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Our study aimed to investigate the relationship between sleep–wake changes and depressive symptoms events among midlife women. We enrolled 1579 women aged 44–56 years who had no clinically relevant depressive symptoms at baseline. Depressive symptoms were assessed at each visit using the Center for Epidemiologic Studies Depression scale. At the third and fourth follow-up visits, women reported their sleep habits. The sleep midpoint was defined as the time to fall asleep plus one-half of the sleep duration. Sleep–wake changes were determined by the difference in the midpoint of sleep between the third and fourth visits, which were 1 year apart. The median follow-up time was 7 years (range 1–7 years). Cox proportional hazard models were fitted to calculate hazard ratios and 95% confidence intervals for the incidence of depressive symptoms associated with sleep–wake changes. After adjusting for potential confounding factors, the hazard ratio (95% confidence interval) of depressive symptoms for severe sleep midpoint changes was 1.51 (1.12, 2.05) compared with mild sleep midpoint changes. This relationship remained statistically significant and changed little when additionally controlling for sleep duration, sleep quality, insomnia symptoms, use of sleep medications, use of nervous medications, glucose, insulin, lipids, dietary energy intake, and C-reactive protein. Our findings indicate that exposure to long-term severe sleep–wake changes increases the risk of depressive symptoms in midlife women. [ABSTRACT FROM AUTHOR]

Sleep is rigorously controlled by circadian rhythms, and any discrepancy between these rhythms and the external environment might result in circadian rhythm sleep disorders. Circadian rhythm sleep disturbances (CRSDs) are linked to detrimental health outcomes, including cancer and psychiatric illnesses. This systematic literature review explores the significance of disturbances of sleep and circadian rhythm. A systematic literature survey was conducted using PubMed, Scopus, Web of Science, Embase, and Cochrane Library databases. We used the following search terms: "Circadian clock," "sleep," "Circadian rhythm," sleep disorders," "drugs to cure sleep and circadian rhythm," and "CRSD." for articles published between 2018 and 2023. This comprehensive review presents evidence from human research to assess the concept that sleep and circadian rhythms have direct effects on physiological processes in the human body and are significant underlying factors contributing to major health concerns. The first part of this review focussed on sleep and circadian rhythm, circadian clock and effects of altered metabolism." The second part discussed recent evidence that the circadian clock system plays a fundamental rolein health risk, adverse effects on health, and their connection with disturbances of sleep and circadian rhythm. These research lines are still in their early stages, but they have nonetheless established a conceptual framework that could be highly significant for comprehending metabolic health and illness. [ABSTRACT FROM AUTHOR]

Sleep and circadian rhythms are observed broadly throughout animal phyla and influence neural plasticity and cognitive function. However, the few phylogenetically conserved cellular and molecular pathways that are implicated in these processes are largely focused on neuronal cells. Research on these topics has traditionally segregated sleep homeostatic behavior from circadian restactivity rhythms. Here we posit an alternative perspective, whereby mechanisms underlying the integration of sleep and circadian rhythms that affect behavioral state, plasticity, and cognition reside within glial cells. The brain-type fatty acid binding protein, FABP7, is part of a larger family of lipid chaperone proteins that regulate the subcellular trafficking of fatty acids for a wide range of cellular functions, including gene expression, growth, survival, inflammation, and metabolism. FABP7 is enriched in glial cells of the central nervous system and has been shown to be a clock-controlled gene implicated in sleep/wake regulation and cognitive processing. FABP7 is known to affect gene transcription, cellular outgrowth, and its subcellular localization in the fine perisynaptic astrocytic processes (PAPs) varies based on time-of-day. Future studies determining the effects of FABP7 on behavioral state- and circadian-dependent plasticity and cognitive processes, in addition to functional consequences on cellular and molecular mechanisms related to neural-glial interactions, lipid storage, and blood brain barrier integrity will be important for our knowledge of basic sleep function. Given the comorbidity of sleep disturbance with neurological disorders, these studies will also be important for our understanding of the etiology and pathophysiology of how these diseases affect or are affected by sleep. [ABSTRACT FROM AUTHOR]

Circadian rhythms are generated by the circadian clock, a self-sustained internal timing system that exhibits 24-h rhythms in the body. Many metabolic, cellular, behavioral and physiological processes are regulated by the circadian clock in coordination with environmental cues. The present study is a comprehensive review of the currently existing evidence concerning the relationship between circadian rhythms and sleep, metabolic, and cardiovascular disorders. We thoroughly searched the online databases PubMed, Scopus, and Web of Science to find the existing clinical studies from the last twenty-three years (2000–2023). Circadian misalignment was found to be associated with an increase in the risk of metabolic disorders, cardiovascular diseases, and obesity, as well as inadequate sleep quality. In this review article, all the included studies had a strength protocol design and all of them were conducted on humans. However, the most common limitations of them were the small sample size and the short time of the intervention. In conclusion, managing the factors that disrupt the optimal function of central and peripheral clocks can help to reduce the risk of metabolic and cardiovascular diseases, improving also sleep quality. Future studies should further explore the underlying mechanisms of the interconnections between circadian clocks and sleep, metabolic, and cardiovascular disorders. This may provide new opportunities for advance chronotherapy approach. [ABSTRACT FROM AUTHOR]

This article, titled "Editorial: Circadian rhythm in cellular endocrinology," discusses the relationship between circadian rhythms and endocrine functions. The circadian clock, an intrinsic timekeeping mechanism, regulates the expression of clock-controlled genes in a tissue-specific manner. Hormonal systems, such as glucocorticoids and melatonin, are subject to circadian regulation and play a role in synchronizing cellular clocks. The article also highlights the impact of circadian rhythms on cardiovascular health, stress responses, and metabolic disorders. Understanding the interaction between circadian and endocrine systems can contribute to the development of therapeutic strategies for various disorders. [Extracted from the article]

Accumulating data have demonstrated that shift work causes a disturbance in circadian rhythms, which is detrimental to physiology and performance. However, the detailed effects of shift work and especially the underlying mechanisms remain to be further investigated. Frequently shifting schedules are widely used in industries, e.g., maritime tasks, oil mining, and aviation. In this work, we investigated the physiological changes and vigilance of 12 subjects who lived on a 30-day frequent shift working schedule in a confined environment, which mimics the common maritime schedules. Elevated and decreased cortisol levels were observed at different stages during the shift, suggesting the occurrence of stress and fatigue. The results of the Karolinska Sleepiness Scale (KSS) indicate increased sleepiness and a changed pattern of the rhythmicity of sleepiness during the shift. The tests of the Psychomotor Vigilance Task (PVT) reveal that the shift led to a continuously decreasing alertness as the shift working schedule progressed, which is prevalently due to the increasingly slower reaction speed. The PVT time-out errors were significantly increased in the early period but decreased in the late period. In addition, we found recoupling of the correlations between multiple physiological and cognitive variables. For instance, heartbeat rate (HR) and breath rate (BR) showed moderate correlations in the control and early periods but little in the late period. Together, these results reveal substantial alterations in diurnal rhythms, affected vigilance and changed coupling of the correlations of diurnal rhythms, physiology and cognition caused by a shift schedule. Our findings may help in the recognition of the detrimental effects of such working schedules and provide clues for the development of potential mitigations. [ABSTRACT FROM AUTHOR]

Adverse childhood experiences (ACEs), which can include child trafficking, are known to program children for disrupted biological cycles, premature aging, microbiome dysbiosis, immune-inflammatory misregulation, and chronic disease multimorbidity. To date, the microbiome has not been a major focus of deprogramming efforts despite its emerging role in every aspect of ACE-related dysbiosis and dysfunction. This article examines: (1) the utility of incorporating microorganism-based, anti-aging approaches to combat ACE-programmed chronic diseases (also known as noncommunicable diseases and conditions, NCDs) and (2) microbiome regulation of core systems biology cycles that affect NCD comorbid risk. In this review, microbiota influence over three key cyclic rhythms (circadian cycles, the sleep cycle, and the lifespan/longevity cycle) as well as tissue inflammation and oxidative stress are discussed as an opportunity to deprogram ACE-driven chronic disorders. Microbiota, particularly those in the gut, have been shown to affect host–microbe interactions regulating the circadian clock, sleep quality, as well as immune function/senescence, and regulation of tissue inflammation. The microimmunosome is one of several systems biology targets of gut microbiota regulation. Furthermore, correcting misregulated inflammation and increased oxidative stress is key to protecting telomere length and lifespan/longevity and extending what has become known as the healthspan. This review article concludes that to reverse the tragedy of ACE-programmed NCDs and premature aging, managing the human holobiont microbiome should become a routine part of healthcare and preventative medicine across the life course. [ABSTRACT FROM AUTHOR]