scholarly journals Role of sleep deprivation in immune-related disease risk and outcomes

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Sergio Garbarino ◽  
Paola Lanteri ◽  
Nicola Luigi Bragazzi ◽  
Nicola Magnavita ◽  
Egeria Scoditti
Keyword(s):  
Sleep Deprivation ◽  
Disease Risk ◽  
Epidemiological Studies ◽  
Adaptive Immune ◽  
Adverse Health Outcomes ◽  
Immune Parameters ◽  
Increased Risk ◽  
Inflammatory State ◽  
Immune Changes

AbstractModern societies are experiencing an increasing trend of reduced sleep duration, with nocturnal sleeping time below the recommended ranges for health. Epidemiological and laboratory studies have demonstrated detrimental effects of sleep deprivation on health. Sleep exerts an immune-supportive function, promoting host defense against infection and inflammatory insults. Sleep deprivation has been associated with alterations of innate and adaptive immune parameters, leading to a chronic inflammatory state and an increased risk for infectious/inflammatory pathologies, including cardiometabolic, neoplastic, autoimmune and neurodegenerative diseases. Here, we review recent advancements on the immune responses to sleep deprivation as evidenced by experimental and epidemiological studies, the pathophysiology, and the role for the sleep deprivation-induced immune changes in increasing the risk for chronic diseases. Gaps in knowledge and methodological pitfalls still remain. Further understanding of the causal relationship between sleep deprivation and immune deregulation would help to identify individuals at risk for disease and to prevent adverse health outcomes.

scholarly journals Occupational Exposure and Multiple Myeloma Risk: An Updated Review of Meta-Analyses

2021 ◽  
Vol 10 (18) ◽  
pp. 4179
Author(s):  
Rebecca Georgakopoulou ◽  
Oraianthi Fiste ◽  
Theodoros N. Sergentanis ◽  
Angeliki Andrikopoulou ◽  
Flora Zagouri ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Occupational Exposure ◽  
Methylene Chloride ◽  
Disease Risk ◽  
Epidemiological Studies ◽  
Preventive Actions ◽  
Increased Risk ◽  
Hazard Surveillance ◽  
Genetic And Environmental Factors ◽  
Meta Analyses

The precise etiology of multiple myeloma remains elusive, but both genetic and environmental factors have been suggested to contribute to disease risk. Several occupational categories and toxic agents have been implicated as potentially causative, yet findings from the literature are inconsistent. The aim of this review was to summarize and critically comment on the accumulated epidemiological evidence, across published meta-analyses, about the association between occupational exposure and risk of multiple myeloma. Overall, results from eleven meta-epidemiological studies underscore a significantly increased risk for firefighters, hairdressers, and employees exposed to engine exhaust, whereas farming and methylene chloride exposure have been non-significantly correlated with the disease. Further epidemiological studies are of utmost importance whilst emphasis should be placed on occupational hazard surveillance, as such studies will obtain a more accurate picture of disease occurrence in working populations, and will enable both the implementation of preventive actions and the evaluation of their effectiveness.

The role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric diseases

2007 ◽  
Vol 45 (12) ◽  
Author(s):  
Rima Obeid ◽  
Andrew McCaddon ◽  
Wolfgang Herrmann
Keyword(s):  
Disease Risk ◽  
Epidemiological Studies ◽  
Nervous System Diseases ◽  
Central Nervous System Diseases ◽  
Dependent Relationship ◽  
Total Homocysteine ◽  
B Vitamin ◽  
Dose Dependent ◽  
Plasma Total Homocysteine

AbstractHyperhomocysteinemia (HHcy) is related to central nervous system diseases. Epidemiological studies show a positive, dose-dependent relationship between plasma total homocysteine (tHcy) concentration and neurodegenerative disease risk. tHcy is a marker of B-vitamin (folate, BClin Chem Lab Med 2007;45:1590–606.

scholarly journals Maternal obesity increases the risk of metabolic disease and impacts renal health in offspring

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Sarah J. Glastras ◽  
Hui Chen ◽  
Carol A. Pollock ◽  
Sonia Saad
Keyword(s):  
Metabolic Disease ◽  
Kidney Disease ◽  
Maternal Obesity ◽  
Disease Risk ◽  
Reproductive Age ◽  
Intrauterine Environment ◽  
Alcoholic Fatty Liver ◽  
Increased Risk ◽  
Epigenetic Modulation

Obesity, together with insulin resistance, promotes multiple metabolic abnormalities and is strongly associated with an increased risk of chronic disease including type 2 diabetes (T2D), hypertension, cardiovascular disease, non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). The incidence of obesity continues to rise in astronomical proportions throughout the world and affects all the different stages of the lifespan. Importantly, the proportion of women of reproductive age who are overweight or obese is increasing at an alarming rate and has potential ramifications for offspring health and disease risk. Evidence suggests a strong link between the intrauterine environment and disease programming. The current review will describe the importance of the intrauterine environment in the development of metabolic disease, including kidney disease. It will detail the known mechanisms of fetal programming, including the role of epigenetic modulation. The evidence for the role of maternal obesity in the developmental programming of CKD is derived mostly from our rodent models which will be described. The clinical implication of such findings will also be discussed.

scholarly journals Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans

2012 ◽  
Vol 113 (6) ◽  
pp. 903-908 ◽  
Author(s):  
Huan Yang ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Jason R. Carter
Keyword(s):  
Sex Differences ◽  
Sleep Deprivation ◽  
Cardiovascular Reactivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Epidemiological Studies ◽  
Total Sleep Deprivation ◽  
Increased Risk ◽  
Forearm Vascular Conductance

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA ( n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA ( n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.

The Role of Mobile Phones in Real World Motor Vehicle Crashes

2015 ◽  
pp. 1366-1375 ◽  
Author(s):  
Suzanne P. McEvoy
Keyword(s):  
Text Messaging ◽  
Motor Vehicle ◽  
Epidemiological Studies ◽  
Motor Vehicle Crashes ◽  
Vehicle Crashes ◽  
Mobile Phone Use ◽  
Relative Risks ◽  
Increased Risk ◽  
Driver Distractions

Early on, road epidemiological studies (Redelmeier & Tibshirani, 1997; McEvoy et al., 2005) indicated an increased risk of motor vehicle crashes, including injury crashes, associated with mobile phone use. However, these studies were unable to assess the relative risks pertaining to specific phone tasks (for example, conversing versus texting). Moreover, direct comparisons of risk between different types of driver distractions, while possible (McEvoy, Stevenson, Woodward, 2007), were difficult to undertake. Naturalistic driving studies using instrumented cars in every day driving have provided more details of the tasks that confer particular risk in relation to phone use and other driver distractions (Klauer et al., 2014; Olson et al., 2009; Klauer et al., 2006; Dingus et al., 2006). Interest generated in these studies has prompted current trials using similar methodologies elsewhere, for example, Australia (Regan et al., 2013). To date, phone tasks involving handling of the phone and/or multiple or prolonged eye glances away from the forward roadway (dialling, reaching for the phone and text messaging) have been shown to significantly increase the risk of crashes and near crashes.

scholarly journals Circadian Rhythms of the Hypothalamus: From Function to Physiology

2021 ◽  
Vol 3 (1) ◽  
pp. 189-226
Author(s):  
Rachel Van Drunen ◽  
Kristin Eckel-Mahan
Keyword(s):  
Circadian Rhythms ◽  
Energy Homeostasis ◽  
Environmental Changes ◽  
Neurological Diseases ◽  
Epidemiological Studies ◽  
Internal Clock ◽  
The Body ◽  
Hypothalamic Nuclei ◽  
Increased Risk

The nearly ubiquitous expression of endogenous 24 h oscillations known as circadian rhythms regulate the timing of physiological functions in the body. These intrinsic rhythms are sensitive to external cues, known as zeitgebers, which entrain the internal biological processes to the daily environmental changes in light, temperature, and food availability. Light directly entrains the master clock, the suprachiasmatic nucleus (SCN) which lies in the hypothalamus of the brain and is responsible for synchronizing internal rhythms. However, recent evidence underscores the importance of other hypothalamic nuclei in regulating several essential rhythmic biological functions. These extra-SCN hypothalamic nuclei also express circadian rhythms, suggesting distinct regions that oscillate either semi-autonomously or independent of SCN innervation. Concurrently, the extra-SCN hypothalamic nuclei are also sensitized to fluctuations in nutrient and hormonal signals. Thus, food intake acts as another powerful entrainer for the hypothalamic oscillators’ mediation of energy homeostasis. Ablation studies and genetic mouse models with perturbed extra-SCN hypothalamic nuclei function reveal their critical downstream involvement in an array of functions including metabolism, thermogenesis, food consumption, thirst, mood and sleep. Large epidemiological studies of individuals whose internal circadian cycle is chronically disrupted reveal that disruption of our internal clock is associated with an increased risk of obesity and several neurological diseases and disorders. In this review, we discuss the profound role of the extra-SCN hypothalamic nuclei in rhythmically regulating and coordinating body wide functions.

scholarly journals Calcium and vitamin D in obesity

2012 ◽  
Vol 25 (1) ◽  
pp. 130-141 ◽  
Author(s):  
Qingming Song ◽  
Igor N. Sergeev
Keyword(s):  
Vitamin D ◽  
Clinical Intervention ◽  
Epidemiological Studies ◽  
Vitamin D Status ◽  
Negative State ◽  
Increased Risk ◽  
Research Findings ◽  
Intervention Trials ◽  
Fat Excretion

New and more effective nutritional measures are urgently needed for the prevention of obesity. The role of Ca and vitamin D in obesity has been recently implicated. Low Ca intake and low vitamin D status have been linked with an increased risk of obesity in epidemiological studies; however, clinical intervention trials designed to test this association have produced controversial results. The suggested anti-obesity mechanisms of Ca and vitamin D include the regulation of adipocyte death (apoptosis), adipogenesis and lipid metabolism. Dietary Ca has been also shown to increase faecal fat excretion. The potential role of Ca and vitamin D in shifting energy balance towards a more negative state is an area of considerable interest. Ultimately, a review of recent research findings does not allow the reaching of a definitive conclusion that increasing Ca intake and rising vitamin D status will influence fat mass and body weight or decrease the risk of obesity and overweight.

scholarly journals Research progress of gut microbiota and frailty syndrome

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1525-1536
Author(s):  
Xiao Wang ◽  
Min Wu
Keyword(s):  
Gut Microbiota ◽  
Health Outcomes ◽  
Clinical Syndrome ◽  
Research Progress ◽  
Circulation System ◽  
Frailty Syndrome ◽  
Adverse Health Outcomes ◽  
Increased Risk ◽  
Research Findings

Abstract Frailty is a clinical syndrome caused by homeostasis imbalance. It is characterized by marked vulnerability to endogenous or exogenous stressors, reduced self-care ability, and increased mortality risk. This aging-related syndrome is common in individuals older than 65 years and carries an increased risk for poor health outcomes. These include falls, incident disability, incapacity, and mortality. In addition, it can result in a poor prognosis for other comorbidities. With the aging population, frailty increases the burden of adverse health outcomes. Studies on frailty are at their infancy. In addition, there is a lack of thorough understanding of its pathogenesis. Several studies have suggested that frailty is caused by chronic inflammation due to enhanced intestinal permeability following gut microbiota imbalance as well as pathogen-related antibodies entering the circulation system. These result in musculoskeletal system disorders and neurodegenerative diseases. However, this assumption has not been validated in large cohort-based studies. Several studies have suggested that inflammation is not the only cause of frailty. Hence, further studies are necessary to extend our understanding of its pathogenesis. This review summarizes the research findings in the field and expands on the possible role of the gut microbiota in frailty syndrome.

scholarly journals Impact of Andropause on Multiple Sclerosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Maria C. Ysrraelit ◽  
Jorge Correale
Keyword(s):  
Multiple Sclerosis ◽  
Age Of Onset ◽  
Adaptive Immune Response ◽  
Epidemiological Studies ◽  
Testosterone Levels ◽  
Adaptive Immune ◽  
Natural Decrease ◽  
And Function ◽  
Gonadal Failure

Andropause results from the natural decrease in testosterone levels that occurs with age. In contrast to menopause, which is a universal, well-characterized process associated with absolute gonadal failure, andropause ensues after gradual decline of both hypothalamic-pituitary-gonadal axis activity, as well as of testicular function, a process which usually develops over a period of many years. Increasing evidence on greater risk of Multiple sclerosis (MS) associated with lower testosterone levels is being reported. Likewise, epidemiological studies have shown a later age of onset of MS in men, relative to women, which could perhaps respond to the decline in protective testosterone levels. In this review, we will discuss the role of androgens in the development and function of the innate and adaptive immune response, as well as in neuroprotective mechanisms relevant to MS. Testosterone effects observed in different animal models and in epidemiological studies in humans will be discussed, as well as their correlation with physical disability and cognitive function levels. Finally, published and ongoing clinical trials exploring the role of androgens, particularly at key stages of sexual maturation, will be reviewed.

scholarly journals Lifetime stress experience: transgenerational epigenetics and germ cell programming

2014 ◽  
Vol 16 (3) ◽  
pp. 297-305 ◽  
Keyword(s):  
Animal Models ◽  
Germ Cell ◽  
Parental Stress ◽  
Disease Risk ◽  
Underlying Disease ◽  
Epidemiological Studies ◽  
Autism Spectrum ◽  
Human Populations ◽  
Epigenetic Marks ◽  
Increased Risk

The transgenerational epigenetic programming involved in the passage of environmental exposures to stressful periods from one generation to the next has been examined in human populations, and mechanistically in animal models. Epidemiological studies suggest that gestational exposures to environmental factors including stress are strongly associated with an increased risk of neurodevelopmental disorders, including attention deficit-hyperactivity disorder, schizophrenia, and autism spectrum disorders. Both maternal and paternal life experiences with stress can be passed on to offspring directly during pregnancy or through epigenetic marks in the germ cell. Animal models of parental stress have examined relevant offspring phenotypes and transgenerational outcomes, and provided unique insight into the germ cell epigenetic changes associated with disruptions in neurodevelopment. Understanding germline susceptibility to exogenous signals during stress exposure and the identification of the types of epigenetic marks is critical for defining mechanisms underlying disease risk.

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