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Abstract

Night work increases diabetes risk. Misalignment between the central circadian “clock” and daily behaviors, typical in night workers, impairs glucose tolerance, likely due to internal misalignment between central and peripheral circadian rhythms. Whether appropriate circadian alignment of eating can prevent internal circadian misalignment and glucose intolerance is unknown. In a 14-day circadian paradigm, we assessed glycemic control during simulated night work with either nighttime or daytime eating. Assessment of central (body temperature) and peripheral (glucose and insulin) endogenous circadian rhythms happened during constant routine protocols before and after simulated night work. Nighttime eating led to misalignment between central and peripheral (glucose) endogenous circadian rhythms and impaired glucose tolerance, whereas restricting meals to daytime prevented it. These findings offer a behavioral approach to preventing glucose intolerance in shift workers.

https://www.science.org/doi/10.1126/sciadv.abg9910

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Abstract

Particular working conditions and/or organization of working time may cause important sleep disturbances that have been proposed to be predictive of cognitive decline. In this regard, circadian rhythm misalignment induced by exposure to night work or long working hours would be responsible for cognitive impairment. Nevertheless, evidence supporting this correlation is limited and several issues still need to be elucidated. In this regard, we conducted a systematic review to evaluate the association between shift/night work and cognitive impairment and address its main determinants. Information provided by the reviewed studies suggested that night work might have serious immediate negative effects especially on cognitive domains related to attention, memory and response inhibition. Furthermore, cognitive performance would progressively worsen over consecutive night shifts or following exposure to very long work shifts. Otherwise, conflicting results emerged regarding the possible etiological role that night work chronic exposure would have on cognitive impairment. Therefore, circadian rhythm desynchronization, lack of sleep and fatigue resulting from night work may negatively impact worker’s cognitive efficiency. However, in light of the considerable methodological variability of the reviewed studies, we proposed to develop a standardized research and evaluation strategy in order to obtain a better and comprehensive understanding of this topic.

https://www.mdpi.com/1660-4601/18/12/6540

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Abstract

Sleep deprivation is highly prevalent and is associated with increased cardiovascular disease (CVD) morbidity and mortality. Age-related alterations in sleep and chronobiology may exaggerate CVD susceptibility in older individuals. The mechanisms responsible for the association between sleep deprivation and CVD are not fully understood, but endothelial dysfunction may play a central role. Our objective was to conduct a systematic literature review to evaluate the evidence on the effects of sleep deprivation on endothelial function (EF). This review adhered to the PRISMA guidelines and was pre-registered with PROSPERO (#CRD42020192485, 07/24/2020). We searched PubMed, Web of Science, Embase, and Cochrane Library for articles published through May 1, 2020. Eligibility criteria included publication in English and use of well-established EF methodologies in adult humans. Two investigators independently performed the literature search, study selection, data extraction, risk-of-bias assessment, and qualitative data synthesis. Out of 3571 articles identified, 24 articles were included in the systematic review. Main findings include the following: (1) shorter sleep duration is associated with lower macrovascular EF; (2) not sleeping 7–9 h/night is linked with impaired microvascular EF; (3) sleep restriction impairs micro- and macrovascular EF; (4) acute total sleep deprivation impairs micro- and macrovascular EF but data on macrovascular EF are less consistent; and (5) shift work impairs macrovascular EF. In conclusion, sleep deprivation impairs EF, which may explain the link between insufficient sleep and CVD. Future investigations should fully elucidate the underlying mechanisms and develop strategies to combat the adverse endothelial effects of sleep deprivation across the lifespan.

https://link.springer.com/article/10.1007/s11357-020-00312-y

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Abstract

Insulin resistance is a main determinant in the development of type 2 diabetes mellitus and a major cause of morbidity and mortality. The circadian timing system consists of a central brain clock in the hypothalamic suprachiasmatic nucleus and various peripheral tissue clocks. The circadian timing system is responsible for the coordination of many daily processes, including the daily rhythm in human glucose metabolism. The central clock regulates food intake, energy expenditure and whole-body insulin sensitivity, and these actions are further fine-tuned by local peripheral clocks. For instance, the peripheral clock in the gut regulates glucose absorption, peripheral clocks in muscle, adipose tissue and liver regulate local insulin sensitivity, and the peripheral clock in the pancreas regulates insulin secretion. Misalignment between different components of the circadian timing system and daily rhythms of sleep–wake behaviour or food intake as a result of genetic, environmental or behavioural factors might be an important contributor to the development of insulin resistance. Specifically, clock gene mutations, exposure to artificial light–dark cycles, disturbed sleep, shift work and social jet lag are factors that might contribute to circadian disruption. Here, we review the physiological links between circadian clocks, glucose metabolism and insulin sensitivity, and present current evidence for a relationship between circadian disruption and insulin resistance. We conclude by proposing several strategies that aim to use chronobiological knowledge to improve human metabolic health.

Key points

• The circadian timing system consists of a central brain clock in the hypothalamic suprachiasmatic nucleus and peripheral clocks in tissues, including the liver, muscle, adipose tissue and pancreas.
• Misalignment between different components of the circadian timing system and daily rhythms of sleep–wake behaviour and food intake might contribute to the development of insulin resistance.
• Strategies to improve metabolic health by circadian synchrony include modulating light exposure, modulating rhythmic behaviour and chronotherapy.
• Circadian molecules are a promising new treatment option for insulin resistance.

https://www.nature.com/articles/s41574-018-0122-1

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Abstract

Circadian rhythmicity is an approximately 24-h cell-autonomous period driven by transcription–translation feedback loops of specific genes, which are referred to as ‘circadian clock genes’. In mammals, the central circadian pacemaker, which is located in the hypothalamic suprachiasmatic nucleus, controls peripheral circadian clocks. The circadian system regulates virtually all physiological processes, which are further modulated by changes in the external environment, such as light exposure and the timing of food intake. Chronic circadian disruption caused by shift work, travel across time zones or irregular sleep–wake cycles has long-term consequences for our health and is an important lifestyle factor that contributes to the risk of obesity, type 2 diabetes mellitus and cancer. Although the hypothalamic–pituitary–thyroid axis is under the control of the circadian clock via the suprachiasmatic nucleus pacemaker, daily TSH secretion profiles are disrupted in some patients with hypothyroidism and hyperthyroidism. Disruption of circadian rhythms has been recognized as a perturbation of the endocrine system and of cell cycle progression. Expression profiles of circadian clock genes are abnormal in well-differentiated thyroid cancer but not in the benign nodules or a healthy thyroid. Therefore, the characterization of the thyroid clock machinery might improve the preoperative diagnosis of thyroid cancer.

Key points

• The hypothalamic–pituitary–thyroid axis is controlled by the central circadian pacemaker located in the suprachiasmatic nucleus.
• Daily TSH secretion profiles are often disrupted in patients with hypothyroidism or hyperthyroidism.
• Circadian dysfunction caused by shift work, travel across time zones or irregular sleep–wake cycles might be a novel lifestyle risk factor for disturbances in thyroid homeostasis in modern societies.
• Disruption of circadian clock genes in vivo and in vitro disturbs cell cycle progression.
• The circadian clock is thought to be disrupted in well-differentiated thyroid cancer.

https://www.nature.com/articles/s41574-019-0237-z

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Abstract

The molecular circadian clock and symbiotic host-microbe relationships both evolved as mechanisms that enhance metabolic responses to environmental challenges. The gut microbiome benefits the host by breaking down diet-derived nutrients indigestible by the host and generating microbiota-derived metabolites that support host metabolism. Similarly, cellular circadian clocks optimize organismal physiology to the environment by influencing the timing and coordination of metabolic processes. Host-microbe interactions are influenced by dietary quality and timing, as well as daily light/dark cycles that entrain circadian rhythms in the host. Together, the gut microbiome and the molecular circadian clock play a coordinated role in neural processing, metabolism, adipogenesis, inflammation, and disease initiation and progression. This review examines the bidirectional interactions between the circadian clock, gut microbiota, and host metabolic systems and their effects on obesity and energy homeostasis. Directions for future research and the development of therapies that leverage these systems to address metabolic disease are highlighted.

Extract:

Our findings support the hypothesis that poor host metabolic outcomes are the result of asynchronous feeding signals, out of coordination with the light entrained circadian clock-driven anticipatory mechanisms regulating nutrient absorption and utilization, which may indirectly affect GM composition throughout the day. Small, achievable changes in behavior (e.g., changing timing of macronutrient consumption and improved sleep hygiene) that modulate GM signaling may harness innate biology to overcome the obesogenic environment that imposes a potential detriment to human health.

Publication History

Published online: March 30, 2021

Identification

DOI: https://doi.org/10.1016/j.cmet.2021.03.015

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Highlights

Although circadian rhythm disruption (CRD) was typically considered to be a risk for chronic diseases solely for shift workers (∼20% of workforce), new epidemiological data suggest more than 80% of the population may be living a shift work lifestyle and thus are at elevated risk for chronic diseases.

Acute CRD compromises health with temporary physical challenges and may be a trigger for underlying latent diseases. Chronic CRD raises the risk for cancer along with a range of diseases affecting the central nervous system, immune and reproductive systems, metabolic organs, endocrine functions, and cardiovascular health.

Recent progress in understanding the molecular mechanisms of circadian timing and diurnal rhythms of tissue-specific gene products has generated testable hypotheses for how the circadian timing system optimizes health and, conversely, how circadian disruption leads to diseases.

Leveraging circadian rhythms to prevent, manage, and treat diseases involves three major strategies: optimizing the circadian lifestyle (‘training the clock’), optimizing timing of therapies (‘clocking the drugs’), and targeting specific circadian clock components (‘drugging the clock’).

Daily rhythms in behavior, physiology, and metabolism are an integral part of homeostasis. These rhythms emerge from interactions between endogenous circadian clocks and ambient light-dark cycles, sleep-activity cycles, and eating-fasting cycles. Nearly the entire primate genome shows daily rhythms in expression in tissue- and locus-specific manners. These molecular rhythms modulate several key aspects of cellular and tissue function with profound implications in public health, disease prevention, and disease management. In modern societies light at night disrupts circadian rhythms, leading to further disruption of sleep-activity and eating-fasting cycles. While acute circadian disruption may cause transient discomfort or exacerbate chronic diseases, chronic circadian disruption can enhance risks for numerous diseases. The molecular understanding of circadian rhythms is opening new therapeutic frontiers placing the circadian clock in a central role. Here, we review recent advancements on how to enhance our circadian clock through behavioral interventions, timing of drug administration, and pharmacological targeting of circadian clock components that are already providing new preventive and therapeutic strategies for several diseases, including metabolic syndrome and cancer.

https://www.sciencedirect.com/science/article/abs/pii/S0165614718301196

© 2018 Elsevier Ltd. All rights reserved.

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Abstract

Electrical activity in the heart exhibits 24-hour rhythmicity, and potentially fatal arrhythmias are more likely to occur at specific times of day. Here, we demonstrate that circadian clocks within the brain and heart set daily rhythms in sinoatrial (SA) and atrioventricular (AV) node activity, and impose a time-of–day dependent susceptibility to ventricular arrhythmia. Critically, the balance of circadian inputs from the autonomic nervous system and cardiomyocyte clock to the SA and AV nodes differ, and this renders the cardiac conduction system sensitive to decoupling during abrupt shifts in behavioural routine and sleep-wake timing. Our findings reveal a functional segregation of circadian control across the heart’s conduction system and inherent susceptibility to arrhythmia.

Extract

It is clear that long-term shift work is associated with an elevated risk of cardiovascular disease, the incidence of cardiac events, and altered electrophysiological parameters^{15,45,46,47,48}. Whether alteration of cardiac conduction parameters during mistimed sleep and shift-work routines increases susceptibility to arrhythmia or other harmful cardiac events in otherwise healthy humans is not yet clear. Nevertheless, it is likely to be of important clinical consideration in patients with pre-existing cardiac dysfunction or injury, as well as in relation to ECG-based diagnoses and pharmacological intervention, where the time of day, patient occupation, and/or sleep–wake history may significantly impact the outcome. Moreover, we show that susceptibility to VT was rarely observed upon cardiomyocyte Bmal1 deletion, indicating that the circadian clock drives increased excitability during the active period of the day at the cost of creating vulnerability to arrhythmias. This suggests that clock function within the heart contributes to the long-known temporal variation in cardiac arrhythmia propensity observed in humans. Given the widespread influence of the circadian clock and established detrimental consequences of clock disruption, any clock-directed intervention must be approached with caution. Nevertheless, our findings offer an important and logical new avenue for therapeutic investigation.

https://www.nature.com/articles/s41467-021-22788-8

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Abstract

Background—In 2019, the IARC concluded that “night shift work is probably carcinogenic to humans (Group 2A), based on limited evidence from human epidemiological studies and sufficient evidence of cancer and strong mechanistic evidence in experimental Animals.” The negative health consequences of night shift work may depend on how the night shifts are scheduled. The aim of this study was to investigate how the characteristics of night work affect the risk of developing breast cancer. Methods—A case–control study was conducted in 2015–2019 in the Lodz region. The case group included 494 women with breast cancer, while the control group included 515 healthy women. Results—Night work was found to be the third most important factor regarding breast cancer after a high BMI and a short or no breastfeeding period and before factors such as early menstruation, late menopause, no pregnancy, and smoking. The harmful effects of night work were influenced by its intensity, frequency, rotation, and the number of night shift years worked. Night work increases the breast cancer risk by 2.34 times, and high-intensity night work increases the breast cancer risk by 2.66 times. Conclusions—Appropriate ergonomic recommendations for night shift work for employers should be considered.

https://www.mdpi.com/1660-4601/18/9/4570/htm

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