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Mentzelou, M.; Papadopoulou, S.K.; Papandreou, D.; Spanoudaki, M.; Dakanalis, A.; Vasios, G.K.; Voulgaridou, G.; Pavlidou, E.; Mantzorou, M.; Giaginis, C. Circadian Rhythms and Sleep, Metabolic and Cardiovascular Disorders. Encyclopedia. Available online: https://encyclopedia.pub/entry/54794 (accessed on 18 May 2024).
Mentzelou M, Papadopoulou SK, Papandreou D, Spanoudaki M, Dakanalis A, Vasios GK, et al. Circadian Rhythms and Sleep, Metabolic and Cardiovascular Disorders. Encyclopedia. Available at: https://encyclopedia.pub/entry/54794. Accessed May 18, 2024.
Mentzelou, Maria, Sousana K. Papadopoulou, Dimitrios Papandreou, Maria Spanoudaki, Antonios Dakanalis, Georgios K. Vasios, Gavriela Voulgaridou, Eleni Pavlidou, Maria Mantzorou, Constantinos Giaginis. "Circadian Rhythms and Sleep, Metabolic and Cardiovascular Disorders" Encyclopedia, https://encyclopedia.pub/entry/54794 (accessed May 18, 2024).
Mentzelou, M., Papadopoulou, S.K., Papandreou, D., Spanoudaki, M., Dakanalis, A., Vasios, G.K., Voulgaridou, G., Pavlidou, E., Mantzorou, M., & Giaginis, C. (2024, February 06). Circadian Rhythms and Sleep, Metabolic and Cardiovascular Disorders. In Encyclopedia. https://encyclopedia.pub/entry/54794
Mentzelou, Maria, et al. "Circadian Rhythms and Sleep, Metabolic and Cardiovascular Disorders." Encyclopedia. Web. 06 February, 2024.
Circadian Rhythms and Sleep, Metabolic and Cardiovascular Disorders
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This entry is adapted from the peer-reviewed paper 10.3390/metabo13030370

Circadian rhythms are generated by the circadian clock, a self-sustained internal timing system that exhibits 24-h rhythms in the body. Many metabolic, cellular, behavioral and physiological processes are regulated by the circadian clock in coordination with environmental cues. 

circadian rhythms metabolic disorders cardiovascular diseases obesity diabetes mellitus sleep quality

1. Circadian Rhythms and Metabolic Diseases

There are a lot of clinical studies that assessed the effect of circadian disruption in human metabolism.
Leproult et al. [1] examined in 26 adults whether circadian misalignment may have adverse cardiometabolic effects independently of sleep loss. The interventions involved 3 days with 10-h bedtimes, followed by 8 days with 5-h bedtimes, with bedtimes always centered at 0300 h (0030–0530 h, circadian alignment) or with bedtimes delayed by 8.5 h on 4 days (0900–1400 h, circadian misalignment) [1]. This study assessed sleep times, circadian phases, food intake and cardiometabolic variables. When sleep was restricted to 5 h, participants sleeping mostly during the day (circadian misalignment) had 47% greater reduction in insulin sensitivity compared with 34% reduction in insulin sensitivity of participants sleeping during the night [1]. This study also documented an increase in high-sensitivity C-reactive protein (hs-CRP) after sleep restriction in the misaligned groups, which was higher compared to the aligned groups. The increased risk of diabetes and cardiovascular disease is unlikely to be solely due to sleep loss and would not be fully mitigated by strategies designed to preserve sleep duration [1]. The findings of this clinical trial are unequivocal due to the carefully execution of the protocol; however, the sample size is quite small [1].
In another study, Morris et al. evaluated the separate effects of the behavioral cycle, circadian phase, and circadian misalignment on glucose metabolism [2]. One protocol included circadian misalignment and the other maintained circadian alignment in 14 healthy adults. In the circadian alignment protocol, the participant’s sleep opportunity occurred between 11:00 and 19:00 h for days 1–8. In the circadian misalignment protocol, the participant’s sleep opportunity occurred between 11:00 and 19:00 h for days 1–3. On day 4 of the circadian misalignment protocol, the participant’s behavioral cycles were shifted by 12 h, and this was remained until the end of that protocol (day 8) [2]. The results of this study supported evidence that separate effects of the endogenous circadian system and of circadian misalignment, independent from effects of the behavioral cycle, may impact on glucose tolerance in humans [2]. These variations in glucose tolerance may be ascribed, at least in part, to different mechanisms: during the biological evening by decreased pancreatic β-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by reduced insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without alterations in early-phase insulin [2]. The fact that the behavioral and environmental conditions remain the same is an undeniable strength, but this study assessed only two behavioral and circadian cycle phases without determining the behavioral cycle on glucose metabolism. However, this study may help the development of behavioral and circadian strategies that could improve glycemic control in day-active people and night workers [2].
To determine whether these findings persist in the shift-work population, the impact of circadian misalignment in a real-life shift worker was evaluated, as well. The intervention included simulated night work comprised of 12-h inverted behavioral and environmental cycles (circadian misalignment) or simulated day work (circadian alignment) [2][3]. For this reason, the above studies measured blood pressure and inflammatory markers across the 24-h behavioral and light/dark cycles when the behavioral and environmental cycle was aligned and misaligned with the endogenous circadian system [2][3]. Their results showed that short-term circadian misalignment increased 24-h blood pressure [2][3]. Moreover, circadian misalignment reduced sleep blood pressure dipping during sleep opportunities, which may be also an independent predictor of adverse cardiovascular events and all-cause mortality [2][3]. Moreover, circadian misalignment increased the inflammatory markers CRP, tumor necrosis factor (TNF)-α, resistin, and interleukin (IL)-6. This suggests that the internal circadian time of food intake may be an important factor to consider in shift workers [2][3]. The strength of these studies included the highly controlled laboratory protocol, which was able to determine the independent impact of circadian misalignment, while the sample size was small [2][3].
Furthermore, another study tested the impact of circadian misalignment, similar to that experienced by real-life shift workers, on 24-h levels of hs-CRP and blood pressure, which are risk factors for cardiovascular disease [4]. For this reason, this study measured hs-CRP and blood pressure levels across the 24-h behavioral and light/dark cycles when the behavioral and environmental cycle was aligned and misaligned. This study also found that short-term circadian misalignment, increased 24-h hs-CRP and 24-h blood pressure in chronic shift workers, which both may increase the prevalence of cardiovascular disease [4].
Moreover, Qian et al. [5] assessed the separated effects of circadian misalignment from effects of circadian phase and environmental/behavioral factors on glucose control in 14 healthy adults using a randomized, cross-over design with two 8-day laboratory protocols [5]. Both protocols involved 3 baseline inpatient days with habitual sleep/wake cycles, followed by 4 inpatient days with the same nocturnal bedtime (circadian alignment) or with 12-h inverted behavioral/environmental cycles (circadian misalignment) [5]. These findings showed that the endogenous circadian system and circadian misalignment, after controlling for behavioral cycle influences, exerted independent and differential impacts on insulin sensitivity and pancreatic β-cell function in diurnally active people as well as night shift workers [5]. The circadian system mainly decreased both dynamic and static β-cell responsivity, while circadian disruption mainly reduced insulin sensitivity without impairing pancreatic β-cell function [5]. The design of this study allowed to distinguish the function of β-cell due to circadian phase and/or circadian disruption. However, the highly controlled diet throughout the study decreased the potential effect of variations in energy intake [5].
Furthermore, Wefer et al. [6] assessed insulin sensitivity by the hyperinsulinemic and euglycemic clamp. Each participant underwent a 3-day control protocol of circadian alignment and after a 3.5-day protocol of circadian misalignment [6]. The findings of this study pointed that short-term circadian misalignment resulted in a significant decrease in insulin sensitivity that was mainly ascribed to the impairment in insulin-stimulated nonoxidative glucose disposal [6]. In addition, the molecular biological clock in skeletal muscle was misaligned relative to the behavioral routine, suggesting that skeletal muscle may be not adjust to a new day–night rhythm within 3 days [6]. Circadian misalignment also led to higher fasting free fatty acids (FFAs) levels, fasting plasma glucose levels, and lower triglyceride levels [6]. Limitations of this study were that it only included male volunteers and the lack of information on sleep quality, which can decrease insulin sensitivity. Future studies should examine whether similar results can be found in individuals at risk for diabetes mellitus [6].
Madjd et al. [7] evaluated the effects of higher energy intake at lunch compared to dinner on weight loss and also on indexes of carbohydrate and lipid metabolism in overweight and obese women (N = 80) who were attending a weight-loss program for 12 weeks [7]. The findings of this study showed that consumption of the main meal at lunch led to more weight loss and a greater improvement in insulin sensitivity as measured by homeostasis model assessment-estimated insulin resistance (HOMA-IR) and fasting insulin concentrations than did eating the main meal at dinner in overweight and obese women [7]. Notably, the findings of this study may have practical implications, indicating that the consumption of a main meal at lunch and not at dinner could improve weight loss when people use a weight-loss program [7]. The principal strength of this study was at first, that it was a randomized, outpatient, clinical trial, in which subjects were following a comprehensive diet plan for weight control [7]. Secondly, the provision of a free diet plan and a daily telephone call from a dietitian to each subject was an encouragement in both groups. In contrast, the main limitation of this study was the short-term intervention period [7].
Bandín et al. [8] analyzed the differences between taking an early (13.00) and late (16.30) lunch in 32 women. In each protocol, participants were provided with standardized meals (breakfast, lunch, and dinner) during the two meal intervention weeks and were studied under two lunch-eating conditions: Early Eating (EE; lunch at 13:00) and Late Eating (LE; lunch 16:30) [8]. The results of this study showed that delaying the timing of an identical meal for a week resulted in decreased resting energy expenditure prior to the meal, unchanged postprandial energy expenditure, reduced fasting carbohydrate oxidation, lowered glucose tolerance, blunted daily profile of free cortisol concentrations, and slowed down thermal effect of food [8]. Chronically, eating at a later time of day may create metabolic disturbances of a larger magnitude and could be implicated in the metabolic alterations that characterize late eaters [8]. However, further studies are strongly required to measure the effect of early and late eating on energy expenditure across 24 h to assess whether meal timing may affect energy expenditure at other times of day. Moreover, there is need to determine the underlying mechanisms, and to resolve whether the endogenous circadian rhythm of cortisol is influenced by meal timing [8].
In the randomized controlled clinical trial of Barger et al. [9], it was assessed whether sleep duration, sleep apnea, and shift work were independent risk factors of cardiovascular diseases. It was found that patients with shorter duration of sleep (less than six hours) had an increased risk of serious cardiovascular events, than those having longer sleep. Patients with obstructive sleep apnea had 12% more risk of cardiovascular events than patients with normal sleep [9]. Overnight shift work had, also, a higher risk than those working in the day. The study design was limited to a self-reported questionnaire, and there was a lack of objective confirmation of these reported sleep-related factors [9]. More to the point, the Berlin questionnaire has not been validated yet in a population of post-acute coronary syndrome patients, but it has been validated in small studies of patients with cardiovascular or cerebrovascular disease [9]. Further research should determine the potential physiological link between sleep duration, sleep disruption, sleep disorders, and cardiovascular risk [9].
Sharma et al. [10] examined the potential effect of rotational shift-work on glucose metabolism Participants underwent an isotope-labeled mixed meal test during a simulated day shift and a simulated night shift, enabling simultaneous measurement of glucose flux and pancreatic β-cell function using the oral minimal model [10]. This study revealed that postprandial glucose concentrations were higher during the night shift; further, the timing of peak insulin and both C-peptide and nadir glucagon suppression after a meal were also delayed due to β-cells weaker responsivity to glucose [10]. In addition, these changes may represent circadian variations in insulin secretory capacity driven by changes in β-cell clock gene expression [10]. The experimental protocol designed very carefully in terms of sleep quantity, energy intake and meal composition [10]. However, further studies are necessary to determine the mechanism(s) of diurnal decline in β-cell function and whether exposure to more prolonged patterns of chronic shiftwork promotes sustained or greater decreases in β-cell function [10].
Jarrin et al. [11] evaluated, also, the potential role of sleep abnormalities and shift work on the development of heart failure due to loss of parasympathetic control. The sample of this study was divided into two groups, with sleep duration shorter <6 h or equal/longer >6 h [11]. Electrocardiogram data derived from polysomnography were applied for obtaining heart rate and heart rate variability during stage 2 and rapid eye movement sleep [11]. The findings of this study showed that patients with short sleep duration insomnia had reduced parasympathetic activity as compared to those with normal sleep duration insomnia [11]. It was also found an increased imbalance between sympathetic and parasympathetic balance [11]. Thus, treating insomnia may reduce the risk of cardiovascular diseases. In the analysis of this study, one strength was the relatively large sample comprised of patients suffering from insomnia on average for 15 years [11]. In contrast, the main limitation was the cross-sectional nature of the study, which precluded the investigation of a causal relation to be assessed between cardiovascular autonomic function, insomnia, and short sleep duration. Moreover, there was no group with normal conditions [11].

2. Interrelationships between Circadian Rhythms, Sleep Disorder, and Metabolic Diseases

There are a lot of clinical studies that assessed the interrelationship between circadian rhythms, sleep disorder, and metabolic diseases in humans. 
Wong et al. [12] investigated whether chronotype and social jet lag covaried with components of cardiometabolic risk in a nonpatient sample of midlife community volunteers and whether any such associations persisted after adjustment for correlated variation in health practices, including behavioral and subjective measures of other sleep characteristics. Their results showed that a mismatch in sleep timing between workdays and free days linked to greater cardiometabolic risk, specifically with components of glycemic control, serum lipids, and adiposity. These effects persisted after adjusting for correlated variation in other sleep parameters and with further adjustment for participant health behaviors. Due to the cross-sectional study design, future prospective studies are strongly recommended to extend the present findings [12].
The cross-sectional study of Ritonja et al. [13] was conducted to determine the association between night work parameters (current night work status, night work duration, and night work intensity) and cardiometabolic risk factors and how it differed by chronotype. This study supported evidence that various night work parameters were related to poorer overall cardiometabolic health, including higher waist circumference and BMI, fasting blood glucose, blood pressure, cardiometabolic risk score, and lower low-density lipoprotein (LDL) cholesterol. One strength of this study was the inclusion of both night work intensity and years of shift work duration in the assessment of night work exposures. The use of objective measures of cardiometabolic indices and chronotype also avoided information bias. Limitations included a small sample size and the cross-sectional design of the study. However, further research is needed to make clear the exact biological pathways between rotating night work and cardiometabolic risk [13].
Hulsegge et al. [14], in their cross-sectional study, investigated relations between shift work and various cardiometabolic risk factors and explored these potential relations in different chronotypes. The findings of this study showed that shift work was not related with an increased risk of cardiometabolic risk factors, except for overweight/BMI. Shift work was not associated with an increased risk of cardiometabolic risk factors, except for overweight/BMI. A strength of the study was the wide variety of objectively measured cardiometabolic risk factors. However, more research is needed on the moderating effects of chronotype to establish whether tailored preventive measures by chronotype may be useful for shift workers [14].
Ji Hee Yu et al. [15] examined whether late chronotype could be associated with metabolic abnormalities and body composition in middle-aged Korean men and women independent of sleep profile and lifestyle factors. Evening chronotype was associated with lower lean mass in men and higher fat mass in women. Moreover, evening type was likely associated with a worse metabolic profile than other chronotypes for several reasons. Thus, chronic circadian misalignment could be one of the reasons explaining metabolic derangements in evening types. The main limitation of this study was its cross-sectional design [15].
The meta-analysis of Rui Zhang et al. [16] explored the association between evening chronotype and circadian misalignment with obesity, type 2 diabetes mellitus (T2 DM), and metabolic syndrome (MetS) in non-shift workers. They found that evening chronotype was associated with unfavorable metabolic indicators including higher BMI, higher fasting glucose level, higher total cholesterol level and lower high-density lipoprotein (HDL)-c level compared with morning chronotype. Moreover, higher social jetlag was associated with larger waist circumference compared with smaller social jetlag. Due to the exposure to artificial light and work demand in modern lifestyle, circadian misalignment may be considered as a quite common phenomenon. This study had the strength that it was the first meta-analysis to assess the association between evening chronotype and circadian misalignment and parameters of MetS in non-shift working adults. The limitations of this study were the heterogeneity and the cross-sectional data [16].
Another cross-sectional clinical study examined the circadian integration of glycemic control in a clinical setting to assess the relationship between morningness–eveningness and glycemic control. This study supported evidence that the sleep–wake pattern of the circadian rhythm correlated with inadequate glycemic control along with low health-related quality of life in patients with type 2 diabetes. The main limitations of this study were the lack of classification (morning, evening, neither group) and the small number of participants. Further studies are required to confirm the relationship among sleep–wake patterns, glycemic control, and lifestyle factors, such as dietary habit, physical activity, and smoking habit [17].
Koopman et al. [18] investigated the association of social jetlag with the MetS and T2 DM in a population-based cohort. They observed an association between social jetlag and the metabolic syndrome only for participants with >2 h social jetlag, compared with participants with <1 h social jetlag. In addition, they suggested that the association between social jetlag and MetS was driven by higher glucose and waist circumference. The limitations of this study were the cross-sectional data as well as the incomplete follow-up data [18].

3. Circadian Rhythms and Cardiovascular Diseases

There are a lot of clinical studies that assessed the relationship between circadian rhythms and cardiovascular diseases (CVDs) in humans. As researchers analyzed before, the randomized controlled trials highlighted the crucial effect in cardiovascular disease, in various aspects [2][3][4][12].
Estarlich et al. [19] investigated whether a circadian pattern in the occurrence of acute coronary syndrome existed and what factors influenced the severity of acute myocardial infraction, its location, the length of hospital stay in patients in Spain, and whether individual risk factors resulted in differing patterns. Acute coronary syndrome seemed to occur more often in the morning hours. Morning was also associated with an increased risk of anterior infarction, which was related to the severity of the disease. The main limitation of this clinical study was the small size of the sample [19].
Sun et al. [20] estimated the association between residential outdoor light at night and risk of CHD among older adults in Hong Kong. They found that individuals living in areas of the region with higher levels of outdoor light at night may be at higher risk of CHD. The important strengths of this clinical study included the prospective study design, the large sample size, the well-characterized population, a wide range of values of light at night, and adjustment for a number of individual and neighborhood-level covariates. The main limitations of this study were the measure of outdoor light at night, lack of data of sleep quality, and weakness of generalization in younger ages [20].
Grimaldi et al. [21] aimed to determine the impact of circadian misalignment on autonomic nervous system control of cardiovascular function. Sleep restriction with circadian misalignment significantly increased urinary norepinephrine levels and reduced nocturnal heart rate variability. Secondly, sleep restriction with circadian misalignment elicited greater increases in nocturnal heart rate when compared to sleep restriction alone. Third, these alterations in autonomic indices did not translate into an augmentation of arterial BP, suggesting that other compensatory mechanisms. These findings demonstrated a clear adverse impact of circadian misalignment on autonomic function in sleep-restricted healthy adults [21].

References

  1. 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.
  2. Morris, C.J.; Yang, J.N.; Garcia, J.I.; Myers, S.; Bozzi, I.; Wang, W.; Buxton, O.M.; Shea, S.A.; Scheer, F.A. Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans. Proc. Natl. Acad. Sci. USA 2015, 112, E2225–E2234.
  3. Morris, C.J.; Purvis, T.E.; Mistretta, J.; Scheer, F.A. Effects of the Internal Circadian System and Circadian Misalignment on Glucose Tolerance in Chronic Shift Workers. J. Clin. Endocrinol. Metab. 2016, 101, 1066–1074.
  4. Morris, C.J.; Purvis, T.E.; Mistretta, J.; Hu, K.; Scheer, F. Circadian Misalignment Increases C-Reactive Protein and Blood Pressure in Chronic Shift Workers. J. Biol. Rhythm. 2017, 32, 154–164.
  5. Qian, J.; Dalla Man, C.; Morris, C.J.; Cobelli, C.; Scheer, F. Differential effects of the circadian system and circadian misalignment on insulin sensitivity and insulin secretion in humans. Diabetes Obes. Metab. 2018, 20, 2481–2485.
  6. Wefers, J.; van Moorsel, D.; Hansen, J.; Connell, N.J.; Havekes, B.; Hoeks, J.; van Marken Lichtenbelt, W.D.; Duez, H.; Phielix, E.; Kalsbeek, A.; et al. Circadian misalignment induces fatty acid metabolism gene profiles and compromises insulin sensitivity in human skeletal muscle. Proc. Natl. Acad. Sci. USA 2018, 115, 7789–7794.
  7. Madjd, A.; Taylor, M.A.; Delavari, A.; Malekzadeh, R.; Macdonald, I.A.; Farshchi, H.R. Beneficial effect of high energy intake at lunch rather than dinner on weight loss in healthy obese women in a weight-loss program: A randomized clinical trial. Am. J. Clin. Nutr. 2016, 104, 982–989.
  8. Bandín, C.; Scheer, F.A.; Luque, A.J.; Ávila-Gandía, V.; Zamora, S.; Madrid, J.A.; Gómez-Abellán, P.; Garaulet, M. Meal timing affects glucose tolerance, substrate oxidation and circadian-related variables: A randomized, crossover trial. Int. J. Obes. 2015, 39, 828–833.
  9. Barger, L.K.; Rajaratnam, S.M.W.; Cannon, C.P.; Lukas, M.A.; Im, K.; Goodrich, E.L.; Czeisler, C.A.; O’Donoghue, M.L. Short Sleep Duration, Obstructive Sleep Apnea, Shiftwork, and the Risk of Adverse Cardiovascular Events in Patients After an Acute Coronary Syndrome. J. Am. Heart Assoc. 2017, 6, e006959.
  10. Sharma, A.; Laurenti, M.C.; Dalla Man, C.; Varghese, R.T.; Cobelli, C.; Rizza, R.A.; Matveyenko, A.; Vella, A. Glucose metabolism during rotational shift-work in healthcare workers. Diabetologia 2017, 60, 1483–1490.
  11. Jarrin, D.C.; Ivers, H.; Lamy, M.; Chen, I.Y.; Harvey, A.G.; Morin, C.M. Cardiovascular autonomic dysfunction in insomnia patients with objective short sleep duration. J. Sleep Res. 2018, 27, e12663.
  12. Wong, P.M.; Hasler, B.P.; Kamarck, T.W.; Muldoon, M.F.; Manuck, S.B. Social Jetlag, Chronotype, and Cardiometabolic Risk. J. Clin. Endocrinol. Metab. 2015, 100, 4612–4620.
  13. Ritonja, J.; Tranmer, J.; Aronson, K.J. The relationship between night work, chronotype, and cardiometabolic risk factors in female hospital employees. Chronobiol. Int. 2019, 36, 616–628.
  14. Hulsegge, G.; Picavet, H.S.J.; van der Beek, A.J.; Verschuren, W.M.M.; Twisk, J.W.; Proper, K.I. Shift work, chronotype and the risk of cardiometabolic risk factors. Eur. J. Public Health 2019, 29, 128–134.
  15. Yu, J.H.; Yun, C.H.; Ahn, J.H.; Suh, S.; Cho, H.J.; Lee, S.K.; Yoo, H.J.; Seo, J.A.; Kim, S.G.; Choi, K.M.; et al. Evening chronotype is associated with metabolic disorders and body composition in middle-aged adults. J. Clin. Endocrinol. Metab. 2015, 100, 1494–1502.
  16. Zhang, R.; Cai, X.; Lin, C.; Yang, W.; Lv, F.; Wu, J.; Ji, L. The association between metabolic parameters and evening chronotype and social jetlag in non-shift workers: A meta-analysis. Front. Endocrinol. 2022, 13, 1008820.
  17. Iwasaki, M.; Hirose, T.; Mita, T.; Sato, F.; Ito, C.; Yamamoto, R.; Someya, Y.; Yoshihara, T.; Tamura, Y.; Kanazawa, A.; et al. Morningness-eveningness questionnaire score correlates with glycated hemoglobin in middle-aged male workers with type 2 diabetes mellitus. J. Diabetes Investig. 2013, 4, 376–381.
  18. Koopman, A.D.M.; Rauh, S.P.; van ’t Riet, E.; Groeneveld, L.; van der Heijden, A.A.; Elders, P.J.; Dekker, J.M.; Nijpels, G.; Beulens, J.W.; Rutters, F. The Association between Social Jetlag, the Metabolic Syndrome, and Type 2 Diabetes Mellitus in the General Population: The New Hoorn Study. J. Biol. Rhythm. 2017, 32, 359–368.
  19. Estarlich, M.; Tolsa, C.; Trapero, I.; Buigues, C. Circadian Variations and Associated Factors in Patients with Ischaemic Heart Disease. Int. J. Environ. Res. Public Health 2022, 19, 15628.
  20. Sun, S.; Cao, W.; Ge, Y.; Ran, J.; Sun, F.; Zeng, Q.; Guo, M.; Huang, J.; Lee, R.S.; Tian, L.; et al. Outdoor light at night and risk of coronary heart disease among older adults: A prospective cohort study. Eur. Heart J. 2021, 42, 822–830.
  21. Grimaldi, D.; Carter, J.R.; Van Cauter, E.; Leproult, R. Adverse Impact of Sleep Restriction and Circadian Misalignment on Autonomic Function in Healthy Young Adults. Hypertens 2016, 68, 243–250.
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Subjects: Physiology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Maria Mentzelou
,
Sousana K. Papadopoulou
,
Dimitrios Papandreou
,
Maria Spanoudaki
,
Antonios Dakanalis
,
Georgios K. Vasios
,
Gavriela Voulgaridou
,
Eleni Pavlidou
,
Maria Mantzorou
,
Constantinos Giaginis
View Times: 76
Revisions: 3 times (View History)
Update Date: 08 Feb 2024
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