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Circadian Misalignment and Metabolic Consequences
Abstract
The human circadian system is controlled by a central master clock in the brain and peripheral clocks in organs such as the liver, heart, pancreas, muscle, and adipose tissues. The main time cue for our central clock is light, while for peripheral clocks, food intake can also be a time cue. When these clocks are synchronized, food-seeking behavior, gastrointestinal activity, and metabolic function are higher during the day and reduced at night whilst people are primed for sleep. Shiftwork changes sleep timing as well as meal and snack timing and content. This can lead to circadian rhythm disruption, changing appetite and energy-regulating hormones as well as impairing metabolic function. This chapter will review mechanisms underpinning adverse metabolic outcomes due to circadian misalignment, and examine evidence from human studies relating to the potential implications of irregular food intake.
... In addition to its established effects on performance and fatigue, increasing evidence points to shift work as a health risk [6][7][8][9][10]; indeed, shift work is associated with greater likelihoods of obesity [11], hypertension [12], diabetes [13], and cardiovascular disease [14]. Though many behavioral, environmental, and physiological factors contribute to these conditions, the unifying factor in shift work is the disruption of the circadian system-caused by the disassociation of regular behavioral cycles (e.g., sleep-wakefulness, rest-activity, fasting-feeding) from the rhythm of the circadian pacemaker, i.e., the "body clock" [8,[15][16][17][18][19]. Circadian disruption and sleep disturbance that arise from this misalignment have both been shown to impair energy metabolism, glucose metabolism, and the production of appetite-regulating hormones, which can lead to weight gain and the development of metabolic disorders [20][21][22][23][24][25][26]. ...
... Considering the significance and prevalence of adverse health outcomes in shift work, there is desire from a public health perspective to identify and better understand suitable targets for intervention. As a modifiable behavior that affects energy balance and the synchronization of metabolite rhythms, food consumption is a plausible candidate for mitigating disease risk [15,[27][28][29][30]. Considerable information about the food choices of shift workers has been gained in various studies via questionnaires, interviews, focus groups, diaries, and 24-h recall [17,27,31]. ...
... While portion size and macronutrients are important factors involved in nutrition, there is growing interest in the role that food timing has on health due to its influence on physiological processes that affect metabolism [9,15]. In previous studies of non-shift working individuals, eating food at night or late in the day has been shown to be associated with impaired glucose metabolism, increased total caloric intake, and reduced weight loss effectiveness [23,[44][45][46][47][48]. ...
Recent studies indicate that the timing of food intake can significantly affect metabolism and weight management. Workers operating at atypical times of the 24-h day are at risk of disturbed feeding patterns. Given the increased risk of weight gain, obesity and metabolic syndrome in shift working populations, further research is required to understand whether their eating behavior could contribute to these increased metabolic risks. The objective of this study was to characterize the dietary patterns of police officers across different types of shifts in their natural environments. Thirty-one police officers (six women; aged 32.1 ± 5.4 years, mean ± SD) from the province of Quebec, Canada, participated in a 28- to 35-day study, comprising 9- to 12-h morning, evening, and night shifts alternating with rest days. Sleep and work patterns were recorded with actigraphy and diaries. For at least 24 h during each type of work day and rest day, participants logged nutrient intake by timestamped photographs on smartphones. Macronutrient composition and caloric content were estimated by registered dieticians using the Nutrition Data System for Research database. Data were analyzed with linear mixed effects models and circular ANOVA. More calories were consumed relative to individual metabolic requirements on rest days than both evening- and night-shift days (p = 0.001), largely sourced from increased fat (p = 0.004) and carbohydrate (trend, p = 0.064) intake. Regardless, the proportions of calories from carbohydrates, fat, and protein did not differ significantly between days. More calories were consumed during the night, between 2300 h and 0600 h, on night-shift days than any other days (p < 0.001). Caloric intake occurred significantly later for night-shift days (2308 h ± 0114 h, circular mean ± SD) than for rest days (1525 h ± 0029 h; p < 0.01) and was dispersed across a longer eating window (13.9 h ± 3.1 h vs. 11.3 h ± 1.8 h, mean ± SD). As macronutrient proportions were similar and caloric intake was lower, the finding of later meals times on night-shift days versus rest days is consistent with emerging hypotheses that implicate the biological timing of food intake—rather than its quantity or composition—as the differentiating dietary factor in shift worker health.
... More than 20 million Americans work night or rotating shifts, which chronically disrupts their circadian rhythms (McMenamin, 2007). Shift workers experience abnormal exposure to light and have disrupted eating and activity/sleeping patterns (Geliebter et al., 2000;de Assis et al., 2003;Bank et al., 2015;Molzof et al., 2017;Molzof et al., 2022). Critically, disruption of the circadian system with shift work is associated with obesity, metabolic syndrome, and cardiovascular disease (CVD) (Kawachi et al., 1995;Boggild and Knutsson, 1999;Sookoian et al., 2007;Vyas et al., 2012;Jankowiak et al., 2016;Torquati et al., 2018). ...
... Epidemiological and clinical studies have shown that aberrant meal timing (e.g., skipping breakfast and eating at night) increases the risk for CVD [reviewed in (St-Onge et al., 2017)]. Shift workers have disrupted rhythms of food intake, including consuming more calories at night and snacking throughout the night, compared to day workers, and this aberrant meal timing has been linked to CVD risk factors (Lennernas et al., 1995;de Assis et al., 2003;Heath et al., 2012;Bank et al., 2015;Molzof et al., 2017;Molzof et al., 2022). Likewise, studies in mice have shown that mistimed feeding, or eating during the inactive phase, caused metabolic dysfunction (Arble et al., 2009;Bray et al., 2012). ...
Shift work chronically disrupts circadian rhythms and increases the risk of developing cardiovascular disease. However, the mechanisms linking shift work and cardiovascular disease are largely unknown. The goal of this study was to investigate the effects of chronically shifting the light-dark (LD) cycle, which models the disordered exposure to light that may occur during shift work, on atherosclerosis. Atherosclerosis is the progressive accumulation of lipid-filled lesions within the artery wall and is the leading cause of cardiovascular disease. We studied ApolipoproteinE -deficient ( ApoE −/− ) mice that are a well-established model of atherosclerosis. Male and female ApoE −/− mice were housed in control 12L:12D or chronic LD shift conditions for 12 weeks and fed low-fat diet. In the chronic LD shift condition, the light-dark cycle was advanced by 6 h every week. We found that chronic LD shifts exacerbated atherosclerosis in female, but not male, ApoE −/− mice. In females, chronic LD shifts increased total serum cholesterol concentrations with increased atherogenic VLDL/LDL particles. Chronic LD shifts did not affect food intake, activity, or body weight in male or female ApoE −/− mice. We also examined eating behavior in female ApoE −/− mice since aberrant meal timing has been linked to atherosclerosis. The phases of eating behavior rhythms, like locomotor activity rhythms, gradually shifted to the new LD cycle each week in the chronic LD shift group, but there was no effect of the LD shift on the amplitudes of the eating rhythms. Moreover, the duration of fasting intervals was not different in control 12L:12D compared to chronic LD shift conditions. Together these data demonstrate that female ApoE −/− mice have increased atherosclerosis when exposed to chronic LD shifts due to increased VLDL/LDL cholesterol, independent of changes in energy balance or feeding-fasting cycles.
... Engaging in shift work is often accompanied by changes to eating behaviours (Banks, Dorrian, Grant, & Coates, 2015;Lowden et al., 2010). While the preponderance of research indicates that total calorie intake per day does not significantly vary between shift workers and non-shift workers, or between shift types (de Assis, Kupek, Nahas, & Bellisle, 2003;Esquirol et al., 2009;Lowden et al., 2010;Reinberg et al., 1979), shift workers tend to eat larger portions of food with macronutrient contents that are higher in salt, sugar and fat (de Assis et al., 2003;Esquirol et al., 2009;Heath et al., 2012). ...
... Further, snacking behaviour amongst shift workers is more common than amongst non-shift workers, particularly during the night shift (Reinberg et al., 1979;Waterhouse, Minors, Atkinson, & Benton, 1997). Although these changes in diet alone could challenge the effectiveness of individuals' metabolic systems, circadian misalignment exacerbates the risk of health disorders because it disrupts metabolic processes (Al-Naimi, Hampton, Richard, Tzung, & Morgan, 2004;Banks et al., 2015;Lowden et al., 2010). Indeed, consuming food during the night shift is associated with greater body fat and can impair postprandial glucose and lipid tolerance (Al-Naimi et al., 2004;Grant et al., 2017;Lund, Arendt, Hampton, English, & Morgan, 2001). ...
... Circadian disruption due to shift work was reported to disrupt behavioral rhythms such as meal timing and lead to significant cardiac and general health consequences. 46,47 Night shift work has been shown to be associated with increased cardiometabolic disease, metabolic syndrome, type 2 diabetes, and cardiovascular heart disease due to its disruption of circadian synchronization. 48,49,50,51,52,53 Other studies have reported various gastrointestinal complaints and difficulties such as menstrual irregularities, dysmenorrhea, and gestational hypertension. ...
Various physiological systems and behaviors such as the sleep-wake cycle, vigilance, body temperature, and the secretion of certain hormones are governed by a 24-hour cycle called the circadian system. While there are many external stimuli involved the regulation of circadian rhythm, the most powerful environmental stimulus is the daily light-dark cycle. Blind individuals with no light perception develop circadian desynchrony. This leads to non-24-hour sleep-wake rhythm disorder, which is associated with sleep-wake disorders, as well as mood disorders and loss of appetite and gastrointestinal disturbances due to disrupted circadian hormone regulation. As the diagnosis is often delayed because of under-recognition in clinical practice, patients must cope with varying degrees of social and academic dysfunction. Most blind individuals report that non-24-hour sleep-wake rhythm disorder affects them more than blindness. In the treatment of totally blind patients suffering from non-24-hour sleep-wake rhythm disorder, the first-line management is behavioral approaches. Drug therapy includes melatonin and the melatonin agonist tasimelteon. Diagnosing blind individuals' sleep disorders is also relevant to treatment because they can be improved with the use of melatonin and its analogues or by phototherapy if they have residual vision. Therefore, assessing sleep problems and planning treatment accordingly for individuals presenting with blindness is an important issue for ophthalmologists to keep in mind.
... Studies have suggested that a desynchrony in the circadian rhythm could trigger metabolic abnormalities. The acute effects of desynchrony are impairment in some physiological processes (e.g., insulin sensitivity, cortisol and melatonin secretion, blood pressure and cardiac modulation by the autonomous nervous system) [129][130][131][132]. In over 40 h of extended wakefulness, polar metabolites had a rhythmic or linear variation. ...
Metabolic syndrome has been associated in many studies with working in shifts. Even if the mechanistic details are not fully understood, forced sleep deprivation and exposure to light, as happens during night shifts, or irregular schedules with late or very early onset of the working program, lead to a sleep–wake rhythm misalignment, metabolic dysregulation and oxidative stress. The cyclic melatonin secretion is regulated by the hypothalamic suprachiasmatic nuclei and light exposure. At a central level, melatonin promotes sleep and inhibits wake-signals. Beside this role, melatonin acts as an antioxidant and influences the functionality of the cardiovascular system and of different metabolic processes. This review presents data about the influence of night shifts on melatonin secretion and oxidative stress. Assembling data from epidemiological, experimental and clinical studies contributes to a better understanding of the pathological links between chronodisruption and the metabolic syndrome related to working in shifts.
... Whilst several physiological, behavioural and environmental factors contribute to these outcomes, the unifying component is the effect that shift work has on the body's circadian system. This system is based on approximately 24-hour rhythms, regulated by a central clock that synchronises the body with the time of day, cued by light exposure (13) . Aligning regular behaviour cycles such as feeding-fasting, sleep-wakefulness, and rest-activity, with the rhythm set by this clock, optimises metabolism (14) . ...
Police officers are at high-risk of developing obesity and cardiometabolic health conditions. Their job presents challenges that contribute to this, predominantly shift work, which causes circadian misalignment and can impair metabolism. Food consumption plays a critical role in the synchronisation of the circadian system. Thus, the aim of this study was to understand the barriers and the impact that different shift types have on the dietary habits of police officers in the UK. A concurrent mixed methods design was used through an online survey that was open to all police officers who were currently working shifts in the UK. 127 police officers were included in the analysis. Diet quality was significantly worse on all shift types than on rest days ( p < 0.001) and was negatively correlated with BMI on all shifts: early-shift = -0.29, p = 0.001], late-shift [rs(105) = - 0.25, p = 0.009], nightshift [rs(104) = -0.24, p = 0.013] and rest-days [rs(117) = -0.31, p = 0.001]. Participants reported that shift work had altered their frequency and timing of food consumption and had increased their reliance on convenience and poor-quality food. Barriers to healthy eating included lacking time (87%), motivation (65%) and cost (48%). Convenience was ranked the highest influence on food choice (49%), followed by price (41.5%). Police officers are faced with unavoidable challenges when it comes to eating healthily. Future police-specific dietary interventions are required, providing practical solutions to these barriers so that behaviour change is more likely to be implemented.
... Shift work also disrupts behavioral rhythms such as the timing of meals, which a growing body of research suggests has consequences for metabolic processes and health (Banks et al., 2015;Skene et al., 2018). In a study of police officers on rotating shift schedules, Kosmadopoulos et al. (2020) found that caloric intake was significantly more dispersed across the 24-h day, with a greater proportion of caloric intake at night, on night-shift days than other types of days. ...
The various non-standard schedules required of shift workers force abrupt changes in the timing of sleep and light-dark exposure. These changes result in disturbances of the endogenous circadian system and its misalignment with the environment. Simulated night-shift experiments and field-based studies with shift workers both indicate that the circadian system is resistant to adaptation from a day- to a night-oriented schedule, as determined by a lack of substantial phase shifts over multiple days in centrally controlled rhythms, such as those of melatonin and cortisol. There is evidence that disruption of the circadian system caused by night-shift work results not only in a misalignment between the circadian system and the external light-dark cycle, but also in a state of internal desynchronization between various levels of the circadian system. This is the case between rhythms controlled by the central circadian pacemaker and clock genes expression in tissues such as peripheral blood mononuclear cells, hair follicle cells, and oral mucosa cells. The disruptive effects of atypical work schedules extend beyond the expression profile of canonical circadian clock genes and affects other transcripts of the human genome. In general, after several days of living at night, most rhythmic transcripts in the human genome remain adjusted to a day-oriented schedule, with dampened group amplitudes. In contrast to circadian clock genes and rhythmic transcripts, metabolomics studies revealed that most metabolites shift by several hours when working nights, thus leading to their misalignment with the circadian system. Altogether, these circadian and sleep-wake disturbances emphasize the all-encompassing impact of night-shift work, and can contribute to the increased risk of various medical conditions. Here, we review the latest scientific evidence regarding the effects of atypical work schedules on the circadian system, sleep and alertness of shift-working populations, and discuss their potential clinical impacts.
... Shift work leads to reduced sleep quality and quantity [1] and is associated with increased fatigue and performance impairments [3][4][5], particularly during the night, when circadian and homeostatic processes promote sleep [6]. The consequences of shift work on the physical health of the workers include an increased risk of metabolic disorders, insulin resistance, type 2 diabetes, cardiovascular disease, mood disorders, obesity, and gastrointestinal disorders [7][8][9][10][11][12][13][14]. Additionally, shift work is linked to exhaustion, absenteeism, presenteeism, and increased social and family conflict [15][16][17][18]. ...
Background:
Residential support workers (RSWs) provide 24-hour care to clients and many work overnight sleepover nightshifts. Although RSWs perform safety-critical tasks and are at high-risk of work stress and exhaustion, the health and safety of RSWs has not been investigated.
Objective:
This explorative workplace case study explored the impact of support work on the eating and driving behaviours of RSWs.
Methods:
Thirteen RSWs who had worked a dayshift (n = 6) or a sleepover nightshift (n = 7) completed questions on the timing of food intake during their shift, motivations for eating during the shift, subjective work performance, alertness and sleepiness post-shift, and driving performance post-shift.
Results:
RSWs reported snacking during the night on a sleepover nightshift. Time available was the biggest determinant for when RSWs ate during a day and sleepover nightshift. Ratings of subjective alertness and sleepiness after eating were not different between shift types, however participants reported an increase in work performance after eating during a dayshift. Driving events were more frequently reported post-sleepover nightshift, compared to post-dayshift.
Conclusions:
Findings demonstrate an impact of shift type on eating and driving behaviours of RSWs and highlight the importance of further investigation of this under-researched group to identify appropriate strategies for improving health and safety.
... 8,9 Observasi terhadap beberapa hewan seperti tikus dan kelinci menunjukkan bahwa stres oksidatif dapat menurunkan motilitas spermatozoa dan menyebabkan kerusakan deoxyribonucleic acid (DNA) pada spermatozoa. 10 Penelitian lain menyatakan bahwa level fragmentasi DNA yang tinggi berhubungan dengan penurunan motilitas, penurunan konsentrasi, dan peningkatan jumlah spermatozoa abnormal. 11,12 Penelitian ini bertujuan untuk mengetahui pengaruh pemberian coklat terhadap kualitas spermatozoa tikus Wistar (Rattus norvegicus) yang terpapar stres. ...
A chocolate compound, flavonoid which is a subgroup of polyphenols, has protective effect on spermatozoa exposed to stress. The flavonoid compound in chocolate, (-)-epicatehin, plays important roles in neutralizing ROS, blocking the production of ROS, and inhibiting enzyme activity of DNA methyltransferase. Stress activates the hypothalamus-pituitary-adrenal (HPA) and simpatoadrenomedular systems that have glucocorticoid as their end product that can cause an increase in essential catabolism and trigger the production of ROS. Oxidative stress can reduce the motility of spermatozoa and cause damage to DNA of spermatozoa. This study was aimed to determine the effect of chocolate (Theobroma cacao) on the quality of spermatozoa in stressed Wistar rats (Rattus norvegicus). This was an experimental study with a post-test only control group design. Samples were spermatozoa of Wistar rats. There were 9 Wistar rats divided into 3 groups, as follows: P0 (control), P1 (stress treatment only), and P2 (stress treatment and chocolate administration). The results showed that there were no significant differences in concentration and motility, albeit, there was a significant difference in morphology of spermatozoa in Wistar rats (Rattus norvegicus). Conclusion: Chocolate (Theobroma cacao) can influence the increase of morphologic quality of spermatozoa in stressed Wistar rats.Keywords: chocolate, stress, spermatozoa Abstrak: Kandungan coklat, yaitu flavonoid merupakan subgrup dari polifenol yang memiliki efek protektif terhadap spermatozoa dari paparan stres. Jenis flavonoid dalam coklat, (-)-epicatehin berperan dalam menetralisir ROS, memblokir produksi ROS, dan menginhibisi aktivitas enzim DNA methyltransferase. Stres mengaktifkan sistem hipotalamus-pituitari-adrenal (HPA) dan simpatoadrenomedular yang memiliki produk akhir glukokortikoid yang dapat menyebabkan peningkatan katabolisme esensial dan memicu produksi ROS. Stres oksidatif dapat menurunkan motilitas spermatozoa dan menyebabkan kerusakan DNA spermatozoa. Penelitian ini bertujuan untuk mengetahui pengaruh pemberian coklat (Theobroma cacao) terhadap kualitas spermatozoa tikus Wistar (Rattus norvegicus) yang terpapar stres. Jenis penelitian ialah eksperimental dengan post-test only control group design. Sampel penelitian ialah spermatozoa tikus Wistar (Rattus norvegicus). Dilakukan perlakuan terhadap 9 ekor tikus Wistar yang dibagi menjadi 3 kelompok, yaitu P0 (kontrol), P1 (perlakuan stres saja), dan P2 (perlakuan stres dan pemberian coklat). Hasil penelitian tidak mendapatkan perbedaan bermakna pada konsentrasi dan motilitas tetapi terdapat perbedaan bermakna pada morfologi spermatozoa tikus Wistar (Rattus norvegicus). Simpulan: Pemberian coklat (Theobroma cacao) berpengaruh terhadap peningkatan kualitas morfologi spermatozoa tikus Wistar (Rattus norvegicus) yang terpapar stres.Kata kunci: coklat, stres, spermatozoa
... Further, the generalizability of the results will be strengthened when samples reflect shiftworker populations more closely. This includes older participants and those with habits such as smoking [62], in addition to the psychological and physical health issues that are especially common among shiftworkers, including obesity [63], metabolic disorders [4,64], sleep disorders [65], and mood disorders [66,67]. Further, shiftworkers report frequent caffeine use whilst on shift [68,69] and this is known to influence gastric upset [70]. ...
Shiftworkers report eating during the night when the body is primed to sleep. This study investigated the impact of altering food timing on subjective responses. Healthy participants (n = 44, 26 male, age Mean ± SD = 25.0 ± 2.9 years, BMI = 23.82 ± 2.59kg/m2) participated in a 7-day simulated shiftwork protocol. Participants were randomly allocated to one of three eating conditions. At 00:30, participants consumed a meal comprising 30% of 24 h energy intake (Meal condition; n = 14, 8 males), a snack comprising 10% of 24 h energy intake (Snack condition; n = 14; 8 males) or did not eat during the night (No Eating condition; n = 16, 10 males). Total 24 h individual energy intake and macronutrient content was constant across conditions. During the night, participants reported hunger, gut reaction, and sleepiness levels at 21:00, 23:30, 2:30, and 5:00. Mixed model analyses revealed that the snack condition reported significantly more hunger than the meal group (p < 0.001) with the no eating at night group reporting the greatest hunger (p < 0.001). There was no difference in desire to eat between meal and snack groups. Participants reported less sleepiness after the snack compared to after the meal (p < 0.001) or when not eating during the night (p < 0.001). Gastric upset did not differ between conditions. A snack during the nightshift could alleviate hunger during the nightshift without causing fullness or increased sleepiness.
... While sleep loss has been the subject of research for more than a century, we still have only an emerging understanding of how changes in sleep impact other healthrelated behaviors. These subsequent changes in health behaviors, including when and what we eat and drink, play a critical role in the observed relationship between sleep changes and increased risk of chronic illness and injury ( Banks et al., 2015;Dorrian et al., 2015). In the laboratory, researchers can control sleep duration and monitor these behavioral changes. ...
An emerging literature is specifically focusing on the effects of sleep deprivation on aspects of social functioning and underlying neural changes. Two critical facets of social behavior emerge that are negatively impacted by sleep deprivation—self-regulation, which includes behavioral and emotional regulation, and social monitoring, which includes perceiving and interpreting cues relating to self and others. Sleep deprived individuals performing tasks with social components show altered brain activity in areas of the prefrontal cortex implicated in self-control, inhibition, evaluation, and decision-making, in proximity to mesocorticolimbic pathways to reward and emotional processing areas. These cognitive changes lead to increased reward seeking and behaviors that promote negative health outcomes (such as increased consumption of indulgence foods). These changes also lead to emotional disinhibition and increased responses to negative stimuli, leading to reductions in trust, empathy, and humor. Concomitant attentional instability leads to impaired social information processing, impairing individual and team performance and increasing likelihood of error, incident, and injury. Together, changes to reward seeking, the foundational components of social interaction, and interpretation of social cues, can result in unpleasant or deviant behavior. These behaviors are perceived and negatively responded to by others, leading to a cycle of conflict and withdrawal. Further studies are necessary and timely. Educational and behavioral interventions are required to reduce health-damaging behaviors, and to reduce emotionally-laden negative interpretation of sleep-deprived exchanges. This may assist with health, and with team cohesion (and improved performance and safety) in the workplace and the home.
... Potential mechanisms by which shift work may lead to CVD include physiological changes due to circadian disruption, and long-term alterations to neuroendocrine and cardiometabolic stress responses 16) . In relation to behavioural pathways, shift workers alter meal and snack timing, which can exacerbate circadian misalignment, negatively impacting on metabolic function 17) . Shift workers are also more likely to choose highsugar and carbohydrate foods 18) . ...
Cardiovascular disease (CVD) risk in train drivers is associated with health conditions that can result in sudden incapacity. Drivers are at high risk on several CVD risk factors with research suggesting that sleep may predict CVD risk, however this relationship has not yet been explored. This study investigated the link between sleep and CVD risk, in relation to hours of work day and days off sleep. N=309 Australian drivers completed cross-sectional survey. A CVD risk score was calculated by summing scores from behavioural and biomedical risk factors. Sleep was most frequently cited as the main reason for decline in perceived health status. Main analyses showed that shorter work day sleep (M=5.79 h) was a significant predictor of increased CVD risk (p=0.013). This relationship was moderated by days off sleep, such that when days off sleep (M=8.17 h) was higher, the effect of work day sleep on CVD risk was weaker (p=0.047). Findings indicate the amount of sleep a driver obtains on non-work days may compensate for adverse health outcomes. Successful management of fatigue in safety critical occupations appears essential not only for the prevention of safety hazards, but also for the long-term health of shift workers. Further investigation is warranted.
... The short-and long-term negative health impacts of shiftwork are well established in the literature and these shiftworkers are particularly vulnerable to higher rates of obesity 7,128) . It is therefore not surprising that health may motivate eating choices on shift. ...
Shiftwork leads to altered eating patterns, with workers often eating foods at all times across the 24h period. Strategies to reduce the burden of shiftwork on the workers should be prioritised and altering these eating patterns is an important area for change. This narrative review examines the current evidence on the individual and environmental factors influencing the eating behaviours of shiftworkers. A systematic search was conducted and yielded 62 articles. These were split into four themes that influence eating patterns; When shiftworkers eat, What type of foods shiftworkers eat, Where the food is sourced from, and Why shiftworkers choose to eat on shift. Irregular working hours was the biggest influence on when workers ate on shift, shift-type was the biggest influence on what workers ate, the majority of food was sourced from canteens and cafeterias, and socialising with colleagues was the biggest reason why workers chose to eat. While more research is needed to explore multiple industries and shift-types, and to investigate the ideal size, type and timing of food on shift, this review has highlighted that future research into shiftworker eating needs to adopt an integrative approach and consider the different individual and social contexts that influence eating patterns.
... Importantly, for all participants, 24 h energy consumption was kept constant. These differences in eating patterns are consistent with the workplace, where employees differentially distribute their food consumption around the clock (Banks et al., 2015). Since this was a proof of concept analysis in a small sample to investigate whether the model would track average performance and sleepiness across this schedule, eating groups were not looked at separately. ...
Technology-supported methods for sleep recording are becoming increasingly affordable. Sleep history feedback may help with fatigue-related decision making - Should I drive? Am I fit for work? This study examines a "sleep tank" model (SleepTank™), which is analogous to the fuel tank in a car, refilled by sleep, and depleted during wake. Required inputs are sleep period time and sleep efficiency (provided by many consumer-grade actigraphs). Outputs include suggested hours remaining to "get sleep" and percentage remaining in tank (Tank%). Initial proof of concept analyses were conducted using data from a laboratory-based simulated nightshift study. Ten, healthy males (18-35y) undertook an 8h baseline sleep opportunity and daytime performance testing (BL), followed by four simulated nightshifts (2000 h-0600 h), with daytime sleep opportunities (1000 h-1600 h), then an 8 h night-time sleep opportunity to return to daytime schedule (RTDS), followed by daytime performance testing. Psychomotor Vigilance Task (PVT) and Karolinska Sleepiness Scale were performed at 1200 h on BL and RTDS, and at 1830 h, 2130 h 0000 h and 0400 h each nightshift. A 40-minute York Driving Simulation was performed at 1730 h, 2030 h and 0300 h on each nightshift. Model outputs were calculated using sleep period timing and sleep efficiency (from polysomnography) for each participant. Tank% was a significant predictor of PVT lapses (p < 0.001), and KSS (p < 0.001), such that every 5% reduction resulted in an increase of two lapses, or one point on the KSS. Tank% was also a significant predictor of %time in the Safe Zone from the driving simulator (p = 0.001), such that every 1% increase in the tank resulted in a 0.75% increase in time spent in the Safe Zone. Initial examination of the correspondence between model predictions and performance and sleepiness measures indicated relatively good predictive value. Results provide tentative evidence that this "sleep tank" model may be an informative tool to aid in individual decision-making based on sleep history.
... Shiftworkers alter their patterns of eating when working, which includes eating during the nightshift when they would typically be asleep (Banks et al., 2015). This is important because food consumption may have a negative impact on performance (Dye & Blundell, 2002). ...
Shiftworkers have impaired performance when driving at night and they also alter their eating patterns during nightshifts. However, it is unknown whether driving at night is influenced by the timing of eating. This study aims to explore the effects of timing of eating on simulated driving performance across four simulated nightshifts. Healthy, non-shiftworking males aged 18–35 years (n = 10) were allocated to either an eating at night (n = 5) or no eating at night (n = 5) condition. During the simulated nightshifts at 1730, 2030 and 0300 h, participants performed a 40-min driving simulation, 3-min Psychomotor Vigilance Task (PVT-B), and recorded their ratings of sleepiness on a subjective scale. Participants had a 6-h sleep opportunity during the day (1000–1600 h). Total 24-h food intake was consistent across groups; however, those in the eating at night condition ate a large meal (30% of 24-h intake) during the nightshift at 0130 h. It was found that participants in both conditions experienced increased sleepiness and PVT-B impairments at 0300 h compared to 1730 and 2030 h (p < 0.001). Further, at 0300 h, those in the eating condition displayed a significant decrease in time spent in the safe zone (p < 0.05; percentage of time within 10 km/h of the speed limit and 0.8 m of the centre of the lane) and significant increases in speed variability (p < 0.001), subjective sleepiness (p < 0.01) and number of crashes (p < 0.01) compared to those in the no eating condition. Results suggest that, for optimal performance, shiftworkers should consider restricting food intake during the night.
Introduction:
Shift workers are at an increased risk of developing obesity and type 2 diabetes. Eating and sleeping out of synchronisation with endogenous circadian rhythms causes weight gain, hyperglycaemia and insulin resistance. Interventions that promote weight loss and reduce the metabolic consequences of eating at night are needed for night shift workers. The aim of this study is to examine the effects of three weight loss strategies on weight loss and insulin resistance (HOMA-IR) in night shift workers.
Methods and analysis:
A multisite 18-month, three-arm randomised controlled trial comparing three weight loss strategies; continuous energy restriction; and two intermittent fasting strategies whereby participants will fast for 2 days per week (5:2); either during the day (5:2D) or during the night shift (5:2N). Participants will be randomised to a weight loss strategy for 24 weeks (weight loss phase) and followed up 12 months later (maintenance phase). The primary outcomes are weight loss and a change in HOMA-IR. Secondary outcomes include changes in glucose, insulin, blood lipids, body composition, waist circumference, physical activity and quality of life. Assessments will be conducted at baseline, 24 weeks (primary endpoint) and 18 months (12-month follow-up). The intervention will be delivered by research dietitians via a combination of face-to-face and telehealth consultations. Mixed-effect models will be used to identify changes in dependent outcomes (weight and HOMA-IR) with predictor variables of outcomes of group, time and group-time interaction, following an intention-to-treat approach.
Ethics and dissemination:
The study protocol was approved by Monash Health Human Research Ethics Committee (RES 19-0000-462A) and registered with Monash University Human Research Ethics Committee. Ethical approval has also been obtained from the University of South Australia (HREC ID: 202379) and Ambulance Victoria Research Committee (R19-037). Results from this trial will be disseminated via conference presentations, peer-reviewed journals and student theses.
Trial registration number:
Australian New Zealand Clinical Trials Registry (ACTRN-12619001035112).
Purpose
This study investigated the relationships between eating habits and sleep quality among university students.
Methods
In a cross-sectional study, university students completed a self-report questionnaire to assess eating habits and meal timing. We assessed subjective sleep quality using the Pittsburgh Sleep Quality Index (PSQI) questionnaire and examined the associations between eating habits and overall sleep quality and its components.
Results
Four hundred ninety-eight students participated in the study. Students who used to skip breakfast, ate late-night snacks, and replaced meals with snacks were at 1.20 times, 1.24 times, and 1.25 times higher likelihood of having poor overall sleep quality, respectively. Multiple logistic regression analysis showed that skipping breakfast (r = − 0.111, P = 0.007), late-night snacks (r = − 0.109, P = 0.007), replacing meals with snacks (r = − 0.126, P = 0.002), and irregular mealtimes (r = − 0.094, P = 0.018) were the best correlates with poor sleep quality. After adjustment to demographic variables, replacing meals with snacks followed by skipping breakfast were the best independent associations with poor sleep quality by the PSQI.
Conclusions
Eating habits and meal timing were significantly associated with sleep quality. We speculate that healthy eating habits may lead to improved sleep quality and sleep components among university students.
Aim:
The aim of this study was to investigate the effects of four consecutive simulated night shifts on glucose homeostasis, mitochondrial function and central and peripheral rhythmicity compared with a simulated day shift schedule.
Methods:
Seventeen healthy adults (8M:9F) matched for sleep, physical activity, and dietary/fat intake participated in this study (night shift work n= 9; day shift work n= 8). Glucose tolerance and insulin sensitivity before and after 4 nights of shift work were measured by an intravenous glucose tolerance test and a hyperinsulinemic euglycemic clamp, respectively. Muscles biopsies were obtained to determine insulin signalling and mitochondrial function. Central and peripheral rhythmicity were assessed by measuring salivary melatonin and expression of circadian genes from hair samples, respectively.
Results:
Fasting plasma glucose increased (4.4±0.1 vs. 4.6±0.1 mmol·L-1 ; P=0.001) and insulin sensitivity decreased (25±7%, P<0.05) following the night shift, with no changes following the day shift. Night shift work had no effect on skeletal muscle protein expression (PGC1α, UCP3, TFAM and mitochondria Complex II-V) or insulin-stimulated pAkt Ser473, pTBC1D4Ser318 and pTBC1D4Thr642. Importantly the metabolic changes after simulated night shifts occurred despite no changes in the timing of melatonin rhythmicity or hair follicle cell clock gene expression across the wake period (Per3, Per1, Nr1d1 and Nr1d2).
Conclusion:
Only four days of simulated night shift work in healthy adults is sufficient to reduce insulin sensitivity which would be expected to increase the risk of T2D. This article is protected by copyright. All rights reserved.
The prevalence of type 2 diabetes continues to rise worldwide and is reaching pandemic proportions. The notion that this is due to obesity, resulting from excessive energy consumption and reduced physical activity, is overly simplistic. Circadian de-synchrony, which occurs when physiological processes are at odds with timing imposed by internal clocks, also promotes obesity and impairs glucose tolerance in mouse models, and is a feature of modern human lifestyles. The purpose of this review is to highlight what is known about glucose metabolism in animal and human models of circadian de-synchrony and examine the evidence as to whether shifts in meal timing contribute to impairments in glucose metabolism, gut hormone secretion and the risk of type 2 diabetes. Lastly, we examine whether restricting food intake to discrete time periods, will prevent or reverse abnormalities in glucose metabolism with the view to improving metabolic health in shift workers and in those more generally at risk of chronic diseases such as type 2 diabetes and cardiovascular disease.
Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation. Pyruvate dehydrogenase (PDH) activity was also reduced due to altered expression of circadian genes Pdk4 and Pdp1, coding for PDH kinase and phosphatase, respectively. PDH inhibition leads to reduced glucose oxidation and diversion of glycolytic intermediates to alternative metabolic pathways, as revealed by metabolome analysis. The impaired glucose metabolism induced by muscle-specific Bmal1 knockout suggests that a major physiological role of the muscle clock is to prepare for the transition from the rest/fasting phase to the active/feeding phase, when glucose becomes the predominant fuel for skeletal muscle.
Shift work was positively associated with higher incidence of metabolic syndrome, obesity, cardiovascular disease, sleep disturbances, decreased immune functions, and cancer. Observed disorders were manifested usually after longer time of shift work (more than 10 years). On the other hand, disturbed daily profile of melatonin and cortisol during shift work were detected even in human self reporting well tolerated shift work. Similarly, changes in thyroid stimulating hormone, prolactin, growth hormone, insulin, and ghrelin were demonstrated. Changes in hormone concentrations are influenced by shift work, sleep or circadian system or combinations of above mentioned regulatory factors. The circadian system consists of the central part localized in the hypothalamus and peripheral oscillators located in all tissues of the body. The central oscillator is predominantly synchronized by light and peripheral oscillators are more responsive to metabolic signals. Under conditions of shift work, central and peripheral oscillators dissociate that causes misalignment of daily rhythms in physiological functions. Synchronization during shift work can be improved by melatonin supplementation and manipulation with light:dark cycles and food regimens. Shift work tolerance is individual. Partial positive selection can be achieved on the basis of several psychological traits. Appropriate schedule can be estimated on the basis of chronotype. Keywords: melatonin, glucocorticoids, insulin, SIRT1, PER, chronotype, synchronization.
In mammals, a network of circadian clocks regulates 24-hr rhythms of behavior and physiology. Circadian disruption promotes obesity and the development of obesity-associated disorders, but it remains unclear to which extent peripheral tissue clocks contribute to this effect. To reveal the impact of the circadian timing system on lipid metabolism, blood and adipose tissue samples from wild-type, ClockΔ19 and Bmal1-/- circadian mutant mice were subjected to biochemical assays and gene expression profiling. We show diurnal variations in lipolysis rates and release of free fatty acids (FFAs) and glycerol into the blood correlating with rhythmic regulation of two genes encoding the lipolysis pacemaker enzymes adipose triglyceride lipase (Atgl) and hormone-sensitive lipase (Hsl) by self-sustained adipocyte clocks. Circadian clock mutant mice show low and non-rhythmic FFA and glycerol blood content together with decreased lipolysis rates and increased sensitivity to fasting. Instead circadian clock disruption promotes the accumulation of triglycerides in WAT, leading to increased adiposity and adipocyte hypertrophy. In summary, circadian modulation of lipolysis rates regulates the availability of lipid-derived energy during the day, suggesting a role for WAT clocks in the regulation of energy homeostasis.
Background:
There is emerging literature demonstrating a relationship between the timing of feeding and weight regulation in animals. However, whether the timing of food intake influences the success of a weight-loss diet in humans is unknown.
Objective:
To evaluate the role of food timing in weight-loss effectiveness in a sample of 420 individuals who followed a 20-week weight-loss treatment.
Methods:
Participants (49.5% female subjects; age (mean ± s.d.): 42 ± 11 years; BMI: 31.4 ± 5.4 kg m(-2)) were grouped in early eaters and late eaters, according to the timing of the main meal (lunch in this Mediterranean population). 51% of the subjects were early eaters and 49% were late eaters (lunch time before and after 1500 hours, respectively), energy intake and expenditure, appetite hormones, CLOCK genotype, sleep duration and chronotype were studied.
Results:
Late lunch eaters lost less weight and displayed a slower weight-loss rate during the 20 weeks of treatment than early eaters (P=0.002). Surprisingly, energy intake, dietary composition, estimated energy expenditure, appetite hormones and sleep duration was similar between both groups. Nevertheless, late eaters were more evening types, had less energetic breakfasts and skipped breakfast more frequently that early eaters (all; P<0.05). CLOCK rs4580704 single nucleotide polymorphism (SNP) associated with the timing of the main meal (P=0.015) with a higher frequency of minor allele (C) carriers among the late eaters (P=0.041). Neither sleep duration, nor CLOCK SNPs or morning/evening chronotype was independently associated with weight loss (all; P>0.05).
Conclusions:
Eating late may influence the success of weight-loss therapy. Novel therapeutic strategies should incorporate not only the caloric intake and macronutrient distribution - as is classically done - but also the timing of food.
Disrupting maternal circadian rhythms through exposure to chronic phase shifts of the photoperiod has lifelong consequences for the metabolic homeostasis of the fetus, such that offspring develop increased adiposity, hyperinsulinaemia and poor glucose and insulin tolerance. In an attempt to determine the mechanisms by which these poor metabolic outcomes arise, we investigated the impact of chronic phase shifts (CPS) on maternal and fetal hormonal, metabolic and circadian rhythms. We assessed weight gain and food consumption of dams exposed to either CPS or control lighting conditions throughout gestation. At day 20, dams were assessed for plasma hormone and metabolite concentrations and glucose and insulin tolerance. Additionally, the expression of a range of circadian and metabolic genes was assessed in maternal, placental and fetal tissue. Control and CPS dams consumed the same amount of food, yet CPS dams gained 70% less weight during the first week of gestation. At day 20, CPS dams had reduced retroperitoneal fat pad weight (-15%), and time-of-day dependent decreases in liver weight, whereas fetal and placental weight was not affected. Melatonin secretion was not altered, yet the timing of corticosterone, leptin, glucose, insulin, free fatty acids, triglycerides and cholesterol concentrations were profoundly disrupted. The expression of gluconeogenic and circadian clock genes in maternal and fetal liver became either arrhythmic or were in antiphase to the controls. These results demonstrate that disruptions of the photoperiod can severely disrupt normal circadian profiles of plasma hormones and metabolites, as well as gene expression in maternal and fetal tissues. Disruptions in the timing of food consumption and the downstream metabolic processes required to utilise that food, may lead to reduced efficiency of growth such that maternal weight gain is reduced during early embryonic development. It is these perturbations that may contribute to the programming of poor metabolic homeostasis in the offspring.
Biological clocks are genetically encoded oscillators that allow organisms to anticipate changes in the light-dark environment that are tied to the rotation of Earth. Clocks enhance fitness and growth in prokaryotes, and they are expressed throughout the central nervous system and peripheral tissues of multicelled organisms in which they influence sleep, arousal, feeding and metabolism. Biological clocks capture the imagination because of their tie to geophysical time, and tools are now in hand to analyse their function in health and disease at the cellular and molecular level.
Adipocytes store excess energy in the form of triglycerides and signal the levels of stored energy to the brain. Here we show that adipocyte-specific deletion of Arntl (also known as Bmal1), a gene encoding a core molecular clock component, results in obesity in mice with a shift in the diurnal rhythm of food intake, a result that is not seen when the gene is disrupted in hepatocytes or pancreatic islets. Changes in the expression of hypothalamic neuropeptides that regulate appetite are consistent with feedback from the adipocyte to the central nervous system to time feeding behavior. Ablation of the adipocyte clock is associated with a reduced number of polyunsaturated fatty acids in adipocyte triglycerides. This difference between mutant and wild-type mice is reflected in the circulating concentrations of polyunsaturated fatty acids and nonesterified polyunsaturated fatty acids in hypothalamic neurons that regulate food intake. Thus, this study reveals a role for the adipocyte clock in the temporal organization of energy regulation, highlights timing as a modulator of the adipocyte-hypothalamic axis and shows the impact of timing of food intake on body weight.
The circadian clock is a highly conserved timing system, resonating physiological
processes to 24-hour environmental cycles. Circadian misalignment is emerging as
a risk factor of metabolic disease. The molecular clock resides in all metabolic
tissues, the dysfunction of which is associated with perturbed energy
metabolism. In this article, we will review current knowledge about molecular
mechanisms of the circadian clock and the role of clocks in the physiology and
pathophysiology of metabolic tissues.
The disruption of the circadian system has been associated with the development of obesity.
We examined the effects of circadian misalignment on sleep, energy expenditure, substrate oxidation, appetite, and related hormones.
Thirteen subjects [aged 24.3 ± 2.5 (mean ± SD) y; BMI (in kg/m(2)): 23.6 ± 1.7 (mean ± SD)] completed a randomized crossover study. For each condition, subjects stayed time blinded in the respiration chamber during 3 light-entrained circadian cycles that resulted in a phase advance (3 × 21 h) and a phase delay (3 × 27 h) compared with during a 24-h cycle. Sleep, energy expenditure, substrate oxidation, and appetite were quantified. Blood and saliva samples were taken to determine melatonin, glucose, insulin, ghrelin, leptin, glucagon-like peptide 1 (GLP-1), and cortisol concentrations.
Circadian misalignment, either phase advanced or phase delayed, did not result in any changes in appetite or energy expenditure, whereas meal-related blood variables (glucose, insulin, ghrelin, leptin, and GLP-1) followed the new meal patterns. However, phase-advanced misalignment caused flattening of the cortisol-secretion pattern (P < 0.001), increased insulin concentrations (P = 0.04), and increased carbohydrate oxidation (P = 0.03) and decreased protein oxidation (P = 0.001). Phase-delayed misalignment increased rapid eye movement sleep (P < 0.001) and the sleeping metabolic rate (P = 0.02), increased glucose (P = 0.02) and decreased GLP-1 (P = 0.02) concentrations, and increased carbohydrate oxidation (P = 0.01) and decreased protein oxidation (P = 0.003).
The main effect of circadian misalignment, either phase advanced or phase delayed, is a concomitant disturbance of the glucose-insulin metabolism and substrate oxidation, whereas the energy balance or sleep is not largely affected. Chronically eating and sleeping at unusual circadian times may create a health risk through a metabolic disturbance. This trial was registered at the International Clinical Trials Registry Platform (http://apps.who.int/trialsearch/) as NTR2926.
Background:
Sleep restriction is associated with development of metabolic ill-health, and hormonal mechanisms may underlie these effects. The aim of this study was to determine the impact of short term sleep restriction on male health, particularly glucose metabolism, by examining adrenocorticotropic hormone (ACTH), cortisol, glucose, insulin, triglycerides, leptin, testosterone, and sex hormone binding globulin (SHBG).
Methodology/principal findings:
N = 14 healthy men (aged 27.4±3.8, BMI 23.5±2.9) underwent a laboratory-based sleep restriction protocol consisting of 2 baseline nights of 10 h time in bed (TIB) (B1, B2; 22:00-08:00), followed by 5 nights of 4 h TIB (SR1-SR5; 04:00-08:00) and a recovery night of 10 h TIB (R1; 22:00-08:00). Subjects were allowed to move freely inside the laboratory; no strenuous activity was permitted during the study. Food intake was controlled, with subjects consuming an average 2000 kcal/day. Blood was sampled through an indwelling catheter on B1 and SR5, at 09:00 (fasting) and then every 2 hours from 10:00-20:00. On SR5 relative to B1, glucose (F(1,168) = 25.3, p<0.001) and insulin (F(1,168) = 12.2, p<0.001) were increased, triglycerides (F(1,168) = 7.5, p = 0.007) fell and there was no significant change in fasting homeostatic model assessment (HOMA) determined insulin resistance (F(1,168) = 1.3, p = 0.18). Also, cortisol (F(1,168) = 10.2, p = 0.002) and leptin (F(1,168) = 10.7, p = 0.001) increased, sex hormone binding globulin (F(1,167) = 12.1, p<0.001) fell and there were no significant changes in ACTH (F(1,168) = 0.3, p = 0.59) or total testosterone (F(1,168) = 2.8, p = 0.089).
Conclusions/significance:
Sleep restriction impaired glucose, but improved lipid metabolism. This was associated with an increase in afternoon cortisol, without significant changes in ACTH, suggesting enhanced adrenal reactivity. Increased cortisol and reduced sex hormone binding globulin (SHBG) are both consistent with development of insulin resistance, although hepatic insulin resistance calculated from fasting HOMA did not change significantly. Short term sleep curtailment leads to changes in glucose metabolism and adrenal reactivity, which when experienced repeatedly may increase the risk for type 2 diabetes.
Mammals have an endogenous timing system in the suprachiasmatic nuclei (SCN) of the hypothalamic region of the brain. This internal clock system is composed of an intracellular feedback loop that drives the expression of molecular components and their constitutive protein products to oscillate over a period of about 24 h (hence the term 'circadian'). These circadian oscillations bring about rhythmic changes in downstream molecular pathways and physiological processes such as those involved in nutrition and metabolism. It is now emerging that the molecular components of the clock system are also found within the cells of peripheral tissues, including the gastrointestinal tract, liver and pancreas. The present review examines their role in regulating nutritional and metabolic processes. In turn, metabolic status and feeding cycles are able to feed back onto the circadian clock in the SCN and in peripheral tissues. This feedback mechanism maintains the integrity and temporal coordination between various components of the circadian clock system. Thus, alterations in environmental cues could disrupt normal clock function, which may have profound effects on the health and well-being of an individual.
Epidemiological studies link short sleep duration and circadian disruption with higher risk of metabolic syndrome and diabetes. We tested the hypotheses that prolonged sleep restriction with concurrent circadian disruption, as can occur in people performing shift work, impairs glucose regulation and metabolism. Healthy adults spent >5 weeks under controlled laboratory conditions in which they experienced an initial baseline segment of optimal sleep, 3 weeks of sleep restriction (5.6 hours of sleep per 24 hours) combined with circadian disruption (recurring 28-hour "days"), followed by 9 days of recovery sleep with circadian re-entrainment. Exposure to prolonged sleep restriction with concurrent circadian disruption, with measurements taken at the same circadian phase, decreased the participants' resting metabolic rate and increased plasma glucose concentrations after a meal, an effect resulting from inadequate pancreatic insulin secretion. These parameters normalized during the 9 days of recovery sleep and stable circadian re-entrainment. Thus, in humans, prolonged sleep restriction with concurrent circadian disruption alters metabolism and could increase the risk of obesity and diabetes.
Due to irregular working hours shiftworkers experience circadian disruption and sleep restriction. There is some evidence to indicate that these factors adversely affect health through changes in snacking behaviour. The aim of this study was to investigate the impact of sleep restriction, prior wake and circadian phase on snacking behaviour during a week of simulated shiftwork. Twenty-four healthy males (age: 22.0 ± 3.6 years, mean ± SD) lived in a sleep laboratory for 12 consecutive days. Participants were assigned to one of two schedules: a moderate sleep restriction condition (n=10) equivalent to a 6-h sleep opportunity per 24h or a severe sleep restriction condition (n=14) equivalent to a 4-h sleep opportunity per 24h. In both conditions, sleep/wake episodes occurred 4h later each day to simulate a rotating shiftwork pattern. While living in the laboratory, participants were served three meals and were provided with either five (moderate sleep restriction condition) or six (severe sleep restriction condition) snack opportunities daily. Snack choice was recorded at each opportunity and assigned to a category (sweet, savoury or healthy) based on the content of the snack. Data were analysed using a Generalised Estimating Equations approach. Analyses show a significant effect of sleep restriction condition on overall and sweet snack consumption. The odds of consuming a snack were significantly greater in the severe sleep restriction condition (P<0.05) compared to the moderate sleep restriction condition. In particular, the odds of choosing a sweet snack were significantly increased in the severe sleep restriction condition (P<0.05). Shiftworkers who are severely sleep restricted may be at risk of obesity and related health disorders due to elevated snack consumption and unhealthy snack choice. To further understand the impact of sleep restriction on snacking behaviour, future studies should examine physiological, psychological and environmental motivators.
Shiftworkers have a higher risk of CHD and type 2 diabetes. They consume a large proportion of their daily energy and carbohydrate intake in the late evening or night-time, a factor which could be linked to their increase in disease risk. We compared the metabolic effects of varying both dietary glycaemic index (GI) and the time at which most daily energy intake was consumed. We hypothesised that glucose control would be optimal with a low-GI diet, consumed predominantly early in the day. A total of six healthy lean volunteers consumed isoenergetic meals on four occasions, comprising either high- or low-GI foods, with 60 % energy consumed predominantly early (breakfast) or late (supper). Interstitial glucose was measured continuously for 20 h. Insulin, TAG and non-esterified fatty acids were measured for 2 h following every meal. Highest glucose values were observed when large 5021 kJ (1200 kcal) high-GI suppers were consumed. Glucose levels were also significantly higher in predominantly late high- v. low-GI meals (P < 0·01). Using an estimate of postprandial insulin sensitivity throughout the day, we demonstrate that this follows the same trend, with insulin sensitivity being significantly worse in high energy consumed in the evening meal pattern. Both meal timing and GI affected glucose tolerance and insulin secretion. Avoidance of large, high-GI meals in the evening may be particularly beneficial in improving postprandial glucose profiles and may play a role in reducing the risk of type 2 diabetes; however, longer-term studies are needed to confirm this.
Mika Kivimaki and colleagues discuss new research that shows an association between shift work and the risk of developing type 2 diabetes among nurses.
Almost all organisms ranging from single cell bacteria to humans exhibit a variety of behavioral, physiological, and biochemical rhythms. In mammals, circadian rhythms control the timing of many physiological processes over a 24-h period, including sleep-wake cycles, body temperature, feeding, and hormone production. This body of research has led to defined characteristics of circadian rhythms based on period length, phase, and amplitude. Underlying circadian behaviors is a molecular clock mechanism found in most, if not all, cell types including skeletal muscle. The mammalian molecular clock is a complex of multiple oscillating networks that are regulated through transcriptional mechanisms, timed protein turnover, and input from small molecules. At this time, very little is known about circadian aspects of skeletal muscle function/metabolism but some progress has been made on understanding the molecular clock in skeletal muscle. The goal of this chapter is to provide the basic terminology and concepts of circadian rhythms with a more detailed review of the current state of knowledge of the molecular clock, with reference to what is known in skeletal muscle. Research has demonstrated that the molecular clock is active in skeletal muscles and that the muscle-specific transcription factor, MyoD, is a direct target of the molecular clock. Skeletal muscle of clock-compromised mice, Bmal1(-/-) and Clock(Δ19) mice, are weak and exhibit significant disruptions in expression of many genes required for adult muscle structure and metabolism. We suggest that the interaction between the molecular clock, MyoD, and metabolic factors, such as PGC-1, provide a potential system of feedback loops that may be critical for both maintenance and adaptation of skeletal muscle.
The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and although rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism and insulin signalling is delayed in circadian mutant mice, and both Clock and Bmal1 (also called Arntl) mutants show impaired glucose tolerance, reduced insulin secretion and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival and synaptic vesicle assembly. Notably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective beta-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the beta-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger the onset of diabetes mellitus.
Epidemiological studies have shown that shift workers are at a greater risk of developing cardiovascular disease which may, in part, be related to metabolic and hormonal changes. Partial sleep deprivation, a common consequence of rotating shift work, has been shown to affect glucose tolerance and insulin sensitivity. The current study investigated the effects of one night of total sleep deprivation, as a proxy for the first night shift, on postprandial glucose, insulin and lipid (triacylglycerols (TAGs) and non-esterified fatty acids (NEFAs)) responses under controlled laboratory conditions in shift workers and non-shift workers. Eleven experienced shift workers (35.7+/-7.2 years, mean+/-s.d.) who had worked in shifts for 8.7+/-5.25 years were matched with 13 non-shift workers who had worked for 32.8+/-6.4 years. After an adaptation night and a baseline sleep night, volunteers were kept awake for 30.5 h, followed by a nap (4 h) and recovery sleep. Blood samples were taken prior to and after a standard breakfast following baseline sleep, total sleep deprivation and recovery sleep. Basal TAG levels prior to the standard breakfast were significantly lower after sleep deprivation, indicating higher energy expenditure. Basal NEFA levels were significantly lower after recovery sleep. Postprandial insulin and TAG responses were significantly increased, and the NEFA response was decreased after recovery sleep, suggestive of insulin insensitivity. Although there were no overall significant differences between non-shift workers and shift workers, non-shift workers showed significantly higher basal insulin levels, lower basal NEFA levels, and an increased postprandial insulin and a decreased NEFA response after recovery sleep. In future, the reasons for these inter-group differences are to be investigated.
This study was designed to investigate postprandial responses to a mixed meal in simulated shift work conditions. Nine normal healthy subjects (six males and three females) were studied on two occasions at the same clock time (1330 h) after consuming test meals, first in their normal environment and secondly after a 9 h phase advance (body clock time 2230 h). Plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), triacylglycerol (TAG) and non-esterified fatty acids (NEFAs) were determined at intervals for 6 h after each test meal. Postprandial plasma glucose, insulin, GIP and GLP-1 profiles were evaluated by calculating areas under the curve (AUC) for the first 2 h and the last 4 h of the sampling together with total AUC. Significantly higher postprandial glucose responses (total AUC) were observed after the phase shift than before (AUC 0-360 min, 2.01 (1.51-2.19) vs 1.79 (1.56-2.04) mmol/l.min; P < 0.02; mean (range)). No significant difference was observed when the first 2 h of each response was compared, but significantly higher glucose levels were observed in the last 4 h of the study after the phase shift than before (AUC 120-360 min, 1.32 (1.08-1.42) vs 1.16 (1.00-1.28) mmol/l.min; P < 0.05). Similar results were obtained for insulin (AUC 0-360 min, 81.72 (30.75-124.97) vs 58.98 (28.03-92.57) pmol/l.min; P < 0.01; AUC 120-360 min, 40.73 (16.20-65.25) vs 25.71 (14.25-37.33) pmol/l.min; P < 0.02). No differences were observed in postprandial plasma GIP and GLP-1 responses before and after the phase shift. Postprandial circulating lipid levels were affected by phase shifting. Peak plasma TAG levels occurred 5 h postprandially before the phase shift. Postprandial rises in plasma TAG were significantly delayed after the phase shift and TAG levels continued to rise throughout the study. Plasma postprandial NEFA levels fell during the first 3 h both before and after the phase shift. Their rate of return to basal levels was significantly delayed after the phase shift compared with before. This study demonstrates that a simulated phase shift can significantly alter pancreatic B-cell responses and postprandial glucose and lipid metabolism.
In mammals, circadian oscillators exist not only in the suprachiasmatic nucleus, which harbors the central pacemaker, but also in most peripheral tissues. It is believed that the SCN clock entrains the phase of peripheral clocks via chemical cues, such as rhythmically secreted hormones. Here we show that temporal feeding restriction under light-dark or dark-dark conditions can change the phase of circadian gene expression in peripheral cell types by up to 12 h while leaving the phase of cyclic gene expression in the SCN unaffected. Hence, changes in metabolism can lead to an uncoupling of peripheral oscillators from the central pacemaker. Sudden large changes in feeding time, similar to abrupt changes in the photoperiod, reset the phase of rhythmic gene expression gradually and are thus likely to act through a clock-dependent mechanism. Food-induced phase resetting proceeds faster in liver than in kidney, heart, or pancreas, but after 1 wk of daytime feeding, the phases of circadian gene expression are similar in all examined peripheral tissues.
Circadian rhythms of behavior are driven by oscillators in the brain that are coupled to the environmental light cycle. Circadian
rhythms of gene expression occur widely in peripheral organs. It is unclear how these multiple rhythms are coupled together
to form a coherent system. To study such coupling, we investigated the effects of cycles of food availability (which exert
powerful entraining effects on behavior) on the rhythms of gene expression in the liver, lung, and suprachiasmatic nucleus
(SCN). We used a transgenic rat model whose tissues express luciferase in vitro. Although rhythmicity in the SCN remained
phase-locked to the light-dark cycle, restricted feeding rapidly entrained the liver, shifting its rhythm by 10 hours within
2 days. Our results demonstrate that feeding cycles can entrain the liver independently of the SCN and the light cycle, and
they suggest the need to reexamine the mammalian circadian hierarchy. They also raise the possibility that peripheral circadian
oscillators like those in the liver may be coupled to the SCN primarily through rhythmic behavior, such as feeding.
To explore how metabolic risk factors for cardiovascular disease (CVD) differ between shift workers and day workers in a defined population. Shift work has been associated with an increased risk of CVD. Risk factors and causal pathways for this association are only partly known.
A working population of 27,485 people from the Västerbotten intervention program (VIP) has been analysed. Cross sectional data, including blood sampling and questionnaires were collected in a health survey.
Obesity was more prevalent among shift workers in all age strata of women, but only in two out of four age groups in men. Increased triglycerides (>1.7 mmol/l) were more common among two age groups of shift working women but not among men. Low concentrations of high density lipoprotein (HDL) cholesterol (men<0.9 and women<1.0 mmol/l) were present in the youngest age group of shift workers in both men and women. Impaired glucose tolerance was more often found among 60 year old women shift workers. Obesity and high triglycerides persisted as risk factors in shift working men and women after adjusting for age and socioeconomic factors, with an OR of 1.4 for obesity and 1.1 for high triglyceride concentrations. The relative risks for women working shifts versus days with one, two, and three metabolic variables were 1.06, 1.20, and 1.71, respectively. The corresponding relative risks for men were 0.99, 1.30, and 1.63, respectively.
In this study, obesity, high triglycerides, and low concentrations of HDL cholesterol seem to cluster together more often in shift workers than in day workers, which might indicate an association between shift work and the metabolic syndrome.
The circadian rhythms of many night-shift workers are maladapted to their imposed behavioural schedule, and this factor may be implicated in the increased occurrence of cardiovascular disease (CVD) reported in shift workers. One way in which CVD risk could be mediated is through inappropriate hormonal and metabolic responses to meals. This study investigated the responses to standard meals at different circadian times in a group of night-shift workers on a British Antarctic Survey station at Halley Bay (75 S) in Antarctica. Twelve healthy subjects (ten men and two women) were recruited. Their postprandial hormone and metabolic responses to an identical mixed test meal of 3330 kJ were measured on three occasions: (i) during daytime on a normal working day, (ii) during night-time at the beginning of a period of night-shift work, and (iii) during the daytime on return from nightworking to daytime working. Venous blood was taken for 9 h after the meal for the measurement of glucose, insulin, triacylglycerol (TAG) and non-esterified fatty acids. Urine was collected 4-hourly (longer during sleep) on each test day for assessment of the circadian phase via 6-sulphatoxymelatonin (aMT6s) assay. During normal daytime working, aMT6s acrophase was delayed (7·71·0 h (...)) compared with that previously found in temperate zones in a comparable age-group. During the night shift a further delay was evident (11·81·9 h) and subjects' acrophases remained delayed 2 days after return to daytime working (12·41·8 h). Integrated postprandial glucose, insulin and TAG responses were significantly elevated during the night shift compared with normal daytime working. Two days after their return to daytime working, subjects' postprandial glucose and insulin responses had returned to pre-shift levels; however, integrated TAG levels remained significantly elevated. These results are very similar to those previously found in simulated night-shift conditions; it is the first time such changes have been reported in real shift workers in field conditions. They provide evidence that the abnormal metabolic responses to meals taken at night during unadapted night shifts are due, at least in part, to a relative insulin resistance, which could contribute to the documented cardiovascular morbidity associated with shift work. When applied to the 20% of the UK workforce currently employed on shift work, these findings have major significance from an occupational health perspective.
The circadian rhythms of most night shift workers do not adapt fully to the imposed behavioural schedule, and this factor is considered to be responsible for many of the reported health problems. One way in which such disturbances might be mediated is through inappropriate hormonal and metabolic responses to meals, on the night shift. Twelve healthy subjects (four males and eight females) were studied on three occasions at the same clock time (1330 h), but at different body clock times, after consuming test meals, first in their normal environment, secondly after a forced 9 h phase advance (body clock time approximately 2230 h) and then again 2 days later in the normal environment. They were given a low-fat pre-meal at 0800 h, then a test meal at 1330 h with blood sampling for the following 9 h. Parameters measured included plasma glucose, non-esterified fatty acids (NEFAs), triacylglycerol (TAG), insulin, C-peptide, proinsulin and glucose-dependent insulinotropic polypeptide, and urinary 6-sulphatoxymelatonin. In contrast with a previous study with a high-fat pre-meal, postprandial glucose and insulin responses were not affected by the phase shift. However, basal plasma NEFAs were lower immediately after the phase shift (P<0·05). Incremental (difference from basal) TAG responses were significantly higher (P<0·05) immediately after the phase shift compared with before. Two-day post-phase shift responses showed partial reversion to baseline values. This study suggests that it takes at least 2 days to adapt to eating meals on a simulated night shift, and that the nutritional content of the pre-meals consumed can have a marked effect on postprandial responses during a simulated phase shift. Such findings may provide a partial explanation for the increased occurrence of cardiovascular disease reported in shift workers.
The circadian clock mechanism in animals involves a transcriptional feedback loop in which the bHLH-PAS proteins CLOCK and BMAL1 form a transcriptional activator complex to activate the transcription of the Period and Cryptochrome genes, which in turn feed back to repress their own transcription. In the mouse liver, CLOCK and BMAL1 interact with the regulatory regions of thousands of genes, which are both cyclically and constitutively expressed. The circadian transcription in the liver is clustered in phase and this is accompanied by circadian occupancy of RNA polymerase II recruitment and initiation. These changes also lead to circadian fluctuations in histone H3 lysine4 trimethylation (H3K4me3) as well as H3 lysine9 acetylation (H3K9ac) and H3 lysine27 acetylation (H3K27ac). Thus, the circadian clock regulates global transcriptional poise and chromatin state by regulation of RNA polymerase II.
© 2015 John Wiley & Sons Ltd.
Unlabelled:
Previous studies have suggested that shiftwork can affect the prevalence of metabolic syndrome. This is thought to be related to disturbance of lipid parameters rather than their effects on glucose metabolism. Several complex mechanisms are suspected to be involved and notably insulin resistance, though the available data are limited. The objective of the present study was to provide further evidence for the effects of shiftwork on glucose and lipid metabolism with a specific focus on insulin resistance. A cross-sectional study has recruited 97 shiftworkers (SWs) (three shifts, 8 h) and 95 strictly day workers (DWs) from the same plant for 2001-2002. Several indices of insulin sensitivity or resistance were calculated, based on formulas of the homeostasis model assessment for insulin resistance (HOMA-IR), the Revised-Quicki, McAuley and Disse indices. The HOMA-β-cell index was used as a reflection of pancreatic secretion. Characteristics of the occupation, habitual diet and lifestyles were recorded. Logistic regression analysis in which pancreatic function or insulin sensitivity was the dependent variable was used to compare alternative models.
Results:
SWs were characterized as having significantly higher triglycerides and free fatty acids and normal but lower blood glucose. The risk of a high β-cell activity was increased almost three-fold in SWs. By adjusting for many confounding factors, SWs had significantly lower insulin sensitivity according to several indices, whereas HOMA-IR was not meaningfully different between shift and DWs. Lower insulin sensitivity and a compensatory pancreas response to maintain a normal glucose tolerance may suggest an intermediate state before development of frank insulin resistance in SWs. Early detection of these moderate alterations of the insulin/glucose balance could be important in the prevention of diabetes.
Circadian rhythms are the daily patterns that occur within an organism, from gene expression to behavior. These rhythms are governed not only externally by environmental cues but also internally, with cell-autonomous molecular clock mechanisms present nearly ubiquitously throughout the cells of organisms. In more complex organisms, it has been suggested that the clock mechanisms serve varied functions depending on the tissue in which they are found. By disrupting core circadian gene function in specific tissues of animal models, the various roles of the circadian clock in differing tissues can begin to be defined. This review provides an overview of the model organisms used to elucidate tissue-specific functions of the molecular circadian clock. © 2014 IUBMB Life, 66(1):34-41, 2014.
Context:
Circadian variation is a fundamental characteristic of plasma glucocorticoids, with a postprandial rise in cortisol an important feature. The diurnal rhythm is presumed to reflect alterations in hypothalamic-pituitary-adrenal axis activity; however, cortisol is produced not only by the adrenal glands but also by regeneration from cortisone by the enzyme 11β-hydroxysteroid dehydrogenase type 1, mainly in liver and adipose tissue.
Objective:
We tested the contribution of peripheral cortisol regeneration to macronutrient-induced circadian variation of plasma cortisol in humans.
Design:
This was a randomized, single-blinded, crossover study.
Setting:
The study was conducted at a hospital research facility.
Participants:
Eight normal-weight healthy men participated in the study.
Interventions:
Subjects were given isocaloric energy isodense flavor-matched liquid meals composed of carbohydrate, protein, fat, or low-calorie placebo during infusion of the stable isotope tracer 9,11,12,12-[2H]4-cortisol.
Outcome measures and results:
Plasma cortisol increased similarly after all macronutrient meals (by ∼90 nmol/L) compared with placebo. Carbohydrate stimulated adrenal secretion and extra-adrenal regeneration of cortisol to a similar degree. Protein and fat meals stimulated adrenal cortisol secretion to a greater degree than extra-adrenal cortisol regeneration. The increase in cortisol production by 11β-hydroxysteroid dehydrogenase type 1 was in proportion to the increase in insulin. The postprandial cortisol rise was not accounted for by decreased cortisol clearance.
Conclusions:
Food-induced circadian variation in plasma cortisol is mediated by adrenal secretion and extra-adrenal regeneration of cortisol. Given that the latter has the more potent effect on tissue cortisol concentrations and that effects on adrenal and extra-adrenal cortisol production are macronutrient specific, this novel mechanism may contribute to the physiological interplay between insulin and glucocorticoids and the contrasting effects of certain diets on postprandial metabolism.
Objective:
Few studies examined the association between time-of-day of nutrient intake and the metabolic syndrome. Our goal was to compare a weight loss diet with high caloric intake during breakfast to an isocaloric diet with high caloric intake at dinner.
Design and methods:
Overweight and obese women (BMI 32.4 ± 1.8 kg/m(2) ) with metabolic syndrome were randomized into two isocaloric (~1400 kcal) weight loss groups, a breakfast (BF) (700 kcal breakfast, 500 kcal lunch, 200 kcal dinner) or a dinner (D) group (200 kcal breakfast, 500 kcal lunch, 700 kcal dinner) for 12 weeks.
Results:
The BF group showed greater weight loss and waist circumference reduction. Although fasting glucose, insulin, and ghrelin were reduced in both groups, fasting glucose, insulin, and HOMA-IR decreased significantly to a greater extent in the BF group. Mean triglyceride levels decreased by 33.6% in the BF group, but increased by 14.6% in the D group. Oral glucose tolerance test led to a greater decrease of glucose and insulin in the BF group. In response to meal challenges, the overall daily glucose, insulin, ghrelin, and mean hunger scores were significantly lower, whereas mean satiety scores were significantly higher in the BF group.
Conclusions:
High-calorie breakfast with reduced intake at dinner is beneficial and might be a useful alternative for the management of obesity and metabolic syndrome.
Daily rhythms are evident across our physiology, ranging from overt behavioural patterns like sleep to intricate molecular rhythms in epigenetic coding. Driving these rhythms at an anatomical and cellular level are circadian clock networks comprising core clock genes and an ever-expanding list of clock-controlled genes. Research over the past decade has revealed an intimate relationship between the clockwork and metabolic processes. In line with this, feeding behaviour in many species exhibits a strong circadian rhythm and, when restricted, food becomes the most potent entraining stimulus for clocks of the body. Critically, there are several indications that disturbance of our daily rhythms contributes to the development of obesity and diabetes. Given our 24-h society, it is important that we understand how the circadian clock influences what and when we eat.
The organisation of timing in mammalian circadian clocks optimally coordinates behavior and physiology with daily environmental cycles. Chronic consumption of a high-fat diet alters circadian rhythms, but the acute effects on circadian organisation are unknown. To investigate the proximate effects of a high-fat diet on circadian physiology, we examined the phase relationship between central and peripheral clocks in mice fed a high-fat diet for 1 week. By 7 days, the phase of the liver rhythm was markedly advanced (by 5 h), whereas rhythms in other tissues were not affected. In addition, immediately upon consumption of a high-fat diet, the daily rhythm of eating behavior was altered. As the tissue rhythm of the suprachiasmatic nucleus was not affected by 1 week of high-fat diet consumption, the brain nuclei mediating the effect of a high-fat diet on eating behavior are likely to be downstream of the suprachiasmatic nucleus.
Life on earth has evolved under the daily rhythm of light and dark. Consequently, most creatures experience a daily rhythm in food availability. In this review, we first introduce the mammalian circadian timing system, consisting of a central clock in the suprachiasmatic nucleus (SCN) and peripheral clocks in various metabolic tissues including liver, pancreas, and intestine. We describe how peripheral clocks are synchronized by the SCN and metabolic signals. Second, we review the influence of the circadian timing system on food intake behavior, activity of the gastrointestinal system, and several aspects of glucose and lipid metabolism. Third, the circadian control of digestion and metabolism may have important implications for several aspects of food intake in humans. Therefore, we review the human literature on health aspects of meal timing, meal frequency, and breakfast consumption, and we describe the potential implications of the clock system for the timing of enteral tube feeding and parenteral nutrition. Finally, we explore the connection between type 2 diabetes and the circadian timing system. Although the past decade has provided exciting knowledge about the reciprocal relation between biological clocks and feeding/energy metabolism, future research is necessary to further elucidate this fascinating relationship in order to improve human health.
Objectives The aim of the investigation was to describe situations with a significant influence on healthy diet and exercise habits among nurses working night shift.
Methods A qualitative descriptive design with a Critical Incident Technique approach was used. Situations were collected by means of interviews with 27 registered/enrolled community nurses.
Results A total of 143 situations were identified comprising two main areas: coping ability at work and coping ability during leisure hours. Coping ability at work included 81 critical incidents grouped into two categories: the nurses’ diet and exercise habits were influenced by social interaction with colleagues at work and by the disruption to their circadian rhythm. Coping ability during leisure hours included 62 critical incidents grouped into two categories: the diet and exercise habits were influenced when the nurses recovered from the disruption to their circadian rhythm and when they took advantage of the freedom of action offered by night work.
Conclusions By identifying the factors that influence diet and exercise habits among nurses working night shift, strategies can be developed in order to strengthen the factors with a positive influence.
While diet-induced obesity has been exclusively attributed to increased caloric intake from fat, animals fed a high-fat diet (HFD) ad libitum (ad lib) eat frequently throughout day and night, disrupting the normal feeding cycle. To test whether obesity and metabolic diseases result from HFD or disruption of metabolic cycles, we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day. Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination. The tRF regimen improved CREB, mTOR, and AMPK pathway function and oscillations of the circadian clock and their target genes' expression. These changes in catabolic and anabolic pathways altered liver metabolome and improved nutrient utilization and energy expenditure. We demonstrate in mice that tRF regimen is a nonpharmacological strategy against obesity and associated diseases.
Disruption of circadian rhythms leads to obesity and metabolic disorders. Timed restricted feeding (RF) provides a time cue and resets the circadian clock, leading to better health. In contrast, a high-fat (HF) diet leads to disrupted circadian expression of metabolic factors and obesity. We tested whether long-term (18 wk) clock resetting by RF can attenuate the disruptive effects of diet-induced obesity. Analyses included liver clock gene expression, locomotor activity, blood glucose, metabolic markers, lipids, and hormones around the circadian cycle for a more accurate assessment. Compared with mice fed the HF diet ad libitum, the timed HF diet restored the expression phase of the clock genes Clock and Cry1 and phase-advanced Per1, Per2, Cry2, Bmal1, Rorα, and Rev-erbα. Although timed HF-diet-fed mice consumed the same amount of calories as ad libitum low-fat diet-fed mice, they showed 12% reduced body weight, 21% reduced cholesterol levels, and 1.4-fold increased insulin sensitivity. Compared with the HF diet ad libitum, the timed HF diet led to 18% lower body weight, 30% decreased cholesterol levels, 10% reduced TNF-α levels, and 3.7-fold improved insulin sensitivity. Timed HF-diet-fed mice exhibited a better satiated and less stressed phenotype of 25% lower ghrelin and 53% lower corticosterone levels compared with mice fed the timed low-fat diet. Taken together, our findings suggest that timing can prevent obesity and rectify the harmful effects of a HF diet.
The present study was done to determine whether weight gain was more prevalent in workers on late shifts than in those on day shifts. A questionnaire about changes in weight, food intake, exercise, and sleep since starting the job on the current shift was given to day-shift and late-shift (evening and night) hospital workers. Data were analyzed for 85 subjects, 36 of whom worked during the day shift and 49 the late shift. The late-shift group reported a mean weight gain of 4.3 kg, which was greater than the mean weight gain of 0.9 kg for the day-shift group (P = 0.02). There were, however, no significant differences in current body mass index (26.7 ± 5.4 SD) between groups. There was a trend for late-shift workers to report eating more since beginning the later shift (P = 0.06). When combined with those reporting exercising less (P = NS), this trend became significant (P = 0.04). Late-shift workers reported eating fewer meals (1.9 ± 0.9 SD) than the day-shift workers (2.5 ± 0.9; P = 0.002). In addition, late-shift workers reported eating the last daily meal later (mean = 22:27, or 10:27 pm) than day-shift workers (17:52 or 5:52 pm; P < 0.00005). Late-shift workers also reported more naps (P = 0.01) and longer naps (P = 0.05) during the work week than did day-shift workers. The reported changes in eating, exercise, and sleep may contribute to the increased weight gain of late-shiftworkers.
Cumulative sleep deprivation is often associated with work patterns involving night shift or early morning shifts. Adaptation of the circadian system to the shift pattern is reported to promote improved duration and quality of sleep and a concurrent improvement in performance. The current study followed twenty-nine operators at a live-in mining operation working to a seven-day, seven-night shift pattern who collected saliva samples for melatonin measurement, recorded sleep using activity monitors and diaries, and underwent performance testing (psychomotor vigilance task) for one complete roster cycle. The time of onset of melatonin secretion changed significantly (P=0.022) across the week of both Day and Night shifts (2104 h ± 16 min versus 2130 h ± 16 min, respectively), but the small magnitude of the change indicates a lack of true circadian rhythm adaptation to the lifestyle. Total sleep time was longer following the seventh Day shift (associated with a period of 24 h off prior to the commencement of Night shifts). There were no other changes in total sleep time. Further, there were no improvements in sleep onset latency or sleep efficiency on Day or Night shifts. However, reaction times recorded at the end of the shifts slowed across the seven Day and seven Night shifts indicative of impairments in psychomotor performance (F(6,168)=6.087, P<0.001). The results suggest that previous reports of adaptation to consecutive night shifts cannot necessarily be applied to onshore or Australian environments. Adaptation is dependent on factors such as light exposure, environmental conditions, shift parameters such as wake-up, work start and work end times and individual characteristics.
Leptin is involved in the hormonal regulation of the reproductive, somatotropic, thyroid, and autonomic axes and ultimately in the regulation of energy balance. In parallel to the metabolic adaptation observed in response to caloric restriction (CR), plasma leptin concentrations are substantially decreased, suggesting a role for this hormone in the drop in energy expenditure beyond that predicted by the changes in body composition (metabolic adaptation).
The aim of the study was to explore the changes in 24-h leptin circadian rhythm in response to CR and to investigate the relationship between these changes and metabolic adaptation.
In a randomized, controlled trial (Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy), 48 subjects were assigned to a control group or one of three CR groups for 6 months. Leptin concentration was assessed every 30 min for 24 h, and leptin circadian variations were fitted by Cosinor analysis. Sedentary energy expenditure and urinary catecholamine excretion were measured for 24 h in a metabolic chamber.
Six months of CR decreased body weight by -11.4 ± 0.6% (mean ± sem; P < 0.001). Mean 24-h circulating leptin concentration decreased by -44 ± 3% (P < 0.001), whereas leptin diurnal amplitude slightly increased over the 6 months of CR. CR caused a metabolic adaptation of -126 ± 25 kcal/d (P <0.001) and a significant decrease in urinary norepinephrine (-13 ± 3%) and T(3) concentrations (10 ± 2%). The metabolic adaptation was significantly and independently related to the changes in 24-h leptin (r(2) = 0 .22, P < 0.01) but not to the changes in leptin amplitude.
Our results confirm an important role for leptin as an independent determinant of the metabolic adaptation in response to CR.
Circadian and seasonal rhythms are a fundamental feature of all living organisms and their organelles. Biological rhythms are responsible for daily food intake; the period of hunger and satiety is controlled by the central pacemaker, which resides in the suprachiasmatic nucleus (SCN) of the hypothalamus, and communicates with tissues via bidirectional neuronal and humoral pathways. The molecular basis for circadian timing in the gastrointestinal tract (GIT) involves interlocking transcriptional/translational feedback loops which culminate in the rhythmic expression and activity of a set of clock genes and related hormones. Interestingly, it has been found that clocks in the GIT are responsible for the periodic activity (PA) of its various segments and transit along the GIT; they are localized in special interstitial cells, with unstable membrane potentials located between the longitudinal and circular muscle layers. The rhythm of slow waves is controlled in various segments of the GIT: in the stomach (about 3 cycles per min), in the duodenum (12 cycle per min), in the jejunum and ileum (from 7 to 10 cycles per min), and in the colon (12 cycles per min). The migrating motor complex (MMC) starts in the stomach and moves along the gut causing peristaltic contractions when the electrical activity spikes are superimposed on the slow waves. GIT hormones, such as motilin and ghrelin, are involved in the generation of MMCs, while others (gastrin, ghrelin, cholecystokinin, serotonin) are involved in the generation of spikes upon the slow waves, resulting in peristaltic or segmental contractions in the small (duodenum, jejunum ileum) and large bowel (colon). Additionally, melatonin, produced by neuro-endocrine cells of the GIT mucosa, plays an important role in the internal biological clock, related to food intake (hunger and satiety) and the myoelectric rhythm (produced primarily by the pineal gland during the dark period of the light-dark cycle). This appears to be an endocrine encoding of the environmental light-dark cycle, conveying photic information which is used by organisms for both circadian and seasonal organization. Motor and secretory activity, as well as the rhythm of cell proliferation in the GIT and liver, are subject to many circadian rhythms, mediated by autonomic cells and some enterohormones (gastrin, ghrelin and somatostatin). Disruption of circadian physiology, due to sleep disturbance or shift work, may result in various gastrointestinal diseases, such as irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD) or peptic ulcer disease. In addition, circadian disruption accelerates aging, and promotes tumorigenesis in the liver and GIT. Identification of the molecular basis and role of melatonin in the regulation of circadian rhythm allows researchers and clinicians to approach gastrointestinal diseases from a chronobiological perspective. Clinical studies have demonstrated that the administration of melatonin improves symptoms in patients with IBS and GERD. Moreover, our own studies indicate that melatonin significantly protects gastrointestinal mucosa, and has strong protective effects on the liver in patients with non-alcoholic steatohepatitis (NASH). Recently, it has been postulated that disruption of circadian regulation may lead to obesity by shifting food intake schedules. Future research should focus on the role of clock genes in the pathophysiology of the GIT and liver.
Sleep duration has been linked to obesity and there is also an emerging literature in animals demonstrating a relationship between the timing of feeding and weight regulation. However, there is a paucity of research evaluating timing of sleep and feeding on weight regulation in humans. The goal of this study was to evaluate the role of sleep timing in dietary patterns and BMI. Participants included 52 (25 females) volunteers who completed 7 days of wrist actigraphy and food logs. Fifty-six percent were "normal sleepers" (midpoint of <5:30 AM) and 44% were "late sleepers" (midpoint of sleep ≥5:30 AM). Late sleepers had shorter sleep duration, later sleep onset and sleep offset and meal times. Late sleepers consumed more calories at dinner and after 8:00 PM, had higher fast food, full-calorie soda and lower fruit and vegetable consumption. Higher BMI was associated with shorter sleep duration, later sleep timing, caloric consumption after 8:00 PM, and fast food meals. In multivariate models, sleep timing was independently associated with calories consumed after 8:00 PM and fruit and vegetable consumption but did not predict BMI after controlling for sleep duration. Calories consumed after 8:00 PM predicted BMI after controlling for sleep timing and duration. These findings indicate that caloric intake after 8:00 PM may increase the risk of obesity, independent of sleep timing and duration. Future studies should investigate the biological and social mechanisms linking timing of sleep and feeding in order to develop novel time-based interventions for weight management.
Our aim was to review published literature on the association between shift work and gastrointestinal (GI) disorders.
A systematic review of the literature was conducted of studies that have reported GI symptoms and diseases among shift workers. We used Medline to search for articles from 1966-2009. Next, we manually searched articles in the reference list of each article and previous reviews.
Twenty studies met the inclusion criteria. Four of six studies showed a significant association between shift work and GI symptoms, and five of six studies reported an association between shift work and peptic ulcer disease. Two of three studies showed an association between shift work and functional GI disease. Only a few studies have examined gastroesophageal reflux disease, chronic inflammatory bowel diseases, or GI cancers in relation to shift work.
Our general judgment is that shift workers appear to have increased risk of GI symptoms and peptic ulcer disease. However, control for potential confounders (eg, smoking, age, socioeconomic status, and other risk factors) was often lacking or insufficient in many of the studies we examined.
Obesity has become a serious public health problem and a major risk factor for the development of illnesses, such as insulin resistance and hypertension. Human homeostatic systems have adapted to daily changes in light and dark in a way that the body anticipates the sleep and activity periods. Mammals have developed an endogenous circadian clock located in the suprachiasmatic nuclei of the anterior hypothalamus that responds to the environmental light-dark cycle. Similar clocks have been found in peripheral tissues, such as the liver, intestine, and adipose tissue, regulating cellular and physiological functions. The circadian clock has been reported to regulate metabolism and energy homeostasis in the liver and other peripheral tissues. This is achieved by mediating the expression and/or activity of certain metabolic enzymes and transport systems. In return, key metabolic enzymes and transcription activators interact with and affect the core clock mechanism. In addition, the core clock mechanism has been shown to be linked with lipogenic and adipogenic pathways. Animals with mutations in clock genes that disrupt cellular rhythmicity have provided evidence for the relationship between the circadian clock and metabolic homeostasis. In addition, clinical studies in shift workers and obese patients accentuate the link between the circadian clock and metabolism. This review will focus on the interconnection between the circadian clock and metabolism, with implications for obesity and how the circadian clock is influenced by hormones, nutrients, and timed meals.
The molecular basis for biological rhythms is formed by clock genes. Clock genes are functional in the liver, within gastrointestinal epithelial cells and neurons of the enteric nervous system. These observations suggest a possible role for clock genes in various circadian functions of the liver and the gastrointestinal tract through the modulation of organ specific clock-controlled genes. Consequently, disruptions in circadian rhythmicity may lead to adverse health consequences. This review will focus on the current understanding of the role of circadian rhythms in the pathogenesis of gastrointestinal- and hepatic disease such as obesity, non-alcoholic fatty liver disease, alcoholic fatty liver disease and alterations in colonic motility.
High-fat feeding in rodents leads to metabolic abnormalities mimicking the human metabolic syndrome, including obesity and insulin resistance. These metabolic diseases are associated with altered temporal organization of many physiological functions. The master circadian clock located in the suprachiasmatic nuclei controls most physiological functions and metabolic processes. Furthermore, under certain conditions of feeding (hypocaloric diet), metabolic cues are capable of altering the suprachiasmatic clock's responses to light. To determine whether high-fat feeding (hypercaloric diet) can also affect resetting properties of the suprachiasmatic clock, we investigated photic synchronization in mice fed a high-fat or chow (low-fat) diet for 3 months, using wheel-running activity and body temperature rhythms as daily phase markers (i.e. suprachiasmatic clock's hands). Compared with the control diet, mice fed with the high-fat diet exhibited increased body mass index, hyperleptinaemia, higher blood glucose, and increased insulinaemia. Concomitantly, high-fat feeding led to impaired adjustment to local time by photic resetting. At the behavioural and physiological levels, these alterations include slower rate of re-entrainment of behavioural and body temperature rhythms after 'jet-lag' test (6 h advanced light-dark cycle) and reduced phase-advancing responses to light. At a molecular level, light-induced phase shifts have been correlated, within suprachiasmatic cells, with a high induction of c-FOS, the protein product of immediate early gene c-fos, and phosphorylation of the extracellular signal-regulated kinases I/II (P-ERK). In mice fed a high-fat diet, photic induction of both c-FOS and P-ERK in the suprachiasmatic nuclei was markedly reduced. Taken together, the present data demonstrate that high-fat feeding modifies circadian synchronization to light.
To study the impact of work hours on eating habits the dietary intake of 96 male industrial workers on day work and two- and three-shift work was investigated using repeated 24 h recall. The intake of energy, 14 nutrients, and coffee and tea was computed, using a nutrient data base, for 8 h work and shifts (day, morning, afternoon, night) and for the 24-h periods including these work shifts. No changes in intake of energy, nutrients and coffee/tea were observed between 8 h morning and afternoon shifts, but there was a reduction in intake during 8 h night shifts. Night shift work caused a redistribution of food and coffee intake, but not an overall 24 h reduction. On the whole, the energy-intake and the quality of food intake (percentages of energy from macronutrients and density of micronutrients) were not affected by shift work, although the intake of carbohydrates was lower in day- and three-shift workers during days off. The intake of alcohol was higher during days off in all groups. In summary, two- and three-shift work in this study affected the circadian distribution of food intakes and coffee consumption, but not the overall 24-h consumption.
Human interdigestive intestinal motility follows a circadian rhythm with reduced nocturnal activity, but circadian pancreatic exocrine secretion is unknown. To determine whether circadian changes in interdigestive pancreatic secretion occur and are associated with motor events, pancreatic enzyme outputs, proximal jejunal motility, and plasma pancreatic polypeptide concentrations were measured during consecutive daytime and nighttime periods (12 h each) in seven healthy volunteers using orojejunal multilumen intubation. Studies were randomly started in the morning or evening. Nocturnally, motility decreased (motor quiescence: 67 +/- 22 vs. 146 +/- 37 min; motility index: 3.59 +/- 0.33 vs. 2.78 +/- 0.40 mmHg/min; both P < 0.05) but amylase output increased (273 +/- 78 vs. 384 +/- 100 U/min; P < 0.05) and protease output remained unchanged (P > 0.05); consequently, enzyme/motility ratio increased. Amylase outputs were always lowest during phase I. Motor but not pancreatic circadian activities were associated with sleep. Pancreatic polypeptide plasma concentrations were unchanged. Consequently, intestinal motor and pancreatic exocrine functions may have different circadian rhythms, i.e., decreased motor and stable secretory activity during the night. However, the association between individual phases of interdigestive motor and secretory activity is preserved. The nocturnal increase in enzyme/motility ratio is probably not caused by increased cholinergic tone.
Based on a 4-day questionnaire survey for all meals and snacks consumed by female workers in a computer factory in Japan, consisting of 44 daytime workers and 93 weekly-rotating shift workers (of whom 47 and 46 were engaged in, respectively, early-shift work and late-shift work during the survey week), the present study aimed to clarify the effects of shift work on their nutrient intakes in association with food consumption patterns. Their dietary intakes for 3 working days and an off day were assessed by self-registered food consumption records with the aid of a photographic method, and intakes of energy, protein, fat, carbohydrate, calcium and iron were estimated. The inter-group differences were prominent in the working days. The shift workers, particularly the late-shift workers, took smaller amounts of energy and nutrients than the daytime workers, implying that the former group's nutritional status has been worsened, judged from the recommended dietary allowance for Japanese. Their inadequate nutrient intake was due to lower meal frequency and poor meal quality, both of which were conditioned by shift work.
With increasing economic and social demands, we are rapidly evolving into a 24-h society. In any urban economy, about 20% of the population are required to work outside the regular 0800-1700 h working day and this figure is likely to increase. Although the increase in shiftwork has led to greater flexibility in work schedules, the ability to provide goods and services throughout the day and night, and possibly greater employment opportunities, the negative effects of shiftwork and chronic sleep loss on health and productivity are now being appreciated. For example, sleepiness surpasses alcohol and drugs as the greatest identifiable and preventable cause of accidents in all modes of transport. Industrial accidents associated with night work are common, perhaps the most famous being Chernobyl, Three Mile Island, and Bhopal.