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Inflammation and sleep quality

Inflammation and sleep quality

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Download references. This research was supported by grants attributed to BDA from the Canadian Institutes of Health Research CIHR, MOP and and the Montreal Heart Institute Foundation. Special thanks to the staff and students of the laboratory and participants of the study for their generous time.

The funding sources played no role in the design, collection, analysis, interpretation of data, nor in the writing of the manuscript. Research Center, Montreal Heart Institute, Belanger Street, Montreal, Quebec, H1T 1C8, Canada.

Psychology Department, Université de Montréal, Montreal, Quebec, Canada. You can also search for this author in PubMed Google Scholar. BDA designed the study, analyzed and interpreted the results, and wrote the manuscript. VB contributed to the literature review and preparation of the manuscript.

Both authors approved the final manuscript. All participants signed the informed consent form which was approved by the Research and Ethics Board of the Montreal Heart Institute. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Impaired sleep quality is associated with concurrent elevations in inflammatory markers: are post-menopausal women at greater risk?. Biol Sex Differ 10 , 34 Download citation.

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Download PDF. Research Open access Published: 08 July Impaired sleep quality is associated with concurrent elevations in inflammatory markers: are post-menopausal women at greater risk? Abstract Background Chronic inflammation and impaired sleep increase the risk for cardiovascular disease.

Methods A fasting blood draw was obtained from healthy men and women 31 were postmenopausal. Conclusion Impaired sleep quality is independently associated with greater inflammation in healthy adult men and women.

Background Sleep impairment, defined as sleep of short duration, presence of insomnia symptoms, or non-restorative sleep, is associated with a number of health outcomes in cross-sectional and prospective epidemiological studies, including increased risk for cardiovascular CV morbidity and mortality [ 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 ].

Methods This study reports on the cross-sectional association between poor sleep quality and inflammatory activity in healthy premenopausal and postmenopausal women and men.

Procedures at follow-up Eligible participants were scheduled for a laboratory appointment at the Montreal Heart Institute.

Analyses Descriptive statistics were used to characterize the sample. Results Descriptive statistics Baseline characteristics of participants are presented in Table 1. Table 1 Sample characteristics Full size table.

Table 2 Bivariate correlations between sleep quality, inflammatory activity, and potential covariates Full size table. Full size image. Discussion The main finding of this study is that poor sleep quality is associated with greater inflammation in healthy adult men and women, independently of age, exercise level, obesity, or symptoms of depression.

Perspectives and significance In summary, poor sleep quality is associated with greater inflammation in apparently healthy individuals without a known sleep disorder, independently of sex and menopausal status.

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Interaction between sleep quality and dietary inflammation on frailty: NHANES — M. Social activity. TIB, time in bed; NWAK, number of nightly awakenings; TWAK, terminal wakefulness; WASO, wake after sleep onset; SOL, sleep onset latency; CRP, C-reactive protein; IL-6, interleukin Model fit indices were evaluated for the measurement model, unadjusted model, and multivariate adjusted model, and the normalized residual covariance was examined to evaluate local fit of the model in any cases where the global fit indices indicated poor fit.

All models described were assessed for global and local model fit issues. The Comparative Fit Index CFI , Root Mean Square Error of Approximation RMSEA , Standardized Root Mean Square Residual SRMR , and the Chi-Squared Test of Model Fit were used to assess global fit.

Descriptive statistics for the covariates and observed sleep inconsistency and inflammatory variables are provided in Table 1.

The coefficients of variation for the inflammatory biomarkers are as follows: 1. The measurement model for average sleep failed to converge, and subsequent analyses were not performed.

The fit indices for the second measurement model i. Overall, the measurement model fit well and was used to examine the full structural model, both unadjusted and multivariate adjusted models. Table 1. Descriptive statistics for covariates, sleep characteristics, and inflammatory markers.

Table 2. Fit indices from structural equation modeling predicting inflammation from sleep inconsistency. The model fit indices for the unadjusted model i. The model exhibited good fit as specified by a CFI 0. Table 3. Results from structural equation modeling predicting inflammation from sleep inconsistency.

The model fit indices for the unadjusted model stratified by sex are presented in Table 2 , and the model results are presented in Table 4. The models exhibited good fit as specified by a CFI 0. Table 4.

Results from unadjusted structural equation modeling predicting inflammation from sleep inconsistency stratified by sex. The model fit indices for the multivariate adjusted model i. However, the CFI 0. Age, sex, BMI, and health status were significant covariates, suggesting that these demographic characteristics help explain some of the variation in inflammation and should therefore be adjusted for in future studies.

The multivariate adjusted model would not converge when stratified by sex. The present study sought to investigate possible associations between an emerging, novel quantification of sleep patterns, sleep inconsistency, and markers of systemic inflammation. Commensurate with our hypothesis, we found that greater sleep inconsistency was associated with greater inflammation.

This association was most robust in women. Importantly, the observed sleep and inflammation variables all loaded onto common factors suggesting that both sleep inconsistency and inflammation were highly correlated across various measures. These common factors were not observed in aggregate i. As such, our analytic approach may signify underlying shared physiologic patterns of sleep inconsistency and inflammation.

Past research on associations between sleep and inflammation has resulted in mixed findings, possibly due to evaluating aggregate measures of sleep rather than examining sleep inconsistency.

However, preliminary research on sleep inconsistency has begun to identify patterns of associations between sleep inconsistency and a variety of inflammatory outcomes. As mentioned previously, one study of older adults found that inconsistency in sleep was associated with elevated peripheral inflammatory cytokines Another study demonstrated that even one night of sleep disruption, as occurs frequently with on-call physicians, can impact an individual's immune modulation Furthermore, in adolescents, sleep inconsistency measured across 1 week via actigraphy, was associated with higher levels of CRP Nevertheless, the literature on sleep inconsistency and inflammation in adults remains limited, and the present study provides further preliminary insight into this association.

Finally, we found that, after controlling for covariates i. Since the adjusted model was no longer significant after the addition of covariates, it can be assumed that part of the relationship between sleep inconsistency and inflammation is due to demographic and clinical factors that account for differences in sleep inconsistency and inflammation.

Previous research has shown that age 43 , sex 44 , BMI 45 , self-rated health 46 , and medication use [e. These clinical and demographic factors have also been independently associated with inflammation [i.

Therefore, the findings of the present study are consistent with prior literature evaluating demographic and clinical predictors of sleep disturbance and inflammation. There are a number of mechanistic pathways that may explain the relationship between sleep inconsistency and inflammation.

For instance, when individuals are woken from sleep on just one occasion, an inflammatory cascade unfolds that can be measured in altered gene expression 53 and multiple awakenings and inconsistent sleep from night-to-night may further exacerbate the inflammatory response.

Inflammation increases during stages 1 and 2 of sleep, as well as rapid eye movement REM sleep, while levels of inflammation during slow wave sleep are comparable to levels of awakening hours Thus, returning to a level of homeostasis during slow wave sleep lower levels of inflammation may represent an integral physiological function of the various stages of sleep.

Such inflammatory profiles may be particularly pronounced in populations known to have increased proportions of REM sleep to slow wave sleep, such as older adults or those suffering from depression 55 — Other factors could contribute to our findings. First, the overall levels of inflammation in this sample deserve further comment.

This minor elevation has been associated with a variety of health outcomes, including those associated with tissue damage or environmental irritants In our sample, mean CRP was 3.

This could indicate that the association between sleep inconsistency and inflammation could be unique to individuals with at least mild systemic inflammation.

Second, the current findings are noteworthy in light of other studies of sleep inconsistency. For instance, while our goal was to take the initial step toward identifying a common sleep inconsistency factor and examine associations with inflammation, previous work has identified that sleep inconsistency may be moderated by sex In the current analyses, females indeed showed greater levels of inflammation.

These sex differences and minor elevation in inflammation specific to our sample could be responsible for at least some of the associations of sleep inconsistency with inflammation. The results of this study may help guide research on the mechanisms linking altered sleep processes and circadian misalignment to adverse health outcomes.

Sleep and circadian processes are involved in the regulation of inflammatory cytokines, and experimental manipulation of both has been shown to increase blood concentrations of inflammatory cytokines 59 — Likewise, inconsistent sleep may reflect a pattern of altered sleep and circadian processes that have implications on inflammatory regulation and health.

For example, recent evidence suggests that sleep inconsistency confers risk for cardiometabolic disease 62 — Given that inflammation plays a critical role in the pathogenesis of metabolic abnormalities 66 , research is needed to explore whether inflammation is a mechanism through which sleep inconsistency and metabolic health are linked.

Because sleep inconsistency is readily modifiable, this line of research may lead to sleep interventions aimed at preventing diseases that have been linked to altered sleep, including cardiovascular disease. Further, our finding of an association between sleep inconsistency and inflammation in women but not men when stratified by sex may be the result of gender differences in biological and socioeconomic factors.

Future research is warranted. There are a number of limitations warranting further comment in this study. First, peripheral markers of inflammation were only available at one time point.

Such cross-sectional data limits our ability to quantify inconsistency in inflammatory processes over time, which has been suggested as a meaningful approach to linking inflammation to other health outcomes 6. Despite the current study being limited in only capturing sleep inconsistency, future research should target comparison of inconsistency across physiologic systems when possible e.

Second, we were limited by the health behavior and comorbidity variables available in MIDUS. In order to extend the current findings, future research should implement collection of more robust time series of data within individuals.

Examining longer epochs of data collection would allow researchers to identify antecedents of changes in sleep patterns or potential response to intervention, such as cognitive behavioral therapy for insomnia.

Third, sources of sleep inconsistency i. Fourth, longitudinal investigations are needed to investigate whether the cross-sectional results hold over time. Lastly, the racial composition of the present sample prohibited important analyses based on race.

This study identified a significant relationship between sleep inconsistency and inflammation. Specifically, a latent factor of sleep inconsistency was found to be related to an overall inflammatory factor; however, this association was no longer significant after controlling for covariates.

These novel findings extend prior work linking poor sleep patterns to physiologic dysfunction, further underscoring sleep inconsistency as a meaningful approach to quantifying sleep. Future research should extend measures of inconsistency to other physiologic systems as well as measuring how sleep inconsistency changes over time in conjunction with markers of inflammation.

JD, DK, and TS contributed to the conception and design of the study. KB organized the database and performed statistical analyses. JD wrote the first draft of the manuscript. JD, ED, DK, TS, and KB wrote sections of the manuscript.

All authors contributed to manuscript revision, read, and approved the submitted version. Research reported here was supported by the National Institute on Aging NIA of the National Institutes of Health NIH under Award Number K23AG PI: JD. Since the MIDUS study has been funded by the following: John D.

and Catherine T. MacArthur Foundation Research Network, NIA PAG, UAG Biomarker data collection was further supported by the NIH National Center for Advancing Translational Sciences NCATS Clinical and Translational Science Award CTSA program as follows: UL1TR Georgetown , UL1TR UCLA , 1UL1RR UW.

The content was solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

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Sleep 38— Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation.

: Inflammation and sleep quality

The connection between sleep and inflammation Majd M. Sleep 35 , 97— J Immunol. Other factors that can vary between men and women—including biological factors, such as the levels of endotoxin in the blood [ 89 ], or social factors, such as the greater impact of depressive symptoms on social stress and loneliness among women [ 17 ]—may be particularly relevant. Such cross-sectional data limits our ability to quantify inconsistency in inflammatory processes over time, which has been suggested as a meaningful approach to linking inflammation to other health outcomes 6. You can also search for this author in PubMed Google Scholar.
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Going to bed at the same time and waking at the same time every day reinforces the healthy circadian rhythms that govern both our sleep and our immune function, including inflammation. Scientists still have a lot to learn about the specifics of the relationship between sleep and inflammation.

Laboratory studies have tested acute, prolonged sleep deprivation—conditions under which sleep is restricted for 24 hours or more—and found this severe degree of sleep loss increases inflammation activity in the body. Scientists have also studied partial sleep deprivation, the kind of chronic, insufficient sleep that so many people experience in their daily lives.

While the study results are mixed, many studies show this form of everyday sleep loss also elevates inflammation. It might surprise you to learn that sleeping too much can also trigger unhealthful inflammation. A study reviewed more than 70 scientific investigations into the relationship between inflammation and sleep.

The long-term effects of poor sleep on health are a major public health concern. The influence sleep can have on inflammation is a significant factor in managing health and guarding against disease over the course of our lives. According to research, it takes as little as a single night.

Research has shown that one night of insufficient sleep is enough to activate pro-inflammatory processes in the body. A study found that one single night of partial sleep resulted in significantly higher levels of NF-kB , a protein complex that acts as a powerful signal to stimulate inflammation throughout the body.

One noteworthy aspect of this study: the researchers found the higher inflammatory response occurred in female subjects, but not in male subjects. The differences in the ways women and men respond to sleep loss are important, and under-studied. This is an area of study that needs more attention.

But every night of sleep counts. Stress is a common obstacle to sleep. Worried, on high alert, agitated and anxious—these emotional and physical states of stress make it difficult to fall asleep and to sleep soundly throughout a full night.

In turn, not getting enough sleep makes us more vulnerable to the physical and emotional effects of stress. Many people fall into a difficult cycle: ending the day stressed out, having a hard time sleeping, feeling exhausted and even more stressed the next day—which leads to more problems sleeping.

This chronic sleep-stress cycle does more than make us tired and irritable. Stress is also a trigger for inflammation. Over time, chronic stress creates systemic, low-grade inflammation that wears at the health of our cells and makes us more vulnerable to disease. Science is now identifying just what that means, and how stress contributes to disease by stimulating inflammation.

A study identified the critical connections between chronic stress, increased inflammation, and the development of a range of diseases including cancer, heart disease, diabetes, and depression. Sleep has a powerful, dual role to play in this complex interaction with stress and inflammation.

Sleeping well can work directly to keep inflammation in check by avoiding the pro-inflammatory activity that occurs in the presence of poor, dysregulated sleep.

And sleep offers us significant protection against stress, itself a major contributor to chronic inflammation—a now known pathway to disease. One of the most exciting areas of sleep and health research involves the human microbiome. Our microbiome is the vast, dynamic, ever-shifting collection of bacteria and other micro-organisms that live within our bodies.

An unhealthy gut contributes to chronic inflammation. How does a gut become unhealthy? Poor diet, stress, medication and illness are all contributors.

So, too are disrupted circadian rhythms and poor sleep. Poor and insufficient sleep appear to change the composition of our natural microbiota, decreasing beneficial bacteria and increasing bacteria associated with disease.

The emerging science points to a powerful two-way street between sleep and gut health. Sleeping well is one way to help maintain a healthy gut.

Both those pillars—healthy sleep and a balanced, thriving gut—can work to limit harmful inflammation, and may help deliver long-term protection against disease. Sleep well can be a potent tool in helping guard against this often silent, and damaging, form of inflammation.

Michael Breus, Ph. Prather, PhD, an associate professor of psychiatry and behavioral sciences at the University of California, San Francisco, told attendees at the Interdisciplinary Autoimmune Summit.

Finally, of course, there are medications that can impact sleep disturbance. The one we think of most commonly is high-dose glucocorticoid, but there are likely others that can mess around with the sleep system.

According to Prather, sleep disturbance is rampant throughout populations of patients with IMIDs. He cited studies from Abad et al. Epidemiologic studies support cross-sectional and longitudinal associations between sleep and markers of inflammation, while experimental studies support the effects of acute sleep loss on increased concentrations of inflammation-inducing cytokines, he added.

In one study — from Irwin et al. In addition, the researchers collected blood samples in the morning during both sleep paradigms and analyzed them for the presence of inflammatory mediators. According to the researchers, the partial sleep deprivation paradigm was associated with an increase in the gene expression of interleukin-6 and TNF alpha.

In addition, although the experimental sleep loss data are mixed, the data linking patient-reported loss disturbance and inflammation levels are not, Prather said. Regarding the possibility that treating inflammation may improve sleep, Prather stated that several biologics are available to treat IMIDs that target proinflammatory cytokines.

However, few studies have tested the effects of these drugs on sleep and sleep quality. Sleep disturbance can lead to increased levels of inflammation, which may contribute to disease course, and there is a small but fairly intriguing set of data on the benefit of cytokine antagonists or inhibitors to improve sleep, but, again, these are only preliminary.

Prather AA. Understanding the Role of Sleep in IMIDs. Presented at: Interdisciplinary Autoimmune Summit. Cerebral microglia recruit monocytes into the brain in response to tumor necrosis factoralpha signaling during peripheral organ inflammation. Shearer, W. Soluble TNF-alpha receptor 1 and IL-6 plasma levels in humans subjected to the sleep deprivation model of spaceflight.

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Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL and CRP. Download references. The author acknowledges research support provided by the US National Institutes of Health Grants R01AG, R01AG, R01AG, R01CA, R01AG and R01CA Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.

You can also search for this author in PubMed Google Scholar. Correspondence to Michael R. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Difficulty initiating or maintaining sleep, early awakening, interrupted or non-restorative sleep, and associated impairments in daytime functioning, which must be present for at least 3 nights per week and last for 3 months or longer.

A stage of sleep, also known as deep sleep, that ischaracterized by synchronized electroencephalogram activity with the presence of slow waves, or delta wave activity. SWS is often viewed as a time of rest for neocortical neurons, in which the brain recovers from activities during the day.

In animals and humans, the sleep—wake cycle, which influences physiological processes including immunity, as well as levels of behavioural arousal. A measure that tracks the electrical activity of the brain; one use is to graphically represent stages of sleep, which are defined by differences in waveform shape, frequency and amplitude.

A measure that tracks the electrical activity of muscle; one use, together with the EEG, is to define stages of sleep, such as rapid eye movement sleep, in which there is low muscle tone or activity accompanied by random and rapid eye movements.

Bursts of oscillatory electroencephalogram activity that occur during stage 2 sleep, caused by a peak of electrical activity in one area of the brain followed by a peak of electrical activity in an adjacent area of the brain.

Large event waveforms of electroencephalogram activity that are considered to be a defining brainwave of stage 2 sleep. They are characterized by a brief negative peak of electrical activity, followed by a longer-duration positive complex and then another negative peak.

HPA axis. A neuroendocrine system that links the hypothalamus, pituitary and adrenal glands and functions to regulate the immune system in response to circadian signalling, behavioural states such as sleep and peripheral inflammatory signals.

A component of the autonomic nervous system that comprises nerve fibres that innervate lymphoid tissues, as well as nearly all other body tissues. The SNS regulates immune cell traffic and immune responses during sleep and in response to stress through the release of noradrenaline.

Also known as the circadian clock. Cycles of oscillation are determined by biochemical signals and synchronized by solar time to influence hour circadian timing in animals and in humans. Imposing a loss of sleep during the night, for either part of the night in other words, partial night sleep deprivation or for the entire night in other words, total night sleep deprivation.

REM sleep. A stage of sleep, also known as paradoxical sleep, that is characterized by desynchronized electroencephalogram activity in a manner similar to waking, accompanied by random and rapid movement of the eyes together with low muscle tone.

REM sleep is viewed as the sleep period in which there is a propensity to dream. The ability of IL-6 to form an agonistic complex with a soluble IL-6 receptor and thereby to activate cells that lack the membrane-bound IL-6 receptor, such as neural cells. A sleep-like state described in invertebrate models, in which a period of behavioural quiescence follows exposure to conditions that induce cellular stress, including exposure to tissue damage or extremes of temperature.

The amount of time spent asleep during the night, measured either by subjective report or objectively, using polysomnography or actigraphy. Short sleep duration is defined as less than the reference amount of 7 hours per night and is typically characterized as being less than 6 hours of sleep per night.

Long sleep duration is typically characterized as being more than 8 hours of sleep per night. The relative distribution of uninterrupted sleep, as opposed to wakefulness, during the night, as measured by sleep efficiency time spent asleep as a percentage of the total time spent in bed and wake time after sleep onset the amount of time spent awake after turning off the lights and initiating sleep.

An acute phase protein that is synthesized by the liver in response to the production of IL-6 by macrophages or T cells. Neuroendocrine hormones that belong to the steroid hormone class, which suppress inflammation and antiviral immune responses, in addition to having a role in the metabolism of protein, fat and glucose.

A state of decreased sensitivity to the anti-inflammatory effects of glucocorticoids, which can be caused by ongoing increases in inflammation as well as by a genetic predisposition. A component of the autonomic nervous system that comprises nerve fibres that innervate visceral tissues to regulate actions of the body when it is at rest, mainly through release of the neurotransmitter acetylcholine.

The state of a cell in which it is no longer able to replicate, which is also characterized by increased release of inflammatory mediators.

An estimate of biological age given by evaluating changes in DNA methylation at particular genomic locations, which is found to be more predictive of mortality risk than is chronological age. A sleep pattern characterized by high levels of sleep efficiency and low levels of awakening or sleep interruption.

Reprints and permissions. Sleep and inflammation: partners in sickness and in health. Nat Rev Immunol 19 , — Download citation. Published : 09 July Issue Date : November Anyone you share the following link with will be able to read this content:.

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Abstract The discovery of reciprocal connections between the central nervous system, sleep and the immune system has shown that sleep enhances immune defences and that afferent signals from immune cells promote sleep. Access through your institution. Buy or subscribe. Change institution.

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Frontiers | Sleep Inconsistency and Markers of Inflammation

Investigators took immune stem cells and immune cells from mice during these undisturbed, fragmented, and sleep recovery phases, analyzed them and compared them at the end of the experiment.

Results in mice were consistent with results in humans. They showed that all mice with fragmented sleep had significant changes to their immune stem cells, producing an increased number of immune cells, and also showed evidence of rewiring and reprogramming.

A notable finding from the mouse group was that even after sleep recovery, the immune stem cells retained this rewiring structure, and they continued to produce additional white blood cells, making the mice susceptible to inflammation and disease.

We can detect a molecular imprint of insufficient sleep in immune stem cells, even after weeks of recovery sleep. There were some stem cell clusters that proliferated and grew in number, while other clusters became smaller.

This reduction in overall diversity and aging of the immune stem cell population is an important contributor to inflammatory diseases and cardiovascular disease. The National Heart, Lung, and Blood Institute , and the National Center for Advancing Translational Sciences part of the National Institutes of Health, helped fund this study.

Description: The left side of the figure shows the sleep time of the humans in the study. Participants in the sleep restriction group the red dots slept less over the six weeks.

The right side of the figure the stem cell analysis. The first graph shows that people in the sleep restriction group again red dots had more stem cells. The red and blue colors show locations in the genome that were re-wired.

Mount Sinai Health System is one of the largest academic medical systems in the New York metro area, with more than 43, employees working across eight hospitals, over outpatient practices, nearly labs, a school of nursing, and a leading school of medicine and graduate education.

Mount Sinai advances health for all people, everywhere, by taking on the most complex health care challenges of our time — discovering and applying new scientific learning and knowledge; developing safer, more effective treatments; educating the next generation of medical leaders and innovators; and supporting local communities by delivering high-quality care to all who need it.

The Health System includes approximately 7, primary and specialty care physicians; 13 joint-venture outpatient surgery centers throughout the five boroughs of New York City, Westchester, Long Island, and Florida; and more than 30 affiliated community health centers.

We are consistently ranked by U. New York Eye and Ear Infirmary of Mount Sinai is ranked No. Vgontzas, A. et al. Circadian interleukin-6 secretion and quantity and depth of sleep.

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Frey, D. The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults. Sauvet, F. Effect of acute sleep deprivation on vascular function in healthy subjects. Haack, M. Diurnal variations of interleukin-6 plasma levels are confounded by blood drawing procedures.

Psychoneuroendocrinology 27 , — Chennaoui, M. Effect of one night of sleep loss on changes in tumor necrosis factor alpha TNF-α levels in healthy men.

What is Inflammation?

One theory focuses on blood vessels. During sleep, blood pressure drops and blood vessels relax. In the deepest sleep phases, cerebrospinal fluid rushes through the brain, sweeping away beta-amyloid protein linked to brain cell damage.

Then, a vicious cycle sets in. This damage makes it harder both to sleep and to retain and consolidate memories. Just one night of lost sleep can keep beta-amyloid levels higher than usual. As a service to our readers, Harvard Health Publishing provides access to our library of archived content.

Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician. When you wake up in the morning, are you refreshed and ready to go, or groggy and grumpy?

For many people, the second scenario is all too common. Improving Sleep: A guide to a good night's rest describes the latest in sleep research, including information about the numerous health conditions and medications that can interfere with normal sleep, as well as prescription and over-the-counter medications used to treat sleep disorders.

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Back to Healio. Aric A. Published by:. Disclosures: Prather reports grant support from the NIH, consulting fees from Fitbit Inc. and being an advisor for NeuroGeneces. Read more about sleep. sleep deprivation. immune-mediated inflammatory diseases. university of california san francisco.

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Inflammafion more Herbal energy elixir about PLOS Subject Areas, ssleep here. Although there Cholesterol-conscious meal ideas a qhality Inflammation and sleep quality between depressive symptoms and xleep of inflammation, it Stomach health issues unclear Lice treatment for pregnant women depressive symptoms at one point in life quakity predict inflammation later in life. Moreover, Ifnlammation extant literature linking sleep with both depressive symptoms and inflammation, there is little research investigating poor sleep as a mechanism linking depressive symptoms with later inflammation. The links between depression and physical health can also vary by gender. In longitudinal analyses with data from the Midlife in the United States MIDUS study, we examined whether depressive symptoms were associated with inflammatory markers 11 years later and whether these associations were mediated by sleep disturbances or moderated by gender. Participants reported depressive symptoms and demographic information at baseline.

Author: Molkis

5 thoughts on “Inflammation and sleep quality

  1. Ich entschuldige mich, aber meiner Meinung nach irren Sie sich. Ich kann die Position verteidigen. Schreiben Sie mir in PM, wir werden umgehen.

  2. Entschuldigen Sie, dass ich mich einmische, aber mir ist es etwas mehr die Informationen notwendig.

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