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Old 31-10-2015, 11:57 PM   #1
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Default Papers related to the importance of sleep.

Sleep and motor learning: implications for physical rehabilitation after stroke

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Sleep is essential for healthy brain function and plasticity underlying learning and memory. In the context of physical impairment such as following a stroke, sleep may be particularly important for supporting critical recovery of motor function through similar processes of reorganisation in the brain. Despite a link between stroke and poor sleep, current approaches to rehabilitative care often neglect the importance of sleep in clinical assessment and treatment. This review assimilates current evidence on the role of sleep in motor learning, with a focus on the implications for physical rehabilitation after stroke. We further outline practical considerations for integrating sleep assessment as a vital part of clinical care.
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Old 01-11-2015, 12:01 AM   #2
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Default Sleep parameters, functional status, and time post-stroke are associated with offline motor skill learning in people with chronic stroke

http://journal.frontiersin.org/artic...015.00225/full

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Background: Mounting evidence demonstrates that individuals with stroke benefit from sleep to enhance learning of a motor task. While stage NREM2 sleep and REM sleep have been associated with offline motor skill learning in neurologically intact individuals, it remains unknown which sleep parameters or specific sleep stages are associated with offline motor skill learning in individuals with stroke.

Methods: Twenty individuals with chronic stroke (>6 months following stroke) and 10 control participants slept for three consecutive nights in a sleep laboratory with polysomnography. Participants practiced a tracking task the morning before the third night and underwent a retention test the morning following the third night. Offline learning on the tracking task was assessed. Pearson’s correlations assessed for associations between the magnitude of offline learning and sleep variables, age, upper-extremity motor function, stroke severity, depression, and time since stroke occurrence.

Results: Individuals with stroke performed with significantly less error on the tracking task following a night of sleep (p = 0.006) while the control participants did not (p = 0.816). Increased sleep efficiency (r = −0.285), less time spent in stage NREM3 sleep (r = 0.260), and more time spent in stage REM sleep (r = −0.266) were weakly-to-moderately associated with increased magnitude of offline motor learning. Furthermore, higher upper-extremity motor function (r = −0.400), lower stroke severity (r = 0.360), and less time since stroke occurrence (r = 0.311) were moderately associated with increased magnitude of offline motor learning.

Conclusion: This study is the first study to provide insight into which sleep stages and individual characteristics may be associated with offline learning in people with stroke. Further research is needed to delineate which factors or combination of factors promote offline motor learning in people with neurologic injury to best promote motor recovery in these individuals.
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Old 01-11-2015, 12:07 AM   #3
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Default REM sleep rebound as an adaptive response to stressful situations

http://journal.frontiersin.org/artic...012.00041/full

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Stress and sleep are related to each other in a bidirectional way. If on one hand poor or inadequate sleep exacerbates emotional, behavioral, and stress-related responses, on the other hand acute stress induces sleep rebound, most likely as a way to cope with the adverse stimuli. Chronic, as opposed to acute, stress impairs sleep and has been claimed to be one of the triggering factors of emotional-related sleep disorders, such as insomnia, depressive- and anxiety-disorders. These outcomes are dependent on individual psychobiological characteristics, conferring even more complexity to the stress-sleep relationship. Its neurobiology has only recently begun to be explored, through animal models, which are also valuable for the development of potential therapeutic agents and preventive actions. This review seeks to present data on the effects of stress on sleep and the different approaches used to study this relationship as well as possible neurobiological underpinnings and mechanisms involved. The results of numerous studies in humans and animals indicate that increased sleep, especially the rapid eye movement phase, following a stressful situation is an important adaptive behavior for recovery. However, this endogenous advantage appears to be impaired in human beings and rodent strains that exhibit high levels of anxiety and anxiety-like behavior.



The Secret Connection Between Anxiety and Sleep

http://neurosciencenews.com/sleep-anxiety-7016/

Quote:
Encountering predators, adapting to a novel environment or expecting a reward ? these stressful or emotionally-salient situations require animals to shift their behavior to a vigilant state, altering their physiological conditions through modulation of autonomic and endocrine functions.

The bed nucleus of the stria terminalis (BNST) is a part of the extended amygdala, which is generally considered as a key player in stress response, fear and anxiety. Through projections to various brain regions including relay nuclei of the autonomic nervous system, hypothalamic regions and the central nucleus of the amygdala, the BNST controls endocrine and autonomic reactions in response to emotionally-salient stimuli, along with behavioral expression of anxiety and fear.
Update 04/07/2017
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Old 01-11-2015, 03:37 PM   #4
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Default Nonpharmacological Treatments of Insomnia for Long-Term Painful Conditions: A Systematic Review and Meta-analysis of Patient-Reported Outcomes in Randomized Controlled Trials

Abstract

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Study Objectives:

Insomnia is a debilitating comorbidity of chronic pain. This study evaluated the effect of nonpharmacological sleep treatments on patient-reported sleep quality, pain, and well-being in people with long-term cancer and non-cancer (e.g., back pain, arthritis, fibromyalgia) pain conditions.


Design:

We systematically searched Cochrane CENTRAL, MEDLINE, Embase, and PsychINFO for relevant studies. Search period was set to inception of these databases to March 2014. Studies were included if they were: original randomized controlled trials (RCTs); testing a nonpharmacological intervention; that targets sleep; in adults; with painful health conditions; that has a control group; includes a measure of sleep quality; and at least one other health and well-being outcome.


Measurement and Findings:

Means and standard deviations of sleep quality, pain, fatigue, depression, anxiety, physical and psychological functioning were extracted for the sleep treatment and control groups at baseline, posttreatment and final follow-up. Methodological details concerning the treatment, participants, and study design were abstracted to guide heterogeneity and subgroup analyses. Eleven RCTs involving 1,066 participants (mean age 45–61 years) met the criteria for the meta-analysis. There was no systematic evidence of publication bias. Nonpharmacological sleep treatments in chronic pain patients were associated with a large improvement in sleep quality (standardized mean difference = 0.78, 95% Confidence Interval [0.42, 1.13]; P < 0.001), small reduction in pain (0.18 [0, 0.36] P < 0.05), and moderate improvement in fatigue (0.38 [0.08, 0.69]; P < 0.01) at posttreatment. The effects on sleep quality and fatigue were maintained at follow-up (up to 1 year) when a moderate reduction in depression (0.31, [0.09, 0.53]; P < 0.01) was also observed. Both cancer and non-cancer pain patients benefited from nonpharmacological sleep treatments. Face-to-face treatments achieved better outcomes than those delivered over the phone/internet.


Conclusions:

Although the body of evidence was small, nonpharmacological sleep interventions may represent a fruitful avenue for optimizing treatment outcomes in patients with chronic pain.

Registration:

PROSPERO registration: CRD42013004131.


Citation:

Tang NK, Lereya T, Boulton H, Miller MA, Wolke D, Cappuccio FP. Nonpharmacological treatments of insomnia for long-term painful conditions: a systematic review and meta-analysis of patient-reported outcomes in randomized controlled trials. SLEEP 2015;38(11):1751–1764.
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Old 03-11-2015, 05:39 PM   #5
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Default Pain in Sleepwalking: A Clinical Enigma

http://www.journalsleep.org/ViewAbstract.aspx?pid=30287

Quote:
Study Objectives:

Sleepwalking is a disorder characterized by arousal specifically from slow wave sleep with dissociated brain activity that may be related to lower nociceptive state. Our objectives were to assess the frequency of chronic pain, headache, and migraine in sleepwalkers compared to controls, examine the impact and determinants of pain in sleepwalkers, and report analgesia frequency during injurious parasomnia episodes.


Design:

Cross-sectional case-control study.


Setting:

Data were collected at the Sleep Disorders Center, Montpellier, France.


Participants:

One hundred patients with sleepwalking were assessed for disease characteristics, sleep (polysomnography, sleepiness, and insomnia), pain (chronic pain, multidimensional pain inventory, headache, and migraine), depressive symptoms, and quality of life compared to 100 adult controls. Pain perception was retrospectively assessed during injurious parasomnia episodes.


Measurements and Results:

Raw association data showed that lifetime headache, migraine, and chronic pain at time of study were significantly associated with sleepwalking (also called somnambulism). Compared to controls, sleepwalkers reported more frequent daytime sleepiness, and depressive and insomnia symptoms. After adjustments, sleepwalking was associated with increased risk for headache and migraine only. Compared to pain-free sleepwalkers, sleepwalkers with chronic pain were more likely to be older and to have greater daytime sleepiness, insomnia, and depressive symptoms, with no difference in polysomnography assessment. Of the 47 sleepwalkers with at least one previous violent parasomnia episode, 78.7% perceived no pain during episodes, allowing them to remain asleep despite injury.


Conclusion:

Our results highlight the clinical enigma of pain in sleepwalking patients with complaints of frequent chronic pain, migraine, and headache during wakefulness but who report retrospectively experience of analgesia during severe parasomnia episodes, suggesting a relationship between dissociated brain activity and nociceptive dysregulation.
Citation:

Lopez R, Jaussent I, Dauvilliers Y. Pain in sleepwalking: a clinical enigma. SLEEP 2015;38(11):1693–1698.


There were several sleepwalkers at the boarding school to which I was sent at the age of eight and they were extraordinarily difficult to wake. We tended to guide them back to bed without waking them. One managed to get out of bed and knock her front teeth out without waking herself or the rest of us and the first we knew about it was when the morning bell was rung and we all awoke to find the dorm looking like an abbatoir.

During my on call nights at the hospital, I tended not to sleep at all if I had patients that needed to be seen two hourly and there were always patients who were in a light sleep in obvious pain. Opiates were supposed to be given four hourly through ports in the IVs, but the timings could go awry if there was an emergency which delayed the drug round.
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Old 19-11-2015, 09:21 AM   #6
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Default Somnambulism analgesia

http://noijam.com/2015/11/19/somnambulism-analgesia/

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I’ve asked the question whether it is possible to feel pain while asleep before. It led to some great discussion, as well as a fascinating first hand report. A recent paper in Sleep (I love these simple, unambiguous journal titles) reported on an experiment that asked known somnambulists about their experiences of pain. A press release from the American Academy of Sleep Medicine detailed some intriguing results:
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Old 10-12-2015, 03:03 PM   #7
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Default Losing Neutrality: The Neural Basis of Impaired Emotional Control without Sleep

http://www.jneurosci.org/content/35/38/13194

Abstract

Quote:
Sleep deprivation has been shown recently to alter emotional processing possibly associated with reduced frontal regulation. Such impairments can ultimately fail adaptive attempts to regulate emotional processing (also known as cognitive control of emotion), although this hypothesis has not been examined directly. Therefore, we explored the influence of sleep deprivation on the human brain using two different cognitive–emotional tasks, recorded using fMRI and EEG. Both tasks involved irrelevant emotional and neutral distractors presented during a competing cognitive challenge, thus creating a continuous demand for regulating emotional processing. Results reveal that, although participants showed enhanced limbic and electrophysiological reactions to emotional distractors regardless of their sleep state, they were specifically unable to ignore neutral distracting information after sleep deprivation. As a consequence, sleep deprivation resulted in similar processing of neutral and negative distractors, thus disabling accurate emotional discrimination. As expected, these findings were further associated with a decrease in prefrontal connectivity patterns in both EEG and fMRI signals, reflecting a profound decline in cognitive control of emotion. Notably, such a decline was associated with lower REM sleep amounts, supporting a role for REM sleep in overnight emotional processing. Altogether, our findings suggest that losing sleep alters emotional reactivity by lowering the threshold for emotional activation, leading to a maladaptive loss of emotional neutrality.


A lack of sleep makes everything harder. Focusing, finishing assignments, and coping with everyday stress can become monumental tasks.

https://www.sciencedaily.com/release...0418151243.htm

Quote:
People with anxiety and depression often have sleep problems. But little has been known about whether or how their poor sleep affects a specific region of the brain known to be involved in regulating negative emotional responses.

Researchers at the University of Illinois at Chicago College of Medicine have found that this area of the brain, the dorsal anterior cingulate cortex, may have to work harder to modify negative emotional responses in people with poor sleep who have depression or anxiety. The finding is reported in the journal Depression and Anxiety.

The research team, led by Heide Klumpp, assistant professor of psychiatry at UIC, used functional MRI to measure the activity in different regions of the brain as subjects were challenged with an emotion-regulation task. Participants were shown disturbing images of violence -- from war or accidents -- and were asked to simply look at the images and not to try to control their reaction or to "reappraise" what they saw in a more positive light.

An example of reappraisal would be to see an image of a woman with a badly bruised face and imagine her as an actress in makeup for a role, rather than as a survivor of violence, Klumpp said.

"Reappraisal is something that requires significant mental energy," she said. "In people with depression or anxiety, reappraisal can be even more difficult, because these disorders are characterized by chronic negativity or negative rumination, which makes seeing the good in things difficult."
Update 19/04/2017
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Old 15-12-2015, 02:21 PM   #8
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Default Humans evolved to get better sleep in less time

http://www.sciencedaily.com/releases...1214130926.htm

Quote:
"Humans are unique in having shorter, higher quality sleep," said anthropologist and study co-author David Samson of Duke, who logged nearly 2,000 hours watching orangutans in REM and non-REM sleep as part of his dissertation research prior to coming to Duke.

The human sleep gap isn't merely the result of round-the-clock access to artificial light from streetlamps and computer screens, the researchers say. A separate study of the sleep habits of people living in three hunter-gatherer societies without electricity in Tanzania, Namibia and Bolivia found they get slightly less shut-eye than those of us with electronic gadgets.

If artificial light and other aspects of modern life were solely responsible for shortening our sleep, we'd expect hunter-gatherer societies without access to electricity to sleep more, Samson said.

Rather, the study by Samson and Duke anthropologist Charlie Nunn suggests that humans replaced sleep quantity with sleep quality long before the glare of smartphones came to be.

The researchers attribute the shift towards shorter, more efficient sleep in part to the transition from sleeping in "beds" in the trees, as our early human ancestors probably did, to sleeping on the ground as we do today.

Once on the ground, Samson said, early humans likely started sleeping near fire and in larger groups in order to keep warm and ward off predators such as leopards and hyenas -- habits which could have enabled our ancestors to get the most out of their sleep in the shortest time possible.

Shorter sleep also freed up time that could be devoted to other things, like learning new skills and forging social bonds, while deeper sleep helped to cement those skills, sharpen memory and boost brainpower, Samson said.
I don't much at night, which often leads to curiosity from those in different time zones.

Being on call and participating in a demanding sport has enabled me to develop the ability to take short sleeps during the day if the opportunity arises.

Those who are ill, injured, anxious/depressed, probably need more in the way of deep sleep and suitable strength and conditioning exercise that they are currently getting.
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Old 08-01-2016, 12:17 AM   #9
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Default LUCID DREAMING MAY HELP US UNRAVEL THE MYSTERIES OF CONSCIOUSNESS

http://neurosciencenews.com/consciou...dreaming-3363/

Quote:
Lucid dreaming is still an understudied subject, but recent advances suggest it’s a hybrid state of waking consciousness and sleep.
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Old 18-01-2016, 04:19 PM   #10
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Default The spectral composition of evening light and individual differences in the suppression of melatonin and delay of sleep in humans

http://onlinelibrary.wiley.com/enhan...c4153c210ced8b

Abstract

Quote:
Abstract:  The effect of light on circadian rhythms and sleep is mediated by a multi-component photoreceptive system of rods, cones and melanopsin-expressing intrinsically photosensitive retinal ganglion cells. The intensity and spectral sensitivity characteristics of this system are to be fully determined. Whether the intensity and spectral composition of light exposure at home in the evening is such that it delays circadian rhythms and sleep also remains to be established. We monitored light exposure at home during 6–8 wk and assessed light effects on sleep and circadian rhythms in the laboratory. Twenty-two women and men (23.1 ± 4.7 yr) participated in a six-way, cross-over design using polychromatic light conditions relevant to the light exposure at home, but with reduced, intermediate or enhanced efficacy with respect to the photopic and melanopsin systems. The evening rise of melatonin, sleepiness and EEG-assessed sleep onset varied significantly (P < 0.01) across the light conditions, and these effects appeared to be largely mediated by the melanopsin, rather than the photopic system. Moreover, there were individual differences in the sensitivity to the disruptive effect of light on melatonin, which were robust against experimental manipulations (intra-class correlation = 0.44). The data show that light at home in the evening affects circadian physiology and imply that the spectral composition of artificial light can be modified to minimize this disruptive effect on sleep and circadian rhythms. These findings have implications for our understanding of the contribution of artificial light exposure to sleep and circadian rhythm disorders such as delayed sleep phase disorder.
From the Wiley Neuroscience twitter feed
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Old 01-03-2016, 12:54 AM   #11
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Default Sleep Loss Boosts Hunger and Unhealthy Food Choices

http://neurosciencenews.com/endocann...p-hunger-3767/

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Sleep-deprived participants in this study—all young, healthy volunteers—were unable to resist what the researchers called “highly palatable, rewarding snacks,” meaning cookies, candy and chips, even though they had consumed a meal that supplied 90 percent of their daily caloric needs two hours before. The effects of sleep loss on appetite were most powerful in the late afternoon and early evening, times when snacking has been linked to weight gain.

“We found that sleep restriction boosts a signal that may increase the hedonic aspect of food intake, the pleasure and satisfaction gained from eating,” said Erin Hanlon, PhD, a research associate in endocrinology, diabetes and metabolism at the University of Chicago. “Sleep restriction seems to augment the endocannabinoid system, the same system targeted by the active ingredient of marijuana, to enhance the desire for food intake.”
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Old 19-03-2016, 08:22 PM   #12
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Default Involvement of Ca2+-Dependent Hyperpolarization in Sleep Duration in Mammals

http://neurosciencenews.com/sleep-calcium-camk2-3884/

Quote:
Highlights
•A simple model predicts Ca2+-dependent hyperpolarization regulates sleep duration
•Impaired/enhanced Ca2+-dependent hyperpolarization decreases/increases sleep duration
•Impaired Ca2+-dependent hyperpolarization increases neural excitability
•Impaired Ca2+/calmodulin-dependent kinases (Camk2a/Camk2b) decreases sleep duration

Summary
The detailed molecular mechanisms underlying the regulation of sleep duration in mammals are still elusive. To address this challenge, we constructed a simple computational model, which recapitulates the electrophysiological characteristics of the slow-wave sleep and awake states. Comprehensive bifurcation analysis predicted that a Ca2+-dependent hyperpolarization pathway may play a role in slow-wave sleep and hence in the regulation of sleep duration. To experimentally validate the prediction, we generate and analyze 21 KO mice. Here we found that impaired Ca2+-dependent K+ channels (Kcnn2 and Kcnn3), voltage-gated Ca2+ channels (Cacna1g and Cacna1h), or Ca2+/calmodulin-dependent kinases (Camk2a and Camk2b) decrease sleep duration, while impaired plasma membrane Ca2+ ATPase (Atp2b3) increases sleep duration. Pharmacological intervention and whole-brain imaging validated that impaired NMDA receptors reduce sleep duration and directly increase the excitability of cells. Based on these results, we propose a hypothesis that a Ca2+-dependent hyperpolarization pathway underlies the regulation of sleep duration in mammals.

“Involvement of Ca2+-Dependent Hyperpolarization in Sleep Duration in Mammals” by Fumiya Tatsuki, Genshiro A. Sunagawa, Shoi Shi, Etsuo A. Susaki, Hiroko Yukinaga, Dimitri Perrin, Kenta Sumiyama, Maki Ukai-Tadenuma, Hiroshi Fujishima, Rei-ichiro Ohno, Daisuke Tone, Koji L. Ode, Katsuhiko Matsumoto, and Hiroki R. Ueda in Neuron. Published online January 191 2016 doi:10.1016/j.neuron.2016.02.032
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Old 22-03-2016, 01:20 PM   #13
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Default Crash risk soars among truck drivers who fail to adhere to sleep apnea treatment

https://www.sciencedaily.com/release...0321081224.htm

Quote:
The largest study of obstructive sleep apnea and crash risk among CMV drivers involved 1,613 truck drivers with sleep apnea and an equal number of controls. The rate of preventable crashes was 5 times higher among truck drivers with sleep apnea who failed to adhere to PAP therapy, compared with matched controls. In contrast, the crash rate of drivers with sleep apnea who were fully or partially adherent with treatment was statistically similar to controls.
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Old 27-03-2016, 12:14 AM   #14
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Default Enhancing Sleep After Brain Injury Reduces Brain Damage and Cognitive Decline in Rats

http://neurosciencenews.com/tbi-slee...oscience-3924/

Quote:
Traumatic brain injury is a major cause of death and disability worldwide. While brain cells at the site of impact are damaged immediately, many more cells can perish in the hours and days after the trauma as damaged axons succumb to injury. Studies suggest that widespread axonal injury contributes to many of the long-lasting problems with learning, memory, and movement commonly associated with head injuries. Molecular waste products also build up in the brain after head injury. Recent studies indicate the brain clears out this molecular buildup during the slow-wave stage of sleep where brain activity synchronizes into high-amplitude waves.
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Old 27-03-2016, 09:03 AM   #15
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Default Neuronal Firing Rate Homeostasis Is Inhibited by Sleep and Promoted by Wake

http://www.cell.com/cell/fulltext/S0...2816%2930060-5

Quote:
Neocortical networks must generate and maintain stable activity patterns despite perturbations induced by learning and experience-dependent plasticity, and this stability must be maintained across distinct behavioral states with very different sensory drive and modulatory tone.
from Adam J Calhoun's twitter feed
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Old 01-04-2016, 12:53 PM   #16
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Default For young adults, sleep problems predict later pain problems

https://www.sciencedaily.com/release...0331124717.htm

Quote:
For at least some groups of "emerging adults," sleep problems are a predictor of chronic pain and worsening pain severity over time, suggests a study in PAIN®, the official publication of the International Association for the Study of Pain® (IASP). The journal is published by Wolters Kluwer.

In contrast, the presence of pain generally doesn't predict worsening sleep problems during the transition between adolescence and young adulthood, according to the new research by Drs. Irma J. Bonvanie and colleagues of University of Groningen, the Netherlands. They believe that early identification and treatment of sleep problems might help reduce later problems with pain in some groups of emerging adults.
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Old 20-04-2016, 07:54 PM   #17
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Default Feel Sleepy During The Day? Your Fatty Diet Could Be To Blame

http://neurosciencenews.com/fatty-di...oscience-4090/

Quote:
University of Adelaide researchers have found that men who consume diets high in fat are more likely to feel sleepy during the day, to report sleep problems at night, and are also more likely to suffer from sleep apnea.
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Old 08-05-2016, 11:11 PM   #18
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Default Smartphones uncover how the world sleeps

https://www.sciencedaily.com/release...0506160105.htm

Quote:
The spread of national averages of sleep duration ranged from a minimum of around 7 hours, 24 minutes of sleep for residents of Singapore and Japan to a maximum of 8 hours, 12 minutes for those in the Netherlands. That's not a huge window, but the researchers say every half hour of sleep makes a big difference in terms of cognitive function and long-term health.

The findings, the researchers say, point to an important lever for the sleep-deprived--a set that the Centers for Disease Control and Prevention is concerned about. A recent CDC study found that across the U.S., one in three adults aren't getting the recommended minimum of seven hours. Sleep deprivation, the CDC says, increases the risk of obesity, diabetes, high blood pressure, heart disease, stroke and stress.

The U-M researchers also found that:

Middle-aged men get the least sleep, often getting less than the recommended 7 to 8 hours.
Women schedule more sleep than men, about 30 minutes more on average. They go to bed a bit earlier and wake up later. This is most pronounced in ages between 30 and 60.
People who spend some time in the sunlight each day tend to go to bed earlier and get more sleep than those who spend most of their time in indoor light.
Habits converge as we age. Sleep schedules were more similar among the older-than-55 set than those younger than 30, which could be related to a narrowing window in which older individuals can fall and stay asleep.
Sleep is more important than a lot of people realize, the researchers say. Even if you get six hours a night, you're still building up a sleep debt, says Walch, doctoral student in the mathematics department and a co-author on the paper.

"It doesn't take that many days of not getting enough sleep before you're functionally drunk," she said. "Researchers have figured out that being overly tired can have that effect. And what's terrifying at the same time is that people think they're performing tasks way better than they are. Your performance drops off but your perception of your performance doesn't."

Aside from the findings themselves, the researchers say the work demonstrates that mobile technology can be a reliable way to gather massive data sets at very low cost.
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Old 02-06-2016, 03:01 PM   #19
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Default Shift work unwinds body clocks, leading to more severe strokes

https://www.sciencedaily.com/release...0601152017.htm

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Statistics show that some 15 million Americans don't work the typical nine-to-five. These employees (or shift workers), who punch in for graveyard or rotating shifts, are more prone to numerous health hazards, from heart attacks to obesity, and now, new research shows shift work may also have serious implications for the brain.
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Old 09-06-2016, 09:14 AM   #20
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Default Shining a light on astrocytes and sleep (Commentary on Pelluru et al.)

http://onlinelibrary.wiley.com/enhan...3b1aad678a7c13

Quote:
The idea that glial cells might be important for sleep has a distinguished pedigree. More than 100 years ago, Ramon y Cajal hypothesized that morphological changes in astrocytic coverage of synapses could be the cellular mechanism gating wakefulness and sleep but, after that perhaps prescient insight (Bellesi et al. 2015), the idea languished despite intriguing suggestions and clues over the intervening years. Glial cells, for example, were known to secrete various sleep-promoting substances in vitro which, when introduced in vivo, increased sleep time or indices of sleep intensity. They were also uniquely positioned to sample synaptic and metabolic activity from neurons, and respond in their own ways to create homeostatic control of these processes. Indeed, difficult experiments in anesthetized animals showed that astrocytes buffer extracellular cation concentrations in ways that suggest that these cells influence a classic index of sleep need (EEG slow-wave activity; SWA) (reviewed by Frank, 2013).

Direct evidence that glial cells really influence sleep in vivo had to wait for a study by Halassa et al. (2009). This study showed that preventing a form of glial chemical exocytosis (‘gliotransmission’) attenuated signs of sleep drive in vivo. Since that study, there has been a resurgence of interest in the role of glia and sleep. A pubmed search with ‘glial’ and ‘sleep’ in the title or abstract finds only a single study in the decade before 2009 and 59 after 2009. This raises two important questions. What does the future hold, and what have we learned?

The future will include the creation of new tools to probe astrocytic function in vivo. Optogenetics is widely used to probe and manipulate neuronal circuits. It involves the expression of light-sensitive ion channels that, when stimulated by specific wavelengths of light, open the channel pore. This has proven to be a highly precise and physiologically relevant tool in neurons because neurons are excitable cells that normally operate via changes in membrane voltage. Several years ago, Deisseroth and colleagues, using an astrocyte-specific viral vector, showed that channelrhodopsin (which passes cations across the membrane) could be expressed in astrocytes in vivo. Upon light stimulation, the pore opened and gliotransmission resulted (Gradinaru et al., 2009). Thus, optogenetics might provide a novel way to interrogate glial function in sleep.

This is precisely what Pelluru et al. (2015), decided to do in their study. They expressed channelrhodopsin in astrocytes in a regionally specific manner. The area they selected was the posterior hypothalamus, in astrocytes that envelop histaminergic neurons. These neurons are known to promote wakefulness; thus the idea being tested was that activation of astrocytes would dampen the activity of these neurons and increase sleep or sleep drive, and that is what they found. After verifying that viral expression of channelrhodopsin was limited to astrocytes, light stimulation increased sleep time and also non-rapid-eye movement SWA. These effects were transient, as might be expected if they were physiological as opposed to pathological.

This then raises the second question: what have we learned? What we have learned is that astrocytes are capable of influencing sleep under these conditions. What we don't know is whether they do so normally. The channelrhodopsin pore is large and does not normally exist in astrocytes. Opening such pores is akin to suddenly and massively perforating the astrocytic plasma membrane, allowing a rush of cations that may never occur normally (given the normal membrane potential of glial cells). This certainly can result in gliotransmission, but possibly a number of other changes that, perhaps not surprisingly, alter surrounding neuronal activity. The use of optogenetics in astrocytes, therefore, highlights a challenge to the field: creating tools designed for glia based on glial, not neuronal, signaling and biology.

Nevertheless, science progresses by such simple elemental steps. The study by Pelluru et al. is important because it pushes the envelope in what we can do to understand the role of glia and sleep. Their results clearly show what might be true. Now, collectively, we must find out whether it is.
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Old 20-06-2016, 05:04 AM   #21
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Default Obstructive Sleep Apnea: A Cluster Analysis at Time of Diagnosis

http://journals.plos.org/plosone/art...l.pone.0157318

Introduction

Quote:
Obstructive sleep apnea (OSA) is a major global health concern, causing considerable cardiovascular and metabolic morbidity and mortality [1]. Although mainly defined by the apnea + hypopnea index (AHI) [2], OSA is nowadays considered a complex, heterogeneous and multi-component condition. It is increasingly recognized that the presence of symptoms, mainly sleepiness but also comorbidities such as cardiovascular and metabolic disease, substantially contributes to prognosis [3].

Treatment for OSA is prescribed not only to normalize symptoms but in a significant percentage of less symptomatic patients it also represents a way of reducing cardiometabolic risk. However, continuous positive airway pressure (CPAP) the first line therapy of OSA fails to improve blood pressure and alter metabolic or inflammatory markers especially in minimally symptomatic obese OSA [4]. This emphasizes the need to offer a combination of multiple modalities of treatment including weight loss by lifestyle interventions or bariatric surgery, physical activity and new medications for reduction of cardiovascular risk specifically dedicated to OSA patients. The pre-requisite for implementing this “personalized OSA medicine” is to have identified the main OSA clusters.

There are few studies that have formally characterized the distinct combinations of symptoms and comorbidities in OSA patients [5, 6] as has been recently done for chronic diseases such as COPD or asthma [7]. We applied cluster analysis to examine the presence of clinically important patient subgroups within a well-characterized national prospective cohort of OSA patients.
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Old 07-07-2016, 09:41 AM   #22
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Default Poor Sleep Health May Contribute to Inflammatory Disease

http://neurosciencenews.com/inflamma...oscience-4627/

Quote:
“It is important to highlight that both too much and too little sleep appears to be associated with inflammation, a process that contributes to depression as well as many medical illnesses,” said Dr. John Krystal, Editor of Biological Psychiatry.

Insufficient sleep is considered a public health epidemic by the Centers for Disease Control and Prevention. Common sleep disturbances, such as insomnia, have been associated with increased risk of inflammatory disease and mortality.

Substances that increase in response to inflammation and circulate in the blood stream, such as C-reactive protein (CRP) and interleukin-6 (IL-6), predict adverse health conditions including cardiovascular events, hypertension, and type 2 diabetes. Many studies have investigated the mechanism behind the association between sleep health and immunity, but variations between studies have made it difficult to understand the effects.

In a recent article, Michael Irwin, Richard Olmstead and Judith Carroll, all of the Cousins Center for Psychoneuroimmunology, UCLA Semel Institute for Neuroscience, University of California, Los Angeles, systematically reviewed existing studies for associations between sleep and inflammatory markers. The meta-analysis examined 72 different articles, which included over 50,000 participants from population-based and clinical studies. The researchers looked at CRP, IL-6, and tumor necrosis factor α (TNFα) as indicators of inflammation.

People with a normal sleep duration get 7-8 hours of shut-eye per night. The analysis showed that sleep disturbance (poor sleep quality or complaints of insomnia) and long sleep duration (more than 8 hours) were associated with increased levels of CRP and IL-6. Shorter sleep duration was associated with increased levels of CRP. No associations were found with TNFα.



Lack of Sleep and Fighting With Partner Increases Inflammation

http://neurosciencenews.com/sleep-fi...ammation-6984/

Researchers find that inflammation markers rise in tired couples who fight.

Quote:
A lack of sleep doesn’t just leave you cranky and spoiling for a fight. Researchers at The Ohio State University Institute for Behavioral Medicine Research say it also puts you at risk for stress-related inflammation.

This type of inflammation is associated with higher risk of cardiovascular disease, diabetes, arthritis and other diseases.

“We know sleep problems are also linked with inflammation and many of the same chronic illnesses. So we were interested to see how sleep related to inflammation among married couples, and whether one partner’s sleep affected the other’s inflammation,” said Stephanie Wilson, lead researcher on the study.

Results of the study were published in the journal Psychoneuroendocrinology.

The research team recruited 43 couples who completed two study visits. Each time, the couples provided blood samples and said how many hours they had slept the previous two nights. Then researchers had the couples try to resolve a topic that sparks conflict in their marriage. Blood samples were taken again following the discussion.

“We found that people who slept less in the past few nights didn’t wake up with higher inflammation, but they had a greater inflammatory response to the conflict. So that tells us less sleep increased vulnerability to a stressor,” Wilson said.

If both partners got less than seven hours of sleep the previous two nights, the couple was more likely to argue or become hostile. For every hour of sleep lost, the researchers noted that levels of two known inflammatory markers rose 6 percent. Couples who used unhealthy tactics in their disagreement had an even greater inflammatory response–about a 10 percent increase with each hour of less sleep.

“Any increase isn’t good, but a protracted increase that isn’t being addressed is where it can become a problem,” Wilson said. “What’s concerning is both a lack of sleep and marital conflict are common in daily life. About half of our study couples had slept less than the recommended seven hours in recent nights.”

That’s higher than the current national average. The CDC reports 35 percent of Americans get less than seven hours of sleep per night.

“Part of the issue in a marriage is that sleep patterns often track together. If one person is restless, or has chronic problems, that can impact the other’s sleep. If these problems persist over time, you can get this nasty reverberation within the couple,” said Janice Kiecolt-Glaser, senior author and director of the Institute for Behavioral Medicine Research.
Update 27/06/2017
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Old 04-08-2016, 05:30 AM   #23
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Default Researchers Discover Sandman’s Role in Sleep Control

http://neurosciencenews.com/sandman-sleep-control-4774/

Quote:
Oxford University researchers have discovered what causes a switch to flip in our brains and wake us up. The discovery, published in the journal Nature, brings us closer to understanding the mystery of sleep.


Inconsistent Sleep Schedule Harms Attention and Creativity in Young Adults

http://neurosciencenews.com/sleep-cr...ttention-6485/

Quote:
‘Most students think they’re getting more sleep than they are,’ Baylor University researcher says.

Skimping on sleep, followed by “catch-up” days with long snoozes, is tied to worse cognition — both in attention and creativity — in young adults, in particular those tackling major projects, Baylor University researchers have found.

“The more variability they showed in their night-to-night sleep, the worse their cognition declined across the week,” said study co-author Michael Scullin, Ph.D., director of Baylor’s Sleep Neuroscience and Cognition Laboratory and assistant professor of psychology and neuroscience in Baylor’s College of Arts & Sciences.

“When completing term projects, students restrict sleep, then rebound on sleep, then repeat,” he said. “Major projects which call for numerous tasks and deadlines — more so than for tests — seem to contribute to sleep variability.”
Update 25/04/2017
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Old 05-08-2016, 12:19 PM   #24
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Default Role of sleep-disordered breathing and sleep-wake disturbances for stroke and stroke recovery

http://www.neurology.org/content/ear...00000000003037

ABSTRACT

Quote:
Background: Sleep-disordered breathing (SDB) and sleep-wake disturbances (SWD) are highly prevalent in stroke patients. Recent studies suggest that they represent both a risk factor and a consequence of stroke and affect stroke recovery, outcome, and recurrence.

Methods: Review of literature.

Results: Several studies have proven SDB to represent an independent risk factor for stroke. Sleep studies in TIA and stroke patients are recommended in view of the very high prevalence (>50%) of SDB (Class IIb, level of evidence B). Treatment of obstructive SDB with continuous positive airway pressure is recommended given the strength of the increasing evidence in support of a positive effect on outcome (Class IIb, level of evidence B). Oxygen, biphasic positive airway pressure, and adaptive servoventilation may be considered in patients with central SDB. Recently, both reduced and increased sleep duration, as well as hypersomnia, insomnia, and restless legs syndrome (RLS), were also suggested to increase stroke risk. Mainly experimental studies found that SWD may in addition impair neuroplasticity processes and functional stroke recovery. Treatment of SWD with hypnotics and sedative antidepressants (insomnia), activating antidepressants or stimulants (hypersomnia), dopaminergic drugs (RLS), and clonazepam (parasomnias) are based on single case observations and should be used with caution.

Conclusions: SDB and SWD increase the risk of stroke in the general population and affect short- and long-term stroke recovery and outcome. Current knowledge supports the systematic implementation of clinical procedures for the diagnosis and treatment of poststroke SDB and SWD on stroke units.
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Old 12-08-2016, 10:04 AM   #25
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Default Exposing the Brain’s Clock

http://neurosciencenews.com/circadia...eep-loss-4836/

Summary:
Quote:
A new study sheds light on numerous functions of our circadian clock, from how the brain maintains performance during the day to how shift workers struggle to maintain attention during early morning hours.
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Old 17-08-2016, 06:03 PM   #26
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Default Dreamless Sleep Store the Day’s Sensory Experiences

http://neurosciencenews.com/sensory-...oscience-4862/

Quote:
Brain boomerang

How the body responds to certain visual cues or the shapes of objects might not seem complicated. But the interpretation, categorization and prioritization of this kind of sensory information is actually highly complex: it requires learning, context and coordinated responses from the brain.

To better understand the neuroscience of this process, Murayama and his colleagues turned to mouse models of touch perception. In 2015, they discovered a two-stage brain circuit that enables mice to discriminate between different floor textures with their paws.

The scientists found that the skin must first send a signal to the brain’s sensory cortex. This message-receiving part of the brain then relays the signal to the higher-order motor cortex—the part of the brain involved in planning, controlling and executing voluntary movements—before the neural signal travels back down to the sensory cortex. This brain boomerang is necessary for tactile processing, the researchers showed, and mice lose their accurate sense of touch without this ‘top-down’ control circuit from the higher-order motor processing center to the more primary sensory area of the brain.

Sleep on it

Building on those results, Murayama’s team sought to determine how the brain turns new sensory experiences into long-term memories. They developed a simple task in which mice familiar with a cage that has an all-smooth floor were introduced to a new cage in which half the floor surface was bumpy.

Mice do not have an innate preference for one texture over the other, but they do have a natural propensity to investigate new things in their environment. Consequently, the animals tended to spend more time exploring the part of the cage with the bumpy floor, indicating that they remembered the all-smooth cage and were less interested in it. But they did this only after a good night’s sleep, or the neurobiological equivalent.

Sleep deprivation impaired the animals’ ability to remember the all-smooth cage. And so did an experimental manipulation in which Murayama’s team used light-activated genetic technology to precisely inactivate the same top-down control circuit they had previously shown was responsible for touch perception.

The timing and direction of the inactivation were critical, however. Silencing the neural signaling bottom-up (from the sensory cortex to the motor cortex) had no effect on tactile memory. Neither did inactivating the top-down pathway (from the motor cortex to the sensory cortex) when the mice wer[e awake or while they were asleep many hours after the initial learning period. Only when the researchers disabled the circuit during deep sleep immediately after the first exploration of the all-smooth cage did the mice subsequently forget the experience.

“Top-down information flow is selectively involved in memory consolidation during sleep,” says RIKEN neuroscientist Daisuke Miyamoto, the first author of the new study.



Deep sleep maintains learning efficiency of the human brain

https://www.nature.com/articles/ncomms15405

Abstract
Quote:
It is hypothesized that deep sleep is essential for restoring the brain’s capacity to learn efficiently, especially in regions heavily activated during the day. However, causal evidence in humans has been lacking due to the inability to sleep deprive one target area while keeping the natural sleep pattern intact. Here we introduce a novel approach to focally perturb deep sleep in motor cortex, and investigate the consequences on behavioural and neurophysiological markers of neuroplasticity arising from dedicated motor practice. We show that the capacity to undergo neuroplastic changes is reduced by wakefulness but restored during unperturbed sleep. This restorative process is markedly attenuated when slow waves are selectively perturbed in motor cortex, demonstrating that deep sleep is a requirement for maintaining sustainable learning efficiency.
Introduction
Quote:
Many of us know from personal experience that a single night of low quality sleep can make mental tasks effortful and inefficient. Accordingly, one theory proposes that sleep is crucial for restoring the brain’s metabolic1 and neural homeostasis2,3, thus ensuring efficient functioning during the next bout of wakefulness. Environmental inputs are constantly experienced when awake and lead to a progressive increase of synaptic strength4,5,6. Perpetual increases in synaptic strength, however, would render the brain highly insensitive to new inputs because neurons would lose their ability to fire selectively and synapses could not be further potentiated, thus saturating neural plasticity7. Additionally, the need for cellular maintenance2 and the removal of potentially neurotoxic waste1 would be markedly enhanced causing an unsustainable level of energy consumption. Deep sleep in particular is thought to be essential for down-regulating synaptic strength3. During deep non-rapid eye movement (NREM) sleep neurons start to oscillate between a depolarized on-state when they fire and a hyperpolarized off-state when they are silent8. Because neurons are highly interconnected, synchronization of on- and off-states within larger neuronal assemblies drives 0.5–4.5 Hz oscillations, termed ‘slow waves’, which are typically detected in the surface electroencephalogram (EEG) or local field potentials during NREM sleep9. Slow wave activity (SWA, EEG power between 1 and 4.5 Hz) is highest shortly after falling asleep, that is, when the sleep need is still high, while it is markedly reduced at the end of the night after restorative processes have taken place10. However, until now the proposal that SWA is necessary for restorative processes has been mainly supported by correlative evidence demonstrating that neural plasticity induced while awake (for example, by practicing a specific task) leads to more SWA during sleep11,12. This effect is highly localized with SWA being significantly higher in brain areas that were activated during the task than in non-task areas, suggesting that the brain responds to a locally increased need for sleep3,5,11,13. However, in order to demonstrate that slow waves are directly responsible for restorative processes, one has to establish a causal relationship between these phenomena. Such an endeavor has thus far proved impossible due to the inability to manipulate SWA in humans on a local level. Here, we introduce a novel perturbation approach where real time closed-loop acoustic stimulation was timed to coincide precisely with the vulnerable down-phase of EEG slow waves2. We targeted SWA in primary motor cortex (M1), taking advantage of well-established behavioural and neurophysiological markers of motor training-induced neuroplasticity to estimate the effect of locally perturbed deep sleep in M1. We demonstrate that the capacity to undergo neuroplastic changes in response to learning is reduced by wakefulness but restored during unperturbed sleep. This restorative process is markedly attenuated when slow waves are selectively perturbed in motor cortex.
Update 23/05/2017



Reactivation or transformation? Motor memory consolidation associated with cerebral activation time-locked to sleep spindles

http://journals.plos.org/plosone/art...l.pone.0174755

Abstract

Quote:
Motor memory consolidation is thought to depend on sleep-dependent reactivation of brain areas recruited during learning. However, up to this point, there has been no direct evidence to support this assertion in humans, and the physiological processes supporting such reactivation are unknown. Here, simultaneous electroencephalographic and functional magnetic resonance imaging (EEG-fMRI) recordings were conducted during post-learning sleep to directly investigate the spindle-related reactivation of a memory trace formed during motor sequence learning (MSL), and its relationship to overnight enhancement in performance (reflecting consolidation). We show that brain regions within the striato-cerebello-cortical network recruited during training on the MSL task, and in particular the striatum, were also activated during sleep, time-locked to spindles. Interestingly, the consolidated trace in the striatum was not simply strengthened, but was transformed/reorganized from rostrodorsal (associative) to caudoventral (sensorimotor) subregions. Moreover, the degree of the reactivation was correlated with overnight improvements in performance. Altogether, the present findings demonstrate that striatal reactivation linked to sleep spindles in the post-learning night, is related to motor memory consolidation.
Update 21/04/2017
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Old 08-09-2016, 12:29 AM   #27
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Default Effects of Restricted Time in Bed on Antidepressant Treatment Response: A Randomized Controlled Trial

http://www.psychiatrist.com/jcp/arti.../15m09879.aspx

Quote:
Objective: Antidepressant response onset is delayed in individuals with major depressive disorder (MDD). This study compared remission rates and time to remission onset for antidepressant medication delivered adjunctively to nightly time in bed (TIB) restriction of 6 hours or 8 hours for the initial 2 weeks.

Methods: Sixty-eight adults with DSM-IV–diagnosed MDD (mean ± SD age = 25.4 ± 6.6 years, 34 women) were recruited from September 2009 to December 2012 in an academic medical center. Participants received 8 weeks of open-label fluoxetine 20–40 mg and were randomized to 1 of 3 TIB conditions for the first 2 weeks: 8-hour TIB (n = 19); 6-hour TIB with a 2-hour bedtime delay (late bedtime, n = 24); or 6-hour TIB with a 2-hour rise time advance (early rise time, n = 25). Clinicians blinded to TIB condition rated symptom severity weekly. Symptom severity, remission rates, and remission onset as rated by the 17-item Hamilton Depression Rating Scale were the primary outcomes.

Results: Mixed effects models indicated lower depression severity for the 8-hour TIB compared to the 6-hour TIB group overall (F8, 226.9 = 2.1, P < .05), with 63.2% of 8-hour TIB compared to 32.6% of 6-hour TIB subjects remitting by week 8 (χ21 = 4.9, P < .05). Remission onset occurred earlier for the 8-hour TIB group (hazard ratio = 0.43; 95% CI, 0.20–0.91; P < .03), with no differences between 6-hour TIB conditions.

Conclusions: Two consecutive weeks of nightly 6-hour TIB does not accelerate or improve antidepressant response. Further research is needed to determine whether adequate sleep opportunity is important to antidepressant treatment response.
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Old 23-09-2016, 04:39 PM   #28
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Default 'I won't be able to cope with my pain if I don't sleep well.'

https://www.sciencedaily.com/release...0921084808.htm

Quote:
Researchers from the Sleep and Pain Lab in the Department of Psychology have demonstrated that conditions like back pain, fibromyalgia, and arthritis are directly linked with negative thoughts about insomnia and pain, and this can be effectively managed by cognitive-behavioural therapy (CBT).
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Old 13-10-2016, 09:38 AM   #29
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Default Chronic Low Quality Sleep Impairs Postural Control in Healthy Adults

http://journals.plos.org/plosone/art...l.pone.0163310

Introduction

Quote:
Sleep is essential for health and sleep disturbances (insufficient duration, poor quality, and irregular timing) can cause a number of disorders [1]. With respect to sleep research, the duration is the most frequently investigated measure because it is easily obtained by an individual inquiry. The appropriate sleep duration for adults has been suggested to be more than 9 hours per night [2], while other authors claimed that a minimum of 7–8 hours of sleep would be sufficient [3]. Several factors, such as work demands, can reduce the sleeping duration below the recommended values eliciting a wide range of effects on mood, cognitive and motor functions [4].

Sleep disorders have a negative impact on postural control (PC) and the standing posture is crucial to perform different tasks, from reaching to locomotion [5]. Moreover, sleep disorders and subsequent PC deterioration are related to work accidents, like driving accidents [6] and falls among frail populations, such as the elderly [7].

Several studies reported that PC deteriorated after one night without sleep [8–16]. However, other studies only found significant differences in PC with sleep deprivation (SD) when the eyes were closed [17–23]. It is well-known that PC performance decreased with eyes closed [24] and this effect might be accentuated with SD [17–23].

Nevertheless, most of the evidence showing that PC was impaired by sleep deprivation was obtained from experiments with participants that were prevented from sleeping for one complete night, that is an acute SD. Furthermore, most of the studies did not monitor objectively the sleep conditions of the participants in the days prior to the tests.

Partial SD or sleep restriction during several days or weeks is a relatively common condition that consists of sleeping below the basal needs and it can occur in three ways [3]. In the first one, sleep fragmentation, sleep is not physiologically consolidated and the normal sequence of sleep stages is disrupted, resulting in less time in consolidated physiological sleep, because fragmentation by brief arousals decreases sleep quality. The second type involves loss of specific physiological sleep stages, and it is referred to as selective sleep stage deprivation. It can occur if sleep fragmentation is isolated to a specific sleep stage. The third type of partial SD is named sleep restriction or sleep debt, which is characterized by reduced sleep duration [3]. The first and the last types are the most prevalent conditions.

Thus, sleep deprivation or restriction is related to the total sleep time, loss of one or more sleep phases and also with the sleep quality. Therefore, low sleep quality is a type of sleep deprivation. Research has shown that inadequate sleep can affect vigilance, information integration, reasoning abilities and motor control performance, such as posture control. To maintain effective performance, sleep quality is as important as sleep quantity. Consequently, subjects should be assessed about their sleep patterns such as sleep interruptions, sleep latency, total sleep time, and frequency of awakenings.

However, the objective assessment of sleep quality is not trivial and it has not received the same attention as acute SD. In fact, to our knowledge, there is no research about the effect of chronic SD and the reduction of sleep quality on PC. In this respect, we hypothesize that chronic partial sleep deprivation and the reduction of sleep quality can affect negatively postural control. Therefore, the objective of the present study is to assess experimentally the effects of the decrease of quality of sleep on PC.
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Old 15-10-2016, 03:10 AM   #30
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Default Exposing the Brain’s Clock

https://www.somasimple.com/forums/ne...ote=1&p=224614

Quote:
Summary: A new study sheds light on numerous functions of our circadian clock, from how the brain maintains performance during the day to how shift workers struggle to maintain attention during early morning hours.
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Old 25-10-2016, 08:30 PM   #31
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Default Gut Microbiota and Glucometabolic Alterations in Response to Recurrent Partial Sleep Deprivation in Normal-weight Young Individuals

http://www.sciencedirect.com/science...12877816301934

Highlights

Possibly the first results of how short sleep impacts the human gut microbiota.

Two nights of short sleep does not significantly impact beta diversity.

The Firmicutes to Bacteriodetes ratio is significantly affected by sleep loss.

Fecal short-chain fatty acid levels do not change depending on sleep duration.

Increased insulin resistance after sleep loss is unrelated to alterations in the microbiota.

Abstract
Quote:
Objective

Changes to the microbial community in the human gut have been proposed to promote metabolic disturbances that also occur after short periods of sleep loss (including insulin resistance). However, whether sleep loss affects the gut microbiota remains unknown.

Methods

In a randomized within-subject crossover study utilizing a standardized in-lab protocol (with fixed meal times and exercise schedules), we studied nine normal-weight men at two occasions: after two nights of partial sleep deprivation (PSD; sleep opportunity 02:45-07:00h), and after two nights of normal sleep (NS; sleep opportunity 22:30-07:00h). Fecal samples were collected within 24 hours before, and after two in-lab nights, of either NS or PSD. In addition, participants underwent an oral glucose tolerance test following each sleep intervention.

Results

Microbiota composition analysis (V4 16S rRNA gene sequencing) revealed that after two days of PSD vs. after two days of NS, individuals exhibited an increased Firmicutes:Bacteroidetes ratio and of the families Coriobacteriaceae and Erysipelotrichaceae, with decreases in Tenericutes (all P<0.05) – previously all associated with metabolic perturbations in animal or human models. However, no PSD vs. NS effect on beta diversity or on fecal short-chain fatty acid concentrations was found. Fasting and postprandial insulin sensitivity decreased after PSD (all P<0.05).

Discussion

Our findings demonstrate that short-term sleep loss induces subtle effects on human microbiota. To what extent changes to the microbial community contribute to metabolic consequences of sleep loss warrants further investigations in larger and more prolonged sleep studies, to also assess how sleep loss impacts the microbiota in individuals who already are metabolically compromised.
Keywords
Bacteroidetes; Firmicutes; insulin resistance; intestinal microbiome; short-chain fatty acid; sleep restriction
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Old 16-11-2016, 12:07 AM   #32
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Default Rotating waves during human sleep spindles organize global patterns of activity that repeat precisely through the night

https://elifesciences.org/content/5/e17267

Abstract
Quote:
During sleep, the thalamus generates a characteristic pattern of transient, 11-15 Hz sleep spindle oscillations, which synchronize the cortex through large-scale thalamocortical loops. Spindles have been increasingly demonstrated to be critical for sleep-dependent consolidation of memory, but the specific neural mechanism for this process remains unclear. We show here that cortical spindles are spatiotemporally organized into circular wave-like patterns, organizing neuronal activity over tens of milliseconds, within the timescale for storing memories in large-scale networks across the cortex via spike-time dependent plasticity. These circular patterns repeat over hours of sleep with millisecond temporal precision, allowing reinforcement of the activity patterns through hundreds of reverberations. These results provide a novel mechanistic account for how global sleep oscillations and synaptic plasticity could strengthen networks distributed across the cortex to store coherent and integrated memories.
eLife digest
Quote:
When you wake up in the morning after a good night's sleep you feel refreshed. You can also think more clearly because your memory has been re-organized, a process called memory consolidation. The problem that the brain has to solve during sleep is how to integrate memories of experiences that happened during the day with old memories, without losing the older memories.

Scientists know that waves of electrical activity, referred to as spindles, help to consolidate and integrate memories during sleep. Spindles are active in the cerebral cortex, the part of your brain used for thinking, in the time between dream sleep and deep sleep. Yet it is not known exactly how these bursting patterns of electrical activity help to strengthen memories.

Now, Muller et al. explored how the spindles could strengthen and connect parts of memories stored in distant parts of the brain. First, a computer algorithm analyzed electrical recordings of brain activity taken while five patients with epilepsy slept. The patients were being monitored to help with their seizures, and the recordings showed that spindles do not occur at the same time throughout the cortex as previously thought. Instead, the spindle is a wave that begins in portion of the cortex near the ear, spirals through the cortex toward the top of back of the head and then on to the forehead area before circling back.

These repeated circular waves of electrical activity strengthen connections between brain cells in distant parts of the brain. For example, these waves may help strengthen connections between the cells of the cortex that separately store memories of the sound, sight and feel of an event during the day, whether that’s being bitten by a dog or talking with a friend. Next, Muller et al. plan to develop computer models of the spindles and verify whether their models make accurate predictions by studying spindles in sleeping mice and rats.


Decoding material-specific memory reprocessing during sleep in humans

https://www.nature.com/articles/ncomms15404

Abstract
Quote:
Neuronal learning activity is reactivated during sleep but the dynamics of this reactivation in humans are still poorly understood. Here we use multivariate pattern classification to decode electrical brain activity during sleep and determine what type of images participants had viewed in a preceding learning session. We find significant patterns of learning-related processing during rapid eye movement (REM) and non-REM (NREM) sleep, which are generalizable across subjects. This processing occurs in a cyclic fashion during time windows congruous to critical periods of synaptic plasticity. Its spatial distribution over the scalp and relevant frequencies differ between NREM and REM sleep. Moreover, only the strength of reprocessing in slow-wave sleep influenced later memory performance, speaking for at least two distinct underlying mechanisms between these states. We thus show that memory reprocessing occurs in both NREM and REM sleep in humans and that it pertains to different aspects of the consolidation process.
Introduction
Quote:
Sleep helps us retain new memories1,2. A reactivation of newly encoded memory traces in the sleeping brain is thought to underlie this effect. Replay of learning-related neuronal firing patterns has been observed in single-cell recordings of the hippocampus and neocortex in animals3,4,5,6. Importantly, this sleep-dependent activation of neurons has recently been shown to promote synaptic plasticity7. Reactivation of neuronal ensembles involved in motor learning is associated with changes in the task-related spiking behaviour of these neurons in the rodent brain8. Furthermore, oscillation related to memory replay during sleep have been linked to greater memory strength and precision in rats9. The dynamics of this memory trace reactivation in humans, however, are still poorly understood. When memory content was associated with auditory or olfactory cues during learning, a re-exposure to these cues during sleep can improve later recall performance10,11. Moreover, activity on the level of brain areas suggests reactivation during sleep12,13. It is unclear whether this re-expression of learning-related activity reflects the specific content of a previous learning task. Recent advances in multivariate pattern classification (MVPC) methods have made it possible to investigate covert cognitive processes in continuous brain activity. Using such methods on brain activity measured with functional magnetic resonance imaging (fMRI), Horikawa et al.14 have recently shown that it is possible to decode the content of visual imagery occurring at sleep onset. In the present study, we used MVPC to test whether the human sleep electroencephalogram (EEG) contains information about what has previously been learned and thus indicates reprocessing of memory content.
Update 20/05/2015
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Old 16-11-2016, 12:09 AM   #33
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I've not been posting here as much as I would like ( less free time!) but I really appreciate all the stuff you post Jo.
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Old 16-11-2016, 12:10 AM   #34
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How kind! Thankyou Paul.
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Old 16-11-2016, 12:42 PM   #35
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Default Study explores how immune system functions during sleep

https://www.sciencedaily.com/release...1115132547.htm

Quote:
T cells are a type of white blood cells and are the foundation of the human body's immune system. Large quantities of T cells are present in the bloodstream and are ready to attack viruses and other pathogens that invade the body. Even during a deep resting phase, the body is able to release T cells, growth hormones and epinephrine back into circulation to fight pathogens when needed. Researchers conducted a "sleep-wake" study to determine how lack of sleep affects the immune system.

Fourteen young male volunteers with an average age of 25 participated in two 24-hour (8 p.m. to 8 p.m.) studies. In one study, the volunteers were allowed to sleep between 11 p.m. and 7 a.m. During the other study, the men were kept awake for 24 hours. Blood samples were taken from each volunteer at varying intervals (90 minutes to three hours) throughout each 24-hour period.

Among the sleeping group, all measured T cell subsets were reduced within three hours of falling asleep. However, T cell numbers remained high in subjects who were not allowed to sleep. While the research showed that the T cells left the bloodstream, where they went is a mystery. "It is an unsolved question as to where the cells are redistributed during sleep since we cannot follow their migratory route in healthy humans. … There are some hints from previous studies that these cells accumulate in lymph nodes during sleep," the researchers wrote.

The rapid drop in circulating T cells during sleep "show[s] that even one night without sleep affects the adaptive immune system," says first author Luciana Besedovsky. "This … might be one reason why regular sleep is so important for general health."
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Old 22-11-2016, 09:54 PM   #36
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Default How the 24-hour society is stealing time from the night

https://aeon.co/ideas/how-the-24-hou...3091d-69418129



Quote:
Burmese monks know that it is time to get up when it is light enough to see the veins in their hands. Muslims base their getting up on the passage in the Quran that defines daybreak as the time when it is possible to distinguish between a dark and a light thread. In parts of Madagascar, questions about how long something takes might receive the answer ‘the time of rice-cooking’ (about half an hour) or ‘the frying of a locust’ (a quick moment).

In a world without clocks, it is natural cues or events that give some sense of time. Each day sees the sun and moon rise and set. The tides rise and fall. Seasons come and go, and return again. Planets move across the sky and come back to their starting point. It is a world of endless cycles but essentially changeless.
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Old 26-11-2016, 11:30 PM   #37
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Default Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training

http://journals.plos.org/plosone/art...l.pone.0167029

Abstract

Quote:
Background

Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation.

Methods

Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated.

Results

Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway.

Conclusions

Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.
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Old 29-11-2016, 01:56 PM   #38
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Default A new study reports the parieto-occipital areas of the brain appear to be more susceptible to a lack of sleep in children.

http://neurosciencenews.com/sleep-de...children-5618/

“The process of sleep may be involved in brain ‘wiring’ in childhood and thus affect brain maturation,” explains Salome Kurth, first author of the study published in Frontiers in Human Neuroscience, and a researcher at the University Hospital of Zurich. “This research shows an increase in sleep need in posterior brain regions in children.”

This contrasts with what researchers know about the effects of sleep deprivation in adults, where the effect is typically concentrated in the frontal regions of the brain.

After staying up too late, both children and adults need a period of deep sleep to recover.




Pediatric sleep apnea and depressive disorders risk: A population-based 15-year retrospective cohort study

http://journals.plos.org/plosone/art...l.pone.0181430

Abstract

Quote:
Background

Studies have shown a higher risk of depressive disorders in children with sleep apnea than in those without sleep apnea. However, the association between sleep apnea and subsequent depressive disorders in the pediatric population remains undetermined. Thus, this study investigated the risk of depressive disorders among pediatric patients with sleep apnea.

Methods

In this study, the population-based National Health Insurance Research Database of Taiwan was used to identify patients who had first been diagnosed with sleep apnea between 1999 and 2013. Patients with sleep apnea who were younger than 18 years were included in the sleep apnea group. Controls (those without sleep apnea) were matched to patients with sleep apnea at a 1:10 ratio by age, sex, and index year. Patients who had baseline or inherited depressive disorders before the enrollment date were excluded. The two groups were followed up until December 31, 2013. The primary endpoint was the occurrence of one or more depressive disorders.

Results

At the end of this study, 6,237 children had been enrolled, comprising 567 children with sleep apnea and 5,670 children without sleep apnea. During the mean follow-up period of 5.87 years, a total of 77 children (1.23%) developed one or more depressive disorders; 14 (2.46%) from the sleep apnea group and 63 (1.11%) from the control group. Kaplan–Meier analysis showed that children with sleep apnea had a significantly higher risk of depressive disorders (log-rank test, p = 0.002). After adjusting for covariates, the risk of subsequent depressive disorders among children with sleep apnea was still significantly higher (hazard ratio [HR] = 2.25; 95% confidence interval [CI] = 1.25–4.05; p = 0.006). Moreover, boys with sleep apnea had a significantly higher risk than those without sleep apnea (adjusted HR = 3.77; 95% CI, 1.82–7.54; p < 0.001). Furthermore, in sleep apnea group, children older than 12 years of age had more risk to depression (hazard ratio (HR) = 7.1833, 95% confidence interval (CI), 2.3734 to 21.7411; p = 0.0004).
Update 19/07/2017
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Old 26-12-2016, 01:48 PM   #39
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Default Falling for sleep

https://aeon.co/essays/the-cure-for-...4d89e-69418129

Quote:
The Industrial Revolution radically transformed our perception of sleep from a gracious, transcendent experience to a mechanistic, biomedical process. With mechanistic philosophies on the rise, the machine emerged as a new hero, with its promise of salvation from all human ills. And energy became gold.

Across the Western world, machines and labourers sprouted in concert with coal mines and coffee houses. Industrialisation seeded a global energy crisis – serving as metaphor for our personal energy crisis. Today, oil and coffee are the most commonly traded commodities in the world. We are a society of energy addicts dependent on overly stimulating foods, fluids, information, entertainment and light at night. And, of course on the extensive global network of machinery needed to manufacture and maintain this lifestyle.
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Old 02-01-2017, 08:48 PM   #40
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Default Synchronizing with Brain Clocks

http://jonlieffmd.com/blog/neuronal-...7a05b-90589721

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Up until recently, research into circadian rhythms has focused on central brain clocks that synchronize other cells. The three previous posts have described new research that each living cell has its own individual clocks based on genetic feedback loops combined with epigenetic loops. The three posts described the discovery of individual clocks, the relation to metabolic cycles in tissues and other cells, and the way immune cell cycles alter responses based on clocks. This fourth post in the series describes what is known about the central clocks and how they might be related to brain disease.



The Neural Relationship Between Light and Sleep

http://neurosciencenews.com/light-sleep-6971/

Quote:
Humans are diurnal animals, meaning that we usually sleep at night and are awake during the day, due at least in part to light or the lack thereof. Light is known to affect sleep indirectly by entraining–modifying the length of–our circadian rhythms and also rapidly and directly due to a phenomenon known as masking. But while a great deal is known about how light affects circadian rhythms, little is known about the direct effects of light on sleep: Why do we tend to wake up if the lights are flipped on in the middle of the night? Why does darkness make us sleepy? Caltech researchers in the laboratory of Professor of Biology David Prober say they have discovered at least part of the answer: a specific protein in the brain that responds to light and darkness to set the correct balance between sleep and wakefulness.

Their work is described in a paper appearing online in the journal Neuron on June 22.
Update 25/06/2017
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Old 06-01-2017, 10:07 AM   #41
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Default Taking an Hour Long Afternoon Nap Improves Memory and Cognition in Older Adults

http://neurosciencenews.com/memory-napping-aging-5875/

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Preserving your memory, as well as your ability to think clearly and make decisions, is a key goal for people as they age. Researchers have a growing interest in the role sleep plays in helping older adults maintain their healthy mental function.
Animals and small children, athletes and other high level performers, do this instinctively. I sometimes find it difficult to persuade those recovering from illness and injury that it isn't lazy or decadent.

Those of us who sleep once or more during the day seem to have better tolerance to working very long days, working hard, and dealing with unexpected/unavoidable situations during which very little sleep can be taken, than those who have a more conventional routine.
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Old 27-01-2017, 04:49 PM   #42
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Default One more reason to get a good night's sleep

https://www.ted.com/talks/jeff_iliff..._night_s_sleep

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The brain uses a quarter of the body's entire energy supply, yet only accounts for about two percent of the body's mass. So how does this unique organ receive and, perhaps more importantly, rid itself of vital nutrients? New research suggests it has to do with sleep.
Cranial osteopaths will love this as there is a lot about CSF. We should bear in mind that there is no evidence that what we do with our hands on can influence the process. Does a light doze count as sleep? Probably not.
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Old 27-01-2017, 08:09 PM   #43
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Default Transcriptional Signatures of Sleep Duration Discordance in Monozygotic Twins

https://academic.oup.com/sleep/artic...Sleep-Duration

Abstract

Quote:
Introduction:

Habitual short sleep duration is associated with adverse metabolic, cardiovascular, and inflammatory effects. Co-twin study methodologies account for familial (eg, genetics and shared environmental) confounding, allowing assessment of subtle environmental effects, such as the effect of habitual short sleep duration on gene expression. Therefore, we investigated gene expression in monozygotic twins discordant for actigraphically phenotyped habitual sleep duration.

Methods:

Eleven healthy monozygotic twin pairs (82% female; mean age 42.7 years; SD = 18.1), selected based on subjective sleep duration discordance, were objectively phenotyped for habitual sleep duration with 2 weeks of wrist actigraphy. Peripheral blood leukocyte (PBL) RNA from fasting blood samples was obtained on the final day of actigraphic measurement and hybridized to Illumina humanHT-12 microarrays. Differential gene expression was determined between paired samples and mapped to functional categories using Gene Ontology. Finally, a more comprehensive gene set enrichment analysis was performed based on the entire PBL transcriptome.

Results:

The mean 24-hour sleep duration of the total sample was 439.2 minutes (SD = 46.8 minutes; range 325.4–521.6 minutes). Mean within-pair sleep duration difference per 24 hours was 64.4 minutes (SD = 21.2; range 45.9–114.6 minutes). The twin cohort displayed distinctive pathway enrichment based on sleep duration differences. Habitual short sleep was associated with up-regulation of genes involved in transcription, ribosome, translation, and oxidative phosphorylation. Unexpectedly, genes down-regulated in short sleep twins were highly enriched in immuno-inflammatory pathways such as interleukin signaling and leukocyte activation, as well as developmental programs, coagulation cascade, and cell adhesion.

Conclusions:

Objectively assessed habitual sleep duration in monozygotic twin pairs appears to be associated with distinct patterns of differential gene expression and pathway enrichment. By accounting for familial confounding and measuring real life sleep duration, our study shows the transcriptomic effects of habitual short sleep on dysregulated immune response and provides a potential link between sleep deprivation and adverse metabolic, cardiovascular, and inflammatory outcomes.
Keywords: Sleep duration, Twins, Monozygotic, Gene expression, Leukocyte.
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Old 02-02-2017, 11:22 PM   #44
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Default Universal Immune Mechanism as a Regulator of Sleep

http://neurosciencenews.com/sleep-im...echanism-6049/

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Sleep — one of the most basic, yet most mystifying processes of the human body — has confounded physicians, scientists and evolutionary biologists for centuries.

Now a study conducted in mice and led by investigators at Harvard Medical School and VA Boston Healthcare System reveals that sleep may be regulated in part by several brain-based immune proteins collectively called inflammasome NLRP3.

The researchers say the inflammasome — which works by unleashing a cascade of immune molecules in response to inflammation and infection — emerges as a central promoter of sleep following such events.

A report on the team’s findings was published Jan. 19 in Brain, Behavior and Immunity.

Scientists have known for a while that certain immune molecules enhance sleep and are activated by infection, but this is the first study suggesting a common underlying mechanism that regulates sleep and plays a critical role in recuperative sleep responses.

Results of the study show that the inflammasome recruits a sleep-inducing molecule to trigger somnolence following sleep deprivation and exposure to a bacterial toxin. Animals lacking genes for this protective immune complex showed profound sleep aberrations.”Our research points, for the first time, to the inflammasome acting as a universal sensing mechanism that regulates sleep through the release of immune molecules,” said study senior investigator Mark R. Zielinski, instructor in psychiatry at HMS.

Although warranting further study, the observations suggest that the inflammasome, the constellation of sleep-regulating proteins, may play an evolutionary role as a guardian of brain health and vitality that wards off the effects of sleep deprivation and infection.
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Old 02-02-2017, 11:29 PM   #45
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Default How the Brain Resets During Sleep

http://neurosciencenews.com/sleep-brain-reset-6047/

Quote:
Striking electron microscope pictures from inside the brains of mice suggest what happens in our own brain every day: Our synapses – the junctions between nerve cells – grow strong and large during the stimulation of daytime, then shrink by nearly 20 percent while we sleep, creating room for more growth and learning the next day.

The four-year research project published today in Science offers a direct visual proof of the “synaptic homeostasis hypothesis” (SHY) proposed by Drs. Chiara Cirelli and Giulio Tononi of the Wisconsin Center for Sleep and Consciousness.

This hypothesis holds that sleep is the price we pay for brains that are plastic and able to keep learning new things.

When a synapse is repeatedly activated during waking, it grows in strength, and this growth is believed to be important for learning and memory. According to SHY, however, this growth needs to be balanced to avoid the saturation of synapses and the obliteration of neural signaling and memories. Sleep is believed to be the best time for this process of renormalization, since when asleep we pay much less attention to the external world and are free from the “here and now.”

When synapses get stronger and more effective they also become bigger, and conversely they shrink when they weaken. Thus, Cirelli and Tononi reasoned that a direct test of SHY was to determine whether the size of synapses changes between sleep and wake. To do so, they used a method with extremely high spatial resolution called serial scanning 3-D electron microscopy.

The research itself was a massive undertaking, with many research specialists working for four years to photograph, reconstruct, and analyze two areas of cerebral cortex in the mouse brain. They were able to reconstruct 6,920 synapses and measure their size.

The team deliberately did not know whether they were analyzing the brain cells of a well-rested mouse or one that had been awake. When they finally “broke the code” and correlated the measurements with the amount of sleep the mice had during the six to eight hours before the image was taken, they found that a few hours of sleep led on average to an 18 percent decrease in the size of the synapses. These changes occurred in both areas of the cerebral cortex and were proportional to the size of the synapses.

The scaling occurred in about 80 percent of the synapses but spared the largest ones, which may be associated with the most stable memory traces.


This picture shows 3-D reconstructions of electron microscope images of tree branch-like dendrites. At the end of the branches are cup-like structures called the spines, and in the tips of the spines are synapses. By studying thousands of images like these, the Wisconsin researchers showed that the synapses shrink after the mouse sleeps and grow again during the next wakeful period. NeuroscienceNews.com image is credited to Wisconsin Center for Sleep and Consciousness.

Quote:
“This shows, in unequivocal ultrastructural terms, that the balance of synaptic size and strength is upset by wake and restored by sleep,” Cirelli says. “It is remarkable that the vast majority of synapses in the cortex undergo such a large change in size over just a few hours of wake and sleep.

Tononi adds, “Extrapolating from mice to humans, our findings mean that every night trillions of synapses in our cortex could get slimmer by nearly 20 percent.”

The study was published today in Science along with research from Dr. Richard Huganir’s laboratory at Johns Hopkins University in Baltimore. This study, using biochemical and molecular methods, confirms SHY’s prediction that synapses undergo a process of scaling down during sleep, and identifies genes important for this process.
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Old 04-02-2017, 08:33 PM   #46
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Default Circadian Entrainment to the Natural Light-Dark Cycle across Seasons and the Weekend

http://www.cell.com/current-biology/...822(16)31522-6

Highlights
Quote:
•Living in the modern electrical lighting environment delays the human circadian clock

•The human circadian clock adapts to seasonal changes in the natural light-dark cycle

•A weekend camping trip prevented the typical weekend circadian and sleep delay

Summary
Quote:
Reduced exposure to daytime sunlight and increased exposure to electrical lighting at night leads to late circadian and sleep timing [1, 2, 3]. We have previously shown that exposure to a natural summer 14 hr 40 min:9 hr 20 min light-dark cycle entrains the human circadian clock to solar time, such that the internal biological night begins near sunset and ends near sunrise [1]. Here we show that the beginning of the biological night and sleep occur earlier after a week’s exposure to a natural winter 9 hr 20 min:14 hr 40 min light-dark cycle as compared to the modern electrical lighting environment. Further, we find that the human circadian clock is sensitive to seasonal changes in the natural light-dark cycle, showing an expansion of the biological night in winter compared to summer, akin to that seen in non-humans [4, 5, 6, 7, 8]. We also show that circadian and sleep timing occur earlier after spending a weekend camping in a summer 14 hr 39 min:9 hr 21 min natural light-dark cycle compared to a typical weekend in the modern environment. Weekend exposure to natural light was sufficient to achieve ∼69% of the shift in circadian timing we previously reported after a week’s exposure to natural light [1]. These findings provide evidence that the human circadian clock adapts to seasonal changes in the natural light-dark cycle and is timed later in the modern environment in both winter and summer. Further, we demonstrate that earlier circadian timing can be rapidly achieved through natural light exposure during a weekend spent camping.
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Old 09-02-2017, 12:30 AM   #47
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Default Advanced EEG Reveals Complex Beauty of the Sleeping Brain

http://neurosciencenews.com/eeg-sleeping-brain-6079/

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“During sleep, the brain is engaged in a symphony of activity involving the dynamic interplay of different cortical and sub-cortical networks,” says Michael Prerau, PhD, of the MGH Department of Anesthesia, Critical Care and Pain Management, lead author of the Physiology report. “Due to practical constraints and established practices, current clinical techniques greatly simplify the way the sleep is described, causing massive amounts of information to be lost. We therefore wanted to identify a more comprehensive way of characterizing brain activity during sleep that was easy to understand and quick to learn, yet mathematically principled and robust.”
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Old 11-02-2017, 07:19 AM   #48
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Default Coordinated infraslow neural and cardiac oscillations mark fragility and offline periods in mammalian sleep

http://advances.sciencemag.org/conte.../e1602026.full

Abstract

Quote:
Rodents sleep in bouts lasting minutes; humans sleep for hours. What are the universal needs served by sleep given such variability? In sleeping mice and humans, through monitoring neural and cardiac activity (combined with assessment of arousability and overnight memory consolidation, respectively), we find a previously unrecognized hallmark of sleep that balances two fundamental yet opposing needs: to maintain sensory reactivity to the environment while promoting recovery and memory consolidation. Coordinated 0.02-Hz oscillations of the sleep spindle band, hippocampal ripple activity, and heart rate sequentially divide non–rapid eye movement (non-REM) sleep into offline phases and phases of high susceptibility to external stimulation. A noise stimulus chosen such that sleeping mice woke up or slept through at comparable rates revealed that offline periods correspond to raising, whereas fragility periods correspond to declining portions of the 0.02-Hz oscillation in spindle activity. Oscillations were present throughout non-REM sleep in mice, yet confined to light non-REM sleep (stage 2) in humans. In both species, the 0.02-Hz oscillation predominated over posterior cortex. The strength of the 0.02-Hz oscillation predicted superior memory recall after sleep in a declarative memory task in humans. These oscillations point to a conserved function of mammalian non-REM sleep that cycles between environmental alertness and internal memory processing in 20- to 25-s intervals. Perturbed 0.02-Hz oscillations may cause memory impairment and ill-timed arousals in sleep disorders.
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Old 23-02-2017, 08:19 PM   #49
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Default Prolonged sleep duration as a marker of early neurodegeneration predicting incident dementia

http://www.neurology.org/content/ear...00003732.short

ABSTRACT

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Objective: To evaluate the association between sleep duration and the risk of incident dementia and brain aging.

Methods: Self-reported total hours of sleep were examined in the Framingham Heart Study (n = 2,457, mean age 72 ± 6 years, 57% women) as a 3-level variable: <6 hours (short), 6–9 hours (reference), and >9 hours (long), and was related to the risk of incident dementia over 10 years, and cross-sectionally to total cerebral brain volume (TCBV) and cognitive performance.

Results: We observed 234 cases of all-cause dementia over 10 years of follow-up. In multivariable analyses, prolonged sleep duration was associated with an increased risk of incident dementia (hazard ratio [HR] 2.01; 95% confidence interval [CI] 1.24–3.26). These findings were driven by persons with baseline mild cognitive impairment (HR 2.83; 95% CI 1.06–7.55) and persons without a high school degree (HR 6.05; 95% CI 3.00–12.18). Transitioning to sleeping >9 hours over a mean period of 13 years before baseline was associated with an increased risk of all-cause dementia (HR 2.43; 95% CI 1.44–4.11) and clinical Alzheimer disease (HR 2.20; 95% CI 1.17–4.13). Relative to sleeping 6–9 hours, long sleep duration was also associated cross-sectionally with smaller TCBV (β ± SE, −1.08 ± 0.41 mean units of TCBV difference) and poorer executive function (β ± SE, −0.41 ± 0.13 SD units of Trail Making Test B minus A score difference).

Conclusions: Prolonged sleep duration may be a marker of early neurodegeneration and hence a useful clinical tool to identify those at a higher risk of progressing to clinical dementia within 10 years.

Acoustic Enhancement of Sleep Slow Oscillations and Concomitant Memory Improvement in Older Adults

http://journal.frontiersin.org/artic...017.00109/full

Quote:
Acoustic stimulation methods applied during sleep in young adults can increase slow wave activity (SWA) and improve sleep-dependent memory retention. It is unknown whether this approach enhances SWA and memory in older adults, who generally have reduced SWA compared to younger adults. Additionally, older adults are at risk for age-related cognitive impairment and therefore may benefit from non-invasive interventions. The aim of this study was to determine if acoustic stimulation can increase SWA and improve declarative memory in healthy older adults. Thirteen participants 60–84 years old completed one night of acoustic stimulation and one night of sham stimulation in random order. During sleep, a real-time algorithm using an adaptive phase-locked loop modeled the phase of endogenous slow waves in midline frontopolar electroencephalographic recordings. Pulses of pink noise were delivered when the upstate of the slow wave was predicted. Each interval of five pulses (“ON interval”) was followed by a pause of approximately equal length (“OFF interval”). SWA during the entire sleep period was similar between stimulation and sham conditions, whereas SWA and spindle activity were increased during ON intervals compared to matched periods during the sham night. The increases in SWA and spindle activity were sustained across almost the entire five-pulse ON interval compared to matched sham periods. Verbal paired-associate memory was tested before and after sleep. Overnight improvement in word recall was significantly greater with acoustic stimulation compared to sham and was correlated with changes in SWA between ON and OFF intervals. Using the phase-locked-loop method to precisely target acoustic stimulation to the upstate of sleep slow oscillations, we were able to enhance SWA and improve sleep-dependent memory storage in older adults, which strengthens the theoretical link between sleep and age-related memory integrity.
Quote:
Sleep in older adults is characterized by frequent awakenings and a prominent reduction in REM, SWS, and SWA (Ohayon et al., 2004; Edwards et al., 2010). Although word pair recall in older adults has been associated with duration of non-REM/REM sleep cycles (Mazzoni et al., 1999), REM sleep deprivation has been shown to have no effect on memory consolidation (Hornung et al., 2007). Much is unknown about the specific mechanisms of age-related changes in sleep physiology, but recent evidence suggests that gray-matter atrophy in the medial prefrontal cortex underlies age-related decline in SWA (Mander et al., 2013b). SWA has indeed been shown to be associated with declarative memory performance in older adults (Westerberg et al., 2012; Mander et al., 2013b). Given this evidence implicating SWA, it is biologically plausible that memory storage can be enhanced in older adults by promoting slow wave synchronization during sleep.
Update 26/04/2017
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Old 25-02-2017, 10:33 AM   #50
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Default Bidirectional, Temporal Associations of Sleep with Positive Events, Affect, and Stressors in Daily Life Across a Week

https://link.springer.com/article/10...160-016-9864-y

Abstract
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Background

Sleep is intricately tied to emotional well-being, yet little is known about the reciprocal links between sleep and psychosocial experiences in the context of daily life.

Purpose

The aim of this study is to evaluate daily psychosocial experiences (positive and negative affect, positive events, and stressors) as predictors of same-night sleep quality and duration, in addition to the reversed associations of nightly sleep predicting next-day experiences.

Methods

Daily experiences and self-reported sleep were assessed via telephone interviews for eight consecutive evenings in two replicate samples of US employees (131 higher-income professionals and 181 lower-income hourly workers). Multilevel models evaluated within-person associations of daily experiences with sleep quality and duration. Analyses controlled for demographics, insomnia symptoms, the previous day’s experiences and sleep measures, and additional day-level covariates.

Results

Daily positive experiences were associated with improved as well as disrupted subsequent sleep. Specifically, positive events at home predicted better sleep quality in both samples, whereas greater positive affect was associated with shorter sleep duration among the higher-income professionals. Negative affect and stressors were unrelated to subsequent sleep. Results for the reversed direction revealed that better sleep quality (and, to a lesser degree, longer sleep duration) predicted emotional well-being and lower odds of encountering stressors on the following day.

Conclusions

Given the reciprocal relationships between sleep and daily experiences, efforts to improve well-being in daily life should reflect the importance of sleep.
Keywords

Sleep Daily stress Positive events Positive affect Negative affect
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