrome, diabetes, reproductive difficulties, and breast and prostate cancer, as well as glucose intolerance and cardiovascular function [9][10]. Caffeine has been shown to have both positive and negative effects on behavior, cognition, and health, depending on the amount consumed. When consumed in excess, it can cause sleep disturbances, since its consumption significantly reduces sleep time and causes disturbances in sleep quality [11]. In recent years, electronic devices, including computers and mobile phones, game consoles and tablets, have been associated with poor sleep among young people [12][13]. Some studies [14][15][16] have linked the mere presence of these devices in the bedroom with the tendency to sleep later, and consequently, shorten sleep duration and increase daytime sleepiness [12][13]. This idea was further reinforced as the use of these devices became the subject of great clinical interest: it was not only shown to increase sedentary behavior but also impoverish the quality of subjective sleep, even leading to falling asleep during school hours and increasing daytime sleepiness [12][13]. In the case of children, among the many factors that affect their sleep time are television viewing and the presence of a television in the bedroom [17]. Television-related behaviors can directly disturb sleep time or increase emotional/mental arousal and light exposure, which can be determinants of sleep duration and quality [17]. These inadequate hours of sleep are associated with poor mental and physical health, which include impaired academic performance, depression, injuries, and an increased risk of obesity [17].

2. Sleep and Metabolism

All animals, including humans, evolved over millions of years in a stable, seasonal light–dark environment, in which the intervals between light and dark moments could be distinguished within a 24 h period [7][18][19][20][21]. Because of this repetitive and extremely regulated 24 h cycle, an internal circadian clock developed that allows day–night adjustments of metabolic activities, which are at the base of circadian rhythms [13][22]. The internal clock in humans is in the suprachiasmatic nucleus of the anterobasal hypothalamus, functioning as a stopwatch and regulating gene/protein expression, and thus the flow of all the functions of the organism, such as the use and storage of energy, feeding, sleep–wake cycle, electrical activity and concentration of ions and substances, cyclic changes in metabolism and energy homeostasis [7][18][19][20][21]. It is apparent that the basis of the circadian clock is the light–dark cycle. Therefore, the most important external signal is light, which makes individual and physiological behavior correspond to the external day–night cycle, influencing several hormones with metabolic relevance since they present a circadian oscillation with different daily patterns [7][20][22]. Thus, it is believed that changes in the pattern of light–dark exposure or inappropriate exposure to light can affect the circadian rhythm, causing the internal rhythm to become out of sync with the external environment, damaging sleeping behavior and compromising metabolic processes [20]. A metabolic process that is clearly dependent on the light–dark cycle and the function of the suprachiasmatic nucleus is the melatonin cycle [21]. Falling asleep with the television on or sleeping with the light on has been associated with a change in the brain’s natural sleep cycle and melatonin production [23]. The production and secretion of melatonin by the pineal gland occurs in a nocturnal circadian pattern, with the peak being reached 3–5 h after dark, declining precipitously after waking up [21][24][25]). Since melatonin is rapidly released by the pineal gland soon after its production, it can be said that the concentration of melatonin in the blood reflects its synthesis, and fluctuations in melatonin concentration play an important role in the transmission of essential information to the various organs [21]. In addition to its role in transmitting information, melatonin secretion, and the location of its receptors throughout the body, which include the β cells of the pancreatic islets, mean that, according to some authors, melatonin can play an important role in glucose metabolism [26][27]. In fact, performed in vitro tests [26][27] have verified that prolonged exposure of the β islets of the pancreas to melatonin, with the purpose of simulating the period of sleep, increases the sensitivity of the β receptors to glucose [25]. Sleep loss not only affects the melatonin cycle but has also been linked to disturbances in other metabolic functions, specifically an increase in the appetite-stimulating hormone ghrelin [24][28][29][30]. A sleep restriction of 4 h per night for two consecutive days, as well as one night of total sleep restriction, have been shown to increase daytime plasma ghrelin concentrations in young men, mainly in the early hours of the day [31]. However, sleep deprivation also causes a decrease in leptin, the appetite-suppressing hormone, thus favoring food intake by increasing appetite [24][28][29]. Leptin is an amino acid essentially produced by adipocytes, which is secreted in a circadian manner, suggesting that it is influenced by the circadian clock through its sympathetic input in adipocytes [32][33]. However, leptin can also be expressed by non-adipose tissues, such as stomach tissue, and, to this extent, gastric leptin levels show oscillations, being elevated during the night, leading to a reduction in appetite and promoting satiety and night rest, but low during the day, increasing appetite [30][32][33]. Thus, it is suggested that gastric leptin may be involved in appetite regulation by inducing satiety [30][32][33]. Some authors [34] have associated leptin with increased insulin sensitivity as it promotes fat oxidation and reduces fat accumulation in non-adipose tissues. This effect can be directly mediated by leptin due to AMPK activation in certain skeletal muscles and indirectly through the sympathetic hypothalamic axial nervous system [33]. The activation of AMPK, activated protein kinase, leads to the inhibition of acetyl-coenzyme A (CoA) carboxylase [33][35], which leads to a reduction in the intracellular levels of the malonyl CoA metabolite. The entry of fatty acids into the mitochondria decreases and the oxidation of fatty acids is favored [33]. There are published results [36] which indicate that leptin-dependent sleep disturbances may result in an alteration in leptin-sensitive axial hormones. In addition to leptin, adipocytes are also the main producers of adiponectin, which has anti-diabetic, anti-atherogenic and anti-inflammatory properties [33]. Like leptin, adiponectin improves insulin sensitivity thanks to the activation of AMPK and is also responsible for the decrease in hepatic glucose production due to the decrease in mRNA expression of two essential enzymes involved in gluconeogenesis, namely phosphoenolpyruvate carboxylase and glucose-6-phosphatase [33]. Ghrelin, on the other hand, is an anorexigenic peptide produced in the stomach and other organs, such as the pancreas and hypothalamus, but it is mostly released by the stomach and its levels fluctuate based on food intake [32], with a rapid decrease in ghrelin after eating and an increase immediately before a meal [30][32][37]. It has been shown that ghrelin levels increase by 20% before breakfast, 45% before lunch and 51% at dinner [38]. Despite the absence of food intake, it is possible to find high levels of ghrelin during the first hours of the night, with a peak between midnight and two in the morning, which progressively decreases with food intake [30][32][38]. Sleep deprivation causes an increase in circulating ghrelin levels, and this phenomenon is accompanied by an increased feeling of hunger [32]. The way ghrelin stimulates appetite is through the activation of neuropeptide Y, located in the lateral part of the hypothalamus [32]. Ghrelin is responsible for the feeling of appetite and for weight gain and is also responsible for stimulating the release of growth hormones. This hormone is a hypothalamic neuropeptide that regulates eating, energy metabolism, reproduction, and sleep [39]. Regarding the latter, it stimulates the neurons that promote the wake-to-eat cycle, thus modulating arousal and appetite [37]. There are several studies that describe how the growth hormone is controlled through the homeostasis of the wake–sleep cycle, with an increase in its production during sleep being verified in men, namely in stages three and four of slow-wave sleep (SWS). When the sleep period is interrupted, there is a change in the release of growth hormones, the impact being particularly evident in men, but also detectable in women [30]. Another cycle that is influenced by the circadian rhythm is the cortisol profile, which oscillates over the 24 h, since the decrease in its secretion occurs in the early hours of the night and the peak of its secretion occurs at the time of awakening, decreasing progressively throughout the day [22]. Manipulations of the sleep cycle have minimal effects on the cortisol profile, as it is very difficult to detect changes when sleep is interrupted in the morning, coinciding with the peak of corticotropic activity [30]. Sleep deprivation has also been shown to have a negative influence on the response of adrenocorticotropic hormones, adrenaline and on the sensitivity of serotonin (5-HT) receptors, which over time can lead to changes in the system’s response to stress, seen in changes in humor [24]. Serotonin (5′hydroxyptitanin) has been implicated not only in the regulation of emotions, attention and memory, but also in the regulation of appetite and sleep, and its synthesis in the brain is considered critical since for this to occur, the availability of its precursor, the essential amino acid tryptophan, is necessary, and it can only be obtained by humans from the diet [40][41][42].

3. Sleep and Food Choices

Changes in food choices and eating behaviors are associated with short sleep time [43]. Sleep disturbances have been associated with increased sleepiness and changes in thermoregulatory functions and secretion of the growth hormone by the hypothalamic–pituitary–adrenal gland axis during SWS, which leads to a decrease in energy expenditure [44][45]. This factor was confirmed by Jung et al. (2011), who reported a 7% increase in energy expenditure over 24 h during a day of total elimination of sleep compared to a normal day, which supports the importance of sleep for energy conservation [46], due to a decrease in the practice of physical activity [31][44][45]. However, sleep deprivation also increases the appetite for food intake, and the food choices made at these times result in meals rich in sweet and high-density energy foods, and these phenomena are associated with changes in neuroendocrine control of appetite. Sleep disturbances cause an increase in circulating ghrelin levels and a decrease in leptin levels, which favors an increase in the sensation of appetite and hunger, affecting the energy balance [3][44][45][47][48][49][50][51][52]. The feeling of hunger and appetite due to sleep disturbances makes people choose foods with a high caloric density and rich in carbohydrates, such as sweets, salty snacks, and starchy foods [31][43][53][54][55], verified in girls, with increased intake of sweets and/or fast food and soft drinks in boys [55]. Sleep disorders in children and sleeping less than 7 h/night in adults have been associated with reduced consumption of fruit and vegetables and increased consumption of energy-rich foods with low nutritional value [43]. Adolescents who report sleeping less than 8 h/night tend to consume more total calories from fat than from carbohydrates and protein when compared to those who sleep for 8 or more hours/night [3][43]. In adults, acute sleep deprivation increases caloric intake, mainly due to increased consumption of carbohydrates and fat, as well as increased consumption of snacks [53][54].

4. Sleep and Chronic Diseases

In modern society, a reduction in sleeping hours is quite common, either for occupational or lifestyle reasons. A short period of sleep, described as sleeping less than six hours a night, sleep deprivation and/or even sleep restriction have been associated with several chronic diseases [56]. Thus, sleep deprivation has been associated with an increased risk of diabetes, obesity, hypertension, breast cancer, coronary heart disease, low bone density, increased body mass index and insulin resistance [7][13][14][19][28][47][57][58][59]. However, excessive sleep duration (more than 9 h/night) is also harmful, being related to an increased incidence of premature mortality, cardiovascular disease, and cognitive damage [19].

5. Sleep and Stress

Children aged 8–11 years change their energy intake because of changes in their sleep duration [3]. However, sleep deprivation is also responsible for causing physiological stress, which can itself alter energy balance regulators [3]. In a prospective study [60], it was shown that physical and social stress related to family and/or work matters was associated with an increased risk of incidence and persistence of insomnia. Insomnia is characterized by difficulty initiating and/or maintaining sleep, waking up in the early hours of the day and, in general, dissatisfaction with both the quality and quantity of sleep [57].

6. Sleep and Night Eating Syndrome

Night eating syndrome (NES) is characterized by morning anorexia, hyperphagia in the afternoon and insomnia, and is often due to periods of stress, such as unsuccessful attempts to lose weight [61]. Research demonstrates that patients with NES experience high levels of insomnia and poor sleep quality [62][63][64]. Expanding on the research, when comparing patients with NES with evening hyperphagia to patients with nocturnal ingestions, Loddo et al. found differences in sleep features across NES subgroups. The researchers observed a higher total duration of eating episodes, eating latency following wakening and sleep latency following eating episodes in the evening hyperphagia group [65]. It may be that sleep disturbance is heightened in patients with evening hyperphagia [66]. Zwaan et al. [67] found that across studies, the prevalence of NES in pre-operative bariatric patients ranged from 6 to 64% [67]. The overall prevalence of NES ranges from 2.8 to 8.2% across the eating disorder, obese and bariatric surgery populations [68].

7. Sleep and Cardiovascular Disease

Currently, there is increasing evidence of a relationship between sleep and the risk of cardiovascular disease [69]. Literature reviews [70][71] have demonstrated the link between dysfunctional sleep patterns and their contribution to the increased risk of cardiovascular disease in shift workers. Evidence supports the existence of a relationship between poor quality and duration of sleep, on the one hand, and the activation of the sympathetic nervous system and increased levels of inflammation, on the other, which are believed to be responsible for inducing endothelial dysfunction, a key factor in the onset of atherosclerosis and consequent increases in the risk of cardiovascular diseases [9][69][72].

8. Sleep and Insulin Resistance

Scientific evidence [73][74] has shown that acute sleep loss increases food intake, with damage to glucose tolerance and insulin sensitivity, the latter of which increases in the body to maintain glucose homeostasis [59]. Just as important in this whole process is the intestinal hormone glucagon-like peptide 1, GLP-1, secreted after ingesting nutrients by mouth. GLP-1 can improve insulin resistance and reduce food intake; when there is a deterioration of sleep, GLP-1 signaling may be compromised [75]. It was found that in young males, plasma GLP-1 concentrations in the afternoon were reduced after a night of fragmented sleep compared to a regular night of sleep. However, the general concentration of GLP-1 during the 24 h was not affected, which may be due to the subtlety of the intervention, characterized by a small variation in the time spent in REM sleep relative to the time spent in stage two [75]. In other studies [76][77], SWS duration was correlated with insulin sensitivity, although no relationship with arousal was reported. The exact effect that reduced sleep exerts on insulin sensitivity is not yet known, but hormonal mechanisms, particularly changes in hormones responsible for promoting appetite, are increasingly evident [59].

References

  1. Feng, D.; Lazar, M.A. Clocks, Metabolism, and the Epigenome. Mol. Cell 2012, 47, 158–167.
  2. Firouzi, S.; Poh, B.K.; Ismail, M.N.; Sadeghilar, A. Sleep habits, food intake, and physical activity levels in normal and overweight and obese Malaysian children. Obes. Res. Clin. Pract. 2014, 8, e70–e78.
  3. Fisher, A.; McDonald, L.; Van Jaarsveld, C.H.; Llewellyn, C.; Fildes, A.; Schrempft, S.; Wardle, J. Sleep and energy intake in early childhood. Int. J. Obes. 2014, 38, 926–929.
  4. Baron, K.G.; Reid, K.J. Circadian misalignment and health. Int. Rev. Psychiatry 2014, 26, 139–154.
  5. Bozkurt, N.C.; Cakal, E.; Sahin, M.; Ozkaya, E.C.; Firat, H.; Delibasi, T. The relation of serum 25-hydroxyvitamin-D levels with severity of obstructive sleep apnea and glucose metabolism abnormalities. Endocrine 2012, 41, 518–525.
  6. Adan, A.; Archer, S.N.; Hidalgo, M.P.; Di Milia, L.; Natale, V.; Randler, C. Circadian Typology: A Comprehensive Review. Chrono-Int. 2012, 29, 1153–1175.
  7. Fonken, L.K.; Workman, J.L.; Walton, J.C.; Weil, Z.M.; Morris, J.S.; Haim, A.; Nelson, R.J. Light at night increases body mass by shifting the time of food intake. Proc. Natl. Acad. Sci. USA 2010, 107, 18664–18669.
  8. Ika, K.; Suzuki, E.; Mitsuhashi, T.; Takao, S.; Doi, H. Shift work and diabetes mellitus among male workers in Japan: Does the intensity of shift work matter? Acta Med. Okayama 2013, 67, 25–33.
  9. Lajoie, P.; Aronson, K.J.; Day, A.; Tranmer, J. A cross-sectional study of shift work, sleep quality and cardiometabolic risk in female hospital employees. BMJ Open 2015, 5, e007327.
  10. Leproult, R.; Holmbäck, U.; Van Cauter, E. Circadian Misalignment Augments Markers of Insulin Resistance and Inflammation, Independently of Sleep Loss. Diabetes 2014, 63, 1860–1869.
  11. Sanchez, S.E.; Martinez, C.; Oriol, R.A.; Yanez, D.; Castañeda, B.; Sanchez, E.; Gelaye, B.; Williams, M.A. Sleep quality, sleep patterns and consumption of energy drinks and other caffeinated beverages among Peruvian college students. Health 2013, 5, 26–35.
  12. Hysing, M.; Pallesen, S.; Stormark, K.M.; Jakobsen, R.; Lundervold, A.J.; Sivertsen, B. Sleep and use of electronic devices in adolescence: Results from a large population-based study. BMJ Open 2015, 5, e006748.
  13. Gamble, A.L.; D’Rozario, A.; Bartlett, D.J.; Williams, S.; Bin, Y.S.; Grunstein, R.R.; Marshall, N.S. Adolescent Sleep Patterns and Night-Time Technology Use: Results of the Australian Broadcasting Corporation’s Big Sleep Survey. PLoS ONE 2014, 9, e111700.
  14. Bulck, J.V.D. Television Viewing, Computer Game Playing, and Internet Use and Self-Reported Time to Bed and Time out of Bed in Secondary-School Children. Sleep 2004, 27, 101–104.
  15. Li, S.; Jin, X.; Wu, S.; Jiang, F.; Yan, C.; Shen, X. The Impact of Media Use on Sleep Patterns and Sleep Disorders among School-Aged Children in China. Sleep 2007, 30, 361–367.
  16. Mindell, J.A.; Telofski, L.S.; Wiegand, B.; Kurtz, E.S. A Nightly Bedtime Routine: Impact on Sleep in Young Children and Maternal Mood. Sleep 2009, 32, 599–606.
  17. Cespedes, E.M.; Gillman, M.W.; Kleinman, K.; Rifas-Shiman, S.L.; Redline, S.; Taveras, E.M. Television Viewing, Bedroom Television, and Sleep Duration from Infancy to Mid-Childhood. Pediatrics 2014, 133, e1163–e1171.
  18. Davies, S.K.; Ang, J.E.; Revell, V.L.; Holmes, B.; Mann, A.; Robertson, F.P.; Cui, N.; Middleton, B.; Ackermann, K.; Kayser, M.; et al. Effect of sleep deprivation on the human metabolome. Proc. Natl. Acad. Sci. USA 2014, 111, 10761–10766.
  19. Kasukawa, T.; Sugimoto, M.; Hida, A.; Minami, Y.; Mori, M.; Honma, S.; Honma, K.-I.; Mishima, K.; Soga, T.; Ueda, H.R. Human blood metabolite timetable indicates internal body time. Proc. Natl. Acad. Sci. USA 2012, 109, 15036–15041.
  20. McFadden, E.; Jones, M.E.; Schoemaker, M.J.; Ashworth, A.; Swerdlow, A.J. The Relationship Between Obesity and Exposure to Light at Night: Cross-Sectional Analyses of Over 100,000 Women in the Breakthrough Generations Study. Am. J. Epidemiol. 2014, 180, 245–250.
  21. Reiter, R.J.; Tan, D.-X.; Korkmaz, A.; Ma, S. Obesity and metabolic syndrome: Association with chronodisruption, sleep deprivation, and melatonin suppression. Ann. Med. 2012, 44, 564–577.
  22. Gonnissen, H.K.; Rutters, F.; Mazuy, C.; AP Martens, E.; Adam, T.C.; Westerterp-Plantenga, M.S. Effect of a phase advance and phase delay of the 24-h cycle on energy metabolism, appetite, and related hormones. Am. J. Clin. Nutr. 2012, 96, 689–697.
  23. Raaz, K.M.; Vanadna, J.; Vikram, B.; Manish, K. “Sleeplessness: Associated Disorders & Remedial Measures,” Sleeplessness: Associated Disorders & Remedial Measures. Int. J. Edu. Res. Technol. 2014, 5, 16–22.
  24. Halson, S.L. Sleep in Elite Athletes and Nutritional Interventions to Enhance Sleep. Sports Med. 2014, 44, 13–23.
  25. McMullan, C.J.; Curhan, G.C.; Schernhammer, E.; Forman, J.P. Association of Nocturnal Melatonin Secretion with Insulin Resistance in Nondiabetic Young Women. Am. J. Epidemiol. 2013, 178, 231–238.
  26. Kemp, D.M.; Ubeda, M.; Habener, J.F. Identification and functional characterization of melatonin Mel 1a receptors in pancreatic β cells: Potential role in incretin-mediated cell function by sensitization of cAMP signaling. Mol. Cell. Endocrinol. 2002, 191, 157–166.
  27. Ramracheya, R.D.; Muller, D.S.; Squires, P.E.; Brereton, H.; Sugden, D.; Huang, G.C.; Amiel, S.A.; Jones, P.M.; Persaud, S.J. Function and expression of melatonin receptors on human pancreatic islets. J. Pineal Res. 2008, 44, 273–279.
  28. Burt, J.; Dube, L.; Thibault, L.; Gruber, R. Sleep and eating in childhood: A potential behavioral mechanism underlying the relationship between poor sleep and obesity. Sleep Med. 2014, 15, 71–75.
  29. Calvin, A.D.; Carter, R.E.; Adachi, T.; Macedo, P.G.; Albuquerque, F.N.; van der Walt, C.; Bukartyk, J.; Davison, D.E.; Levine, J.A.; Somers, V.K. Effects of Experimental Sleep Restriction on Caloric Intake and Activity Energy Expenditure. Chest 2013, 144, 79–86.
  30. Leproult, R.; Van Cauter, E. Role of Sleep and Sleep Loss in Hormonal Release and Metabolism. Endocr. Dev. 2010, 17, 11–21.
  31. Benedict, C.; Hallschmid, M.; Lassen, A.; Mahnke, C.; Schultes, B.; Schiöth, H.B.; Born, J.; Lange, T. Acute sleep deprivation reduces energy expenditure in healthy men. Am. J. Clin. Nutr. 2011, 93, 1229–1236.
  32. Cagampang, F.R.; Bruce, K.D. The role of the circadian clock system in nutrition and metabolism. Br. J. Nutr. 2012, 108, 381–392.
  33. Padilha, H.; Crispim, C.; Zimberg, I.; De-Souza, D.; Waterhouse, J.; Tufik, S.; De-Mello, M. A link between sleep loss, glucose metabolism and adipokines. Braz. J. Med. Biol. Res. 2011, 44, 992–999.
  34. Ruderman, N.B.; Saha, A.K. Metabolic Syndrome: Adenosine Monophosphate-activated Protein Kinase and Malonyl Coenzyme A. Obesity 2006, 14, 25S–33S.
  35. Hardie, D.G. AMPK: A Target for Drugs and Natural Products With Effects on Both Diabetes and Cancer. Diabetes 2013, 62, 2164–2172.
  36. Spiegel, K.; Leproult, R.; L’hermite-Balériaux, M.; Copinschi, G.; Penev, P.D.; Van Cauter, E. Leptin Levels Are Dependent on Sleep Duration: Relationships with Sympathovagal Balance, Carbohydrate Regulation, Cortisol, and Thyrotropin. J. Clin. Endocrinol. Metab. 2004, 89, 5762–5771.
  37. Birketvedt, G.S.; Geliebter, A.; Kristiansen, I.; Firgenschau, Y.; Goll, R.; Florholmen, J.R. Diurnal secretion of ghrelin, growth hormone, insulin binding proteins, and prolactin in normal weight and overweight subjects with and without the night eating syndrome. Appetite 2012, 59, 688–692.
  38. Friedman, J. Grelina, Obesidad Mórbida y Bypass Gástrico. Rev. Med. De Costa Rica Y Centroam. 2015, 614, 59–63.
  39. Akalu, Y.; Molla, M.D.; Dessie, G.; Ayelign, B. Physiological Effect of Ghrelin on Body Systems. Int. J. Endocrinol. 2020, 2020, 1385138.
  40. Bravo, R.; Matito, S.; Cubero, J.; Paredes, S.D.; Franco, L.; Rivero, M.; Rodríguez, A.B.; Barriga, C. Tryptophan-enriched cereal intake improves nocturnal sleep, melatonin, serotonin, and total antioxidant capacity levels and mood in elderly humans. Age 2013, 35, 1277–1285.
  41. Mitchell, E.S.; Slettenaar, M.; Quadt, F.; Giesbrecht, T.; Kloek, J.; Gerhardt, C.; Bot, A.; Eilander, A.; Wiseman, S. Effect of hydrolysed egg protein on brain tryptophan availability. Br. J. Nutr. 2011, 105, 611–617.
  42. Peuhkuri, K.; Sihvola, N.; Korpela, R. Diet promotes sleep duration and quality. Nutr. Res. 2012, 32, 309–319.
  43. Dweck, J.S.; Jenkins, S.M.; Nolan, L.J. The role of emotional eating and stress in the influence of short sleep on food consumption. Appetite 2014, 72, 106–113.
  44. Seegers, V.; Petit, D.; Falissard, B.; Vitaro, F.; Tremblay, R.E.; Montplaisir, J.; Touchette, E. Short Sleep Duration and Body Mass Index: A Prospective Longitudinal Study in Preadolescence. Am. J. Epidemiol. 2011, 173, 621–629.
  45. Verhoef, S.P.; Camps, S.G.; Gonnissen, H.K.; Westerterp, K.R.; Westerterp-Plantenga, M.S. Concomitant changes in sleep duration and body weight and body composition during weight loss and 3-mo weight maintenance. Am. J. Clin. Nutr. 2013, 98, 25–31.
  46. Shechter, A.; Rising, R.; Albu, J.B.; St-Onge, M.-P. Experimental sleep curtailment causes wake-dependent increases in 24-h energy expenditure as measured by whole-room indirect calorimetry. Am. J. Clin. Nutr. 2013, 98, 1433–1439.
  47. Baron, K.G.; Reid, K.J.; Van Horn, L.; Zee, P.C. Contribution of evening macronutrient intake to total caloric intake and body mass index. Appetite 2013, 60, 246–251.
  48. Brondel, L.; Romer, M.A.; Nougues, P.M.; Touyarou, P.; Davenne, D. Acute partial sleep deprivation increases food intake in healthy men. Am. J. Clin. Nutr. 2010, 91, 1550–1559.
  49. Chaput, J.-P.; Després, J.-P.; Bouchard, C.; Tremblay, A. The Association between Short Sleep Duration and Weight Gain Is Dependent on Disinhibited Eating Behavior in Adults. Sleep 2011, 34, 1291–1297.
  50. Gonnissen, H.K.J.; Mazuy, C.; Rutters, F.; Martens, E.A.P.; Adam, T.C.; Westerterp-Plantenga, M.S. Sleep Architecture When Sleeping at an Unusual Circadian Time and Associations with Insulin Sensitivity. PLoS ONE 2013, 8, e72877.
  51. Hursel, R.; Rutters, F.; Gonnissen, H.K.; AP Martens, E.; Westerterp-Plantenga, M.S. Effects of sleep fragmentation in healthy men on energy expenditure, substrate oxidation, physical activity, and exhaustion measured over 48 h in a respiratory chamber. Am. J. Clin. Nutr. 2011, 94, 804–808.
  52. St-Onge, M.-P.; Wolfe, S.; Sy, M.; Shechter, A.; Hirsch, J. Sleep restriction increases the neuronal response to unhealthy food in normal-weight individuals. Int. J. Obes. 2014, 38, 411–416.
  53. Beebe, D.W.; Simon, S.; Summer, S.; Hemmer, S.; Strotman, D.; Dolan, L.M. Dietary Intake Following Experimentally Restricted Sleep in Adolescents. Sleep 2013, 36, 827–834.
  54. Simon, S.L.; Field, J.; Miller, L.E.; DiFrancesco, M.; Beebe, D.W. Sweet/Dessert Foods Are More Appealing to Adolescents after Sleep Restriction. PLoS ONE 2015, 10, e0115434.
  55. Tatone-Tokuda, F.; Dubois, L.; Ramsay, T.; Girard, M.; Touchette, E.; Petit, D.; Montplaisir, J.Y. Sex differences in the association between sleep duration, diet and body mass index: A birth cohort study. J. Sleep Res. 2012, 21, 448–460.
  56. Colten, H.R.; Altevogt, B.M.; Institute of Medicine (US) Committee on Sleep Medicine and Research. Extent and Health Consequences of Chronic Sleep Loss and Sleep Disorders. 2006. Available online: https://www.ncbi.nlm.nih.gov/books/NBK19961/ (accessed on 18 April 2023).
  57. Jarrin, D.C.; Chen, I.Y.; Ivers, H.; Morin, C.M. The role of vulnerability in stress-related insomnia, social support and coping styles on incidence and persistence of insomnia. J. Sleep Res. 2014, 23, 681–688.
  58. Kanerva, N.; Kronholm, E.; Partonen, T.; Ovaskainen, M.-L.; Kaartinen, N.E.; Konttinen, H.; Broms, U.; Männistö, S. Tendency Toward Eveningness Is Associated with Unhealthy Dietary Habits. Chrono-Int. 2012, 29, 920–927.
  59. Killick, R.; Banks, S.; Liu, P.Y. Implications of Sleep Restriction and Recovery on Metabolic Outcomes. J. Clin. Endocrinol. Metab. 2012, 97, 3876–3890.
  60. Bernert, R.A. Sleep disturbances and suicide risk: A review of the literature. Neuropsychiatr. Dis. Treat. 2008, 3, 735–743.
  61. Allison, K.C.; Lundgren, J.D.; O’Reardon, J.P.; Geliebter, A.; Gluck, M.E.; Vinai, P.; Mitchell, J.E.; Schenck, C.H.; Howell, M.J.; Crow, S.J.; et al. Proposed diagnostic criteria for night eating syndrome. Int. J. Eat. Disord. 2010, 43, 241–247.
  62. Dorflinger, L.M.; Ruser, C.B.; Masheb, R.M. Night eating among veterans with obesity. Appetite 2017, 117, 330–334.
  63. Cleator, J.; Abbott, J.; Judd, P.; Wilding, J.P.; Sutton, C.J. Correlations between night eating, sleep quality, and excessive daytime sleepiness in a severely obese UK population. Sleep Med. 2013, 14, 1151–1156.
  64. Ivezaj, V.; Lawson, J.L.; Lydecker, J.A.; Duffy, A.J.; Grilo, C.M. Examination of night eating and loss-of-control eating following bariatric surgery. Eat Weight Disord. 2021, 27, 207–213.
  65. Loddo, G.; Zanardi, M.; Caletti, M.T.; Mignani, F.; Petroni, M.L.; Chiaro, G.; Marchesini, G.; Provini, F. Searching food during the night: The role of video-polysomnography in the characterization of the night eating syndrome. Sleep Med. 2019, 64, 85–91.
  66. Lavery, M.E.; Frum-Vassallo, D. An Updated Review of Night Eating Syndrome: An Under-Represented Eating Disorder. Curr. Obes. Rep. 2022, 11, 395–404.
  67. De Zwaan, M.; Burgard, M.A.; Schenck, C.H.; Mitchell, J.E. Night time eating: A review of the literature. Eur. Eat. Disord. Rev. 2003, 11, 7–24.
  68. Kaur, J.; Dang, A.B.; Gan, J.; An, Z.; Krug, I. Night Eating Syndrome in Patients with Obesity and Binge Eating Disorder: A Systematic Review. Front. Psychol. 2022, 12, 6201.
  69. Leng, Y.; Wainwright, N.W.J.; Cappuccio, F.P.; Surtees, P.G.; Hayat, S.; Luben, R.; Brayne, C.; Khaw, K.-T. Daytime Napping and the Risk of All-Cause and Cause-Specific Mortality: A 13-Year Follow-up of a British Population. Am. J. Epidemiol. 2014, 179, 1115–1124.
  70. Spiesshoefer, J.; Linz, D.; Skobel, E.; Arzt, M.; Stadler, S.; Schoebel, C.; Fietze, I.; Penzel, T.; Sinha, A.-M.; Fox, H.; et al. Sleep–the yet underappreciated player in cardiovascular diseases: A clinical review from the German Cardiac Society Working Group on Sleep Disordered Breathing. Eur. J. Prev. Cardiol. 2021, 28, 189–200.
  71. Vyas, M.V.; Garg, A.X.; Iansavichus, A.V.; Costella, J.; Donner, A.; Laugsand, L.E.; Janszky, I.; Mrkobrada, M.; Parraga, G.; Hackam, D.G. Shift work and vascular events: Systematic review and meta-analysis. BMJ 2012, 345, e4800.
  72. Dettoni, J.L.; Consolim-Colombo, F.M.; Drager, L.F.; Rubira, M.C.; de Souza, S.B.P.C.; Irigoyen, M.C.; Mostarda, C.; Borile, S.; Krieger, E.M.; Moreno, H.; et al. Cardiovascular effects of partial sleep deprivation in healthy volunteers. J. Appl. Physiol. 2012, 113, 232–236.
  73. Hogenkamp, P.S.; Nilsson, E.; Nilsson, V.C.; Chapman, C.D.; Vogel, H.; Lundberg, L.S.; Zarei, S.; Cedernaes, J.; Rångtell, F.H.; Broman, J.-E.; et al. Acute sleep deprivation increases portion size and affects food choice in young men. Psychoneuroendocrinology 2013, 38, 1668–1674.
  74. St-Onge, M.-P.; Roberts, A.L.; Chen, J.; Kelleman, M.; O’keeffe, M.; RoyChoudhury, A.; Jones, P.J. Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals. Am. J. Clin. Nutr. 2011, 94, 410–416.
  75. Benedict, C.; Barclay, J.L.; Ott, V.; Oster, H.; Hallschmid, M. Acute sleep deprivation delays the glucagon-like peptide 1 peak response to breakfast in healthy men. Nutr. Diabetes 2013, 3, e78.
  76. Stamatakis, K.A.; Punjabi, N.M. Effects of Sleep Fragmentation on Glucose Metabolism in Normal Subjects. Chest 2010, 137, 95–101.
  77. Tasali, E.; Leproult, R.; Ehrmann, D.A.; Van Cauter, E. Slow-wave sleep and the risk of type 2 diabetes in humans. Proc. Natl. Acad. Sci. USA 2008, 105, 1044–1049.
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Sofia Gomes
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Cátia Ramalhete
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Isabel Ferreira
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Manuel Bicho
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Ana Valente
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Update Date: 08 Jun 2023
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