New Research Identifies 2 Key Lifestyle Factors For Reducing Dementia Risk by mindbodygreen

I'm good with all of these.
New Research Identifies 2 Key Lifestyle Factors For Reducing Dementia Risk

Pink Noise Might Be Stealing Your Best Sleep by Super Age

 Have your doctor vet this and CREATE AN EXACT SLEEP PROTOCOL! Not doing so is incompetence!

• 30% poor sleep (17 posts to May 2019)
• sleep deprivation (7 posts to June 2015)
• sleep disruption (6 posts to January 2018)
• sleep protocol? (14 posts to April 2014)

Pink Noise Might Be Stealing Your Best Sleep

Prevalence of post-stroke poor sleep quality: a meta-analysis of Pittsburgh Sleep Quality Index results

Prevalence is totally useless! You need to create EXACT SLEEP PROTOLS! Are you that fucking incompetent you can't accomplish that?

You've known of poor sleep for how many years and STILL HAVEN'T SOLVED THE PROBLEM? Only 6+ years and why haven't you been fired yet?

30% poor sleep (16 posts to May 2019)

 Prevalence of post-stroke poor sleep quality: a meta-analysis of Pittsburgh Sleep Quality Index results

Yu Zhou¹Bi Guan²Rong Tang³Qiongyao Zhong⁴Liangnan Zeng^5*

• 1Department of Operating Room, Chengdu Fifth People’s Hospital, Chengdu, China
• 2Department of Nursing, Chengdu Fifth People’s Hospital, Chengdu, China
• 3Department of Orthopedics, Chengdu Fifth People’s Hospital, Chengdu, China
• 4Department of Neurology, Chengdu Fifth People’s Hospital, Chengdu, China
• 5Department of Nursing, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China

Objective: To assess the prevalence of post-stroke poor sleep quality using the Pittsburgh Sleep Quality Index (PSQI).

Methods: This study was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Following the PICO framework, a systematic search was conducted in PubMed, CINAHL, Cochrane Library, and Web of Science for relevant cohort, case-control, and cross-sectional studies published up to October 2024. The retrieved literature was then meta-analyzed using Stata 13.0 software.

Results: Eighteen studies were reviewed, showing a total poor sleep quality prevalence of 55% (95%CI = 0.47 to 0.62) and a PSQI score is 8.12 (95%CI = 6.71 to 9.53). Compared to normal people, stroke patients sleep onset latency (SL) was prolonged by 1.36 min (95%CI = 0.82 to 1.90), sleep efficiency (SE) decreased by 1.48% (95%CI = −0.20 to −0.92), and periodic leg movements per hour of sleep (PLMI) increased by 1.07 per hour (95%CI = 0.56 to 1.59). Subgroup analysis showed that, compared with hemorrhagic stroke patients, ischemic stroke patients had higher incidence of poor sleep quality at 52% (95%CI = 0.24 to 0.86); the incidence of poor sleep quality was 59% (95%CI = 0.49 to 0.70) higher in chronic stroke patients compared to acute and subacute stroke patients; the incidence of poor sleep quality was 61% (95%CI = 0.51 to 0.71) higher in community stroke patients than in hospitalized stroke patients; and the incidence of poor sleep quality was 59% (95%CI = 0.58 to 0.61) higher in stroke patients in developing countries than those in developed countries.

Conclusion: Current evidence suggests that quality of sleep worsens after a stroke, with symptoms being widespread. Factors such as stroke type, stroke phase, clinical setting, and research region can all impact sleep quality after stroke. These findings underscore the importance of monitoring sleep quality in these populations and implementing appropriate preventive and interventional strategies.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO, identifier CRD420251161167.

More at link.

Sleep Disorders Predict Parkinson’s or Dementia Years Ahead

 

With your extra risk of dementia and Parkinsons post stroke; DOES YOUR DOCTOR HAVE EXACT  PREVENTION PROTOCOLS? NO? So, your doctor is incompetent? 

Your doctor has known of sleep problems post stroke for years now, has ANYTHING BEEN DONE?

30% poor sleep (14 posts to May 2019)

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

Sleep Disorders Predict Parkinson’s or Dementia Years Ahead

Summary: Two landmark international studies show that brain biomarkers can predict whether people with REM sleep behaviour disorder (iRBD) will develop Parkinson’s disease or dementia with Lewy bodies (DLB). MRI scans revealed that reduced glymphatic system function signals higher risk for Parkinson’s, while increased free water in the basal nucleus of Meynert predicts progression to DLB.

These findings come from the largest imaging studies ever conducted in patients with confirmed iRBD. The results pave the way for earlier diagnosis, targeted monitoring, and preventive treatments before irreversible brain damage occurs.

Key Facts

• Parkinson’s Predictor: Reduced glymphatic fluid circulation doubled Parkinson’s risk.
• DLB Predictor: Higher free water in the basal nucleus of Meynert raised DLB risk 8-fold.
• Clinical Impact: First tools to differentiate disease outcomes years before symptoms.

Source: University of Montreal

An international research team led by Université de Montréal medical professor Shady Rahayel has made a major breakthrough in predicting neurodegenerative diseases.

Thanks to two complementary UdeM studies, scientists are now able to determine, years in advance, which individuals with a particular sleep disorder will develop Parkinson’s disease or dementia with Lewy bodies (DLB).

The studies focus on isolated REM sleep behaviour disorder (iRBD)—a condition in which people yell, thrash, or act out their dreams, sometimes violently enough to injure a bed partner.

“It’s not just restless sleep—it’s a neurological warning sign,” said Rahayel, a neuropsychologist and researcher at the Centre for Advanced Research in Sleep Medicine at Sacré-Cœur Hospital in Montreal.

Roughly 90 per cent of people with this sleep disorder will go on to eventually develop Parkinson’s disease or DLB. Until now, however, it was impossible to know which disease would occur—or when.

First biomarker: predicting Parkinson’s

The first study, led by UdeM doctoral student in neurosciences Violette Ayral and published in Neurology on September 16, involved 428 participants from five countries: Canada, the United States, France, the United Kingdom and Czechia.

It examined the brain’s glymphatic system—a network that clears metabolic waste during sleep, including proteins linked to neurodegeneration. When this system is impaired, waste accumulates, potentially triggering diseases like Parkinson’s.

Using an advanced MRI technique known as DTI-ALPS, researchers measured fluid circulation in specific brain regions in 250 patients with iRBD and 178 healthy control subjects, with an average follow-up of six years.

The key finding: patients with a lower DTI-ALPS index in the left hemisphere of the brain (indicating reduced fluid circulation) were 2.4 times more likely to develop Parkinson’s disease in the years that followed. No such link was found for dementia with Lewy bodies.

“This asymmetry mirrors what we see clinically in early Parkinson’s, where motor symptoms often start on one side of the body – it may mark the very earliest stage of the disease,” said Ayral.

This is the first evidence that glymphatic function, as measured by MRI, can predict progression to Parkinson’s—and the largest international study ever conducted on this topic among patients with polysomnography-confirmed REM sleep disorder.

Second biomarker: predicting DLB

The second study, led by UdeM doctoral student in neuropsychology Celine Haddad and published in Alzheimer’s & Dementia on September 19, focused on 438 participants from the same five countries as the first study.

It took a different approach to predict the onset of DLB —a condition combining Parkinsonian symptoms (tremors, rigidity) and Alzheimer-like symptoms (cognitive impairment, confusion, hallucinations). It’s the second most common degenerative dementia after Alzheimer’s.

Researchers measured the amount of “free water” — water not bound by brain cells and able to flow freely between them — in the basal nucleus of Meynert, a key region for thought and reasoning. This free water is a sign of early microscopic changes, such as inflammation or cell loss, and serves as an indirect marker of neuronal degeneration.

After a median follow-up of 8.4 years, the results were striking: individuals who developed DLB had significantly higher levels of free water in this brain region, making them eight times more likely to convert to this form of dementia. This method proved more sensitive than traditional approaches based on brain atrophy.

“What’s fascinating is that this marker picks up very early changes—even before symptoms emerge,” said Haddad.

Toward precision medicine

These studies represent the largest international imaging research ever done on patients with polysomnography-confirmed iRBD, and pave the way for personalized screening tests to predict which disease will develop before symptoms appear.

Clinicians will be able to tailor medical monitoring to each patient’s trajectory and better target clinical trials for preventive treatments, the researchers say, adding that their early intervention model could transform care for neurodegenerative diseases by addressing them before irreversible damage occurs.

“We already knew that isolated REM sleep behaviour disorder is a warning sign for these diseases,” said Rahayel.

“What we didn’t know was who would develop what. Thanks to these complementary studies, we now have tools to better predict and personalize care.”

About this sleep and Parkinson’s disease research news

Author: Julie Gazaille
Source: University of Montreal
Contact: Julie Gazaille – University of Montreal
Image: The image is credited to Neuroscience News

Original Research: Open access.
“DTI-ALPS associates with differential phenoconversion in patients with isolated REM sleep behaviour disorder: a multicenter MRI study” by Shady Rahayel et al. Neurology

Sleep mediates the association between stroke and all cause mortality in the NHANES cohort

 You address those issues by CREATING EXACT SLEEP PROTOCOLS! You failed; you're fired!

You knew of the need over 6 years ago and still incompetently DID NOTHING to solve the problem!

30% poor sleep (14 posts to May 2019)

Sleep mediates the association between stroke and all cause mortality in the NHANES cohort

• Yike Zhu & 
• Chuansen Lu 

Scientific Reports volume 15, Article number: 28280 (2025) Cite this article

Abstract

This study examines the associations among stroke, sleep, and all-cause mortality and explores the mediating role of sleep using data from the National Health and Nutrition Examination Survey (NHANES). This cohort study used NHANES data from 2005 to 2018. The primary endpoint was all-cause mortality. Multivariate Logistic regression was used to analyze the association between stroke and sleep, while Cox regression and subgroup analyses were employed to examine associations between stroke/sleep and all-cause mortality. Mediation analysis assessed the role of sleep in the stroke-mortality relationship. Statistical analyses were performed using R software. Among the 27,302 participants included with a mean follow-up of 111.05 months, 1046 experienced a stroke, 4666 had poor sleep patterns, and 3807 deaths occurred. In the multivariable-adjusted model, stroke was significantly associated with all-cause mortality (HR = 6.08, 95% CI = 5.37–6.87, P < 0.001); compared with poor sleep patterns, both moderate and healthy sleep patterns were significantly associated with a lower risk of stroke (Moderate: HR = 0.97, 95% CI = 0.97–0.98, P < 0.001; Healthy: HR = 0.97, 95% CI = 0.96–0.97, P < 0.001) and all-cause mortality (Moderate vs. Poor: HR = 0.64, 95% CI = 0.57–0.72, P < 0.001; Healthy vs. Poor: HR = 0.60, 95% CI = 0.54–0.67, P < 0.001). Mediation analysis showed that sleep mediated 1.4% of the stroke-mortality association. This study demonstrates that sleep significantly mediate the association between stroke and all-cause mortality, highlighting the importance of addressing sleep issues in stroke populations.

Sleep Learning: How Synapses Strengthen While We Rest

Since 30% of survivors have sleep problems, has your doctor done ONE DAMN THING about it in the last 5 years? NO? So, you don't have a functioning stroke doctor, do you?

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now. Of course your doctor needs to get this testing done on stroke survivors if they are competent at all!

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 Or is your doctor so incompetent that s/he is not even trying to create recovery protocols for stroke survivors? Mine knew nothing and did nothing as proven by writing three prescriptions of E.T.(Evaluate and Treat to the therapists. I could train a chimp to do that!

In my opinion competence is immediately installing protocols upon published research. Does your incompetent? doctor think that is too high a bar? FIRE THEM! And if your doctor is still there after doing nothing your board of directors is completely incompetent!

 The latest here:

Sleep Learning: How Synapses Strengthen While We Rest

Summary: New research reveals how synaptic connections in the cerebral cortex can strengthen during sleep, offering insight into how the brain continues learning even while we rest. Using computer simulations, researchers demonstrated that synaptic activity during sleep follows known “synaptic learning rules” when neural activity reaches specific thresholds.

This means that under certain conditions, learning can occur during sleep—a concept long speculated but now theoretically supported. The findings may also shed light on sleep-related brain disorders and pave the way for new strategies in cognitive health and memory enhancement.

Key Facts:

• Sleep-Driven Plasticity: Synaptic strength can increase during sleep if certain activity thresholds and learning rules are met.
• Theoretical Sleep Learning: The study predicts conditions under which “sleep learning” is scientifically plausible.
• Clinical Relevance: Insights could inform understanding and treatment of sleep-linked brain disorders like neuropsychiatric diseases.

Source: Japan Science and Technology Agency

In the cerebral cortex, numerous neurons exchange information through junctions known as synapses. The strength of each synaptic connection changes depending on the activity levels of the neurons involved, and these changes are thought to form the basis of learning and memory.

There are several established principles governing the relationship between neuronal activity patterns and changes in synaptic strength, referred to as “synaptic learning rules” (1).

Although it is well known that sleep plays a crucial role in learning and memory, how synaptic connections are altered during sleep has remained unclear.

A research group led by Professor Hiroki Ueda of the Graduate School of Medicine, The University of Tokyo, has demonstrated that the strength of synaptic connections in the cerebral cortex during sleep changes depending on synaptic learning rules and the level of neuronal activity during sleep.

They revealed that it was possible to theoretically predict the conditions under which “sleep learning ⁽²⁾ ” may occur.

The researchers used computational simulations to reproduce the activity of neural networks composed of various types of interconnected neurons, and they investigated changes in synaptic connections during the neural activity observed in the sleep-wake states.

These results showed that synaptic connections in the cerebral cortex are strengthened during sleep when specific levels of neural activity were accompanied by typical synaptic learning rules.

This finding clarified the conditions under which synaptic strengthening can occur even during sleep, thereby enabling theoretical predictions of when “sleep learning” is possible.

Based on these predictions, these insights are expected to lead to a deeper understanding of the relationship between sleep, learning and memory.

Moreover, they may contribute to elucidating the mechanisms of brain disorders associated with sleep disturbances, such as neuropsychiatric conditions.

These findings were published in the online version of the American scientific journal PLOS Biology on June 12, 2025.

This result was achieved in the Ueda Biological Timing Project, a research area of the Exploratory Research for Advanced Technology (ERATO) by the Japan Science and Technology Agency (JST). Under this project, JST pursues “systems biology for understanding humans” using the sleep-wake rhythm as a model system and aims to understand information on “biological time,” which transcends from molecules to individual humans livingin society.

Notes:

(*1) Synaptic learning rules

Rules that describe how the strength of synaptic connections between neurons changes depending on the timing and frequency of neural activity. Examples include Hebbian rule and spike-timing-dependent plasticity (STDP).

(*2) Sleep learning

The enhancement of memory and learning performance through the organization and integration of new information by the brain during sleep.

About this sleep and learning research news

Author: Satomi Kobayashi
Source: Japan Science and Technology Agency
Contact: Satomi Kobayashi – Japan Science and Technology Agency
Image: The image is credited to Neuroscience News

Original Research: Open access.
“A unified framework to model synaptic dynamics during the sleep–wake cycle” by Hiroki Ueda et al. PLOS Biology

Effect of Pink Noise on EEG and Memory Performance in Memory Task

 Since 30% of survivors have sleep problems, has your doctor done ONE DAMN THING about it in the last 4 years? NO? So you don't have a functioning stroke doctor, do you?

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now. Of course your doctor needs to get this testing done on stroke survivors if they are competent at all!

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 The latest here:

Effect of Pink Noise on EEG and Memory Performance in Memory Task

Akari Hatayama; Atsushi Matsubara; Sota Nakashima; Seiji Nishifuji

All Authors

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Abstract

Document Sections

• I.
  Introduction
• II.
  METHODS
• III.
  RESULTS AND DISCUSSION
• IV.
  CONCLUSION

Authors

Figures

References

Citations

Keywords

Metrics

Abstract:

Recently, improvement of memory ability by listening noise in deep sleep has attracted extensive attention for its promising potential to prevent older adults from degrading cognitive function such as mild cognitive impairment and dementia. In particular, pink noise with 1/f-characteristics was frequently used to facilitate synchronization of neural oscillatory activities. However, the effect of pink noise on short-term memory task including memory encoding and recall during awake state has not been well investigated. We conducted a simple memory task consisting of memorization of ten fish names during which pink noise was presented and recalling them before and after mental arithmetic for seven healthy young males. Memory recall performance and amplitudes of electroencephalogram (EEG) for noise-added trials were compared with those for control trials without additive noise. The beta and gamma wave amplitudes in the noise-added trials for participants with higher memory performance in the noise-added trials than the control trials were larger than the amplitudes in the control trials by about 10 points, whereas the former amplitudes for participants with lower memory performance in the noise-added trials were smaller than the latter amplitudes. There is a possibility that pink noise could affect the memory ability through the enhancement of beta and gamma wave.

Published in: 2021 IEEE 10th Global Conference on Consumer Electronics (GCCE)

Date of Conference: 12-15 October 2021

Date Added to IEEE Xplore: 01 December 2021

ISBN Information:

Print on Demand(PoD) ISSN: 2378-8143

DOI: 10.1109/GCCE53005.2021.96220

Can Pink Noise Enhance Sleep and Memory? Early Research Drives a Color Noise Buzz.

 

What is your doctors sleep protocol for you? Doesn't have one! You don't have a functioning stroke doctor! Why are you there?

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now.

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 The latest here:

Can Pink Noise Enhance Sleep and Memory? Early Research Drives a Color Noise Buzz.

— "There's still a lot of work we have to do," says one researcher

by Associated Press May 21, 2024

(AP Photo/Laura Bargfeld)

You may have heard of white noise used to mask background sounds. Now, it has colorful competition.

There's a growing buzz around pink noise, brown noise, green noise -- a rainbow of soothing sounds -- and their theoretical effects on sleep, concentration, and the relaxation response.

The science is new with only a few small studies behind it, but that hasn't stopped thousands of people from listening to hours of these noises on YouTube and on meditation apps that provide a palette of color noises with paid subscriptions.

What Is Pink Noise?

To understand pink noise, start with white, the most familiar of the color noises.

White noise is similar to static on a radio or TV. Sound engineers define it as having equal volume across all the frequencies audible to the human ear. It gets its name from white light, which contains all the visible color wavelengths.

But the high frequencies of white noise can sound harsh. Pink noise turns down the volume on those higher frequencies, so it sounds lower in pitch and more like the natural sound of rain or the ocean.

Brown noise sounds even lower in pitch, giving it a pleasing, soothing rumble.

Pink and brown, like white, have standard definitions to audio experts. Other color noises are more recent creations with very flexible definitions.

What's the Science Behind Color Noises?

White noise and pink noise may provide small benefits for people with attention deficit-hyperactivity disorder (ADHD), according to a recent review of limited ADHDopens in a new tab or window studiesopens in a new tab or window. In theory, it wakes up the brain, said ADHD researcher and co-author Joel Nigg, PhD, of Oregon Health & Science University in Portland.

"The noise provides stimulation to the brain without providing information, and so it doesn't distract," Nigg said.

White noise has been used to treat ringing or buzzing in the ear, called tinnitusopens in a new tab or window.

Scientists at Northwestern University are studying how short pulses of pink noise can enhance the slow brain waves of deep sleep. In small studies, these pink-noise pulses have shown promise in improving memory and the relaxation response.

Pink noise has a frequency profile "very similar to the distribution of brain wave frequencies we see in slow-wave sleep because these are large, slow waves," said Roneil Malkani, MD, associate professor of neurology at Northwestern University Feinberg School of Medicine.

If Northwestern's research pans out, it could lead to a medical device to improve sleep or memory through personalized pulses of pink noise. But many scientific questions remain unanswered, Malkani said. "There's still a lot of work we have to do."

Is There Any Harm in Trying Color Noises?

If color noises feel calming and help you drown out distractions, it makes sense to use them. Keep them at a quiet level, of course, to prevent hearing loss and take "plenty of breaks for the ears to rest," Nigg said.

Presence of Self-Reported Sleep Alterations After Stroke and Their Relationship With Disability: A Longitudinal Study.

What is your doctors sleep protocol for you? Doesn't have one! You don't have a functioning stroke doctor! Why are you there?

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now.

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 The latest here:

 Presence of Self-Reported Sleep Alterations After Stroke and Their Relationship With Disability: A Longitudinal Study.

Marcela Rangel, Leonardo Silva, Estefany Gonçalves, Andressa Silva, Luci Teixeira-Salmela, Aline Scianni

BACKGROUND: Sleep disorders have a prevalence of 30% to 70% in post-stroke individuals. The presence of sleep disorders and poor sleep quality after stroke can affect important functions and lead to worse outcomes. However, most studies are restricted to the acute post-stroke stage only.

OBJECTIVE: To investigate the frequency of self-reported sleep alterations in a sample of chronic stroke individuals and to identify which self-reported sleep alterations were associated with disability.

METHODS: Prospective exploratory study. Self-reported sleep alterations were measured by the Pittsburgh Sleep Quality Index, Insomnia Severity Index, Epworth Sleepiness Scale, and STOP-Bang Questionnaire. The dependent variable was measured 3 years after the first contact by the Modified Rankin Scale (mRS). Step-wise multiple linear regression analysis was employed to identify which sleep alterations were associated with disability.

RESULTS: Sixty-five individuals with stroke participated. About 67.7% of participants had poor sleep quality, 52.4% reported insomnia symptoms, 33.9% reported excessive daytime sleepiness, and 80.0% were classified as intermediate or high risk for obstructive sleep apnea. Only risk for obstructive sleep apnea was significantly associated with disability and explained 5% of the variance in the mRS scores.

CONCLUSION: Self-reported sleep alterations had a considerable frequency in a sample of chronic stroke individuals. The risk of obstructive sleep apnea was associated with disability in the chronic stage of stroke. Sleep alterations must be considered and evaluated in the rehabilitation process even after a long period since the stroke onset.

Obstructive Sleep ApneaSleep ApneaStroke

Neurology

Shorter dream-stage sleep may be related to earlier death

Useless. Describes a problem, OFFERS NO EXACT SOLUTION.

Absolutely nothing here is going to help with 30% of survivors having sleep problems. Damn it all, solve stroke problems, don't just do quote useless guidelines.

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now.

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 The latest here:

 

Shorter dream-stage sleep may be related to earlier death

Time and time again, adequate sleep has been shown to be critical to daily functioning and long-term health. Sleep serves numerous roles: recovering energy for the brain, clearing waste products, and forming memories. Prior studies have clearly linked shortened sleep times to heart disease, obesity, reduced cognitive performance, worsened mood, and even a shorter life. There is now new research that suggests that lack of a certain type of sleep (the dream stage of sleep) may be related to an earlier death in middle-aged and older people.

What is REM sleep?

Normal sleep is broken down into two sleep types: rapid eye movement (REM) and non-rapid eye movement (NREM). NREM is further classified by depth of sleep; N1 and N2 are lighter sleep stages, and N3 is deep sleep, which is most restorative. (REM is the stage where vivid dreaming occurs.) Brainwave activity during this time appears similar to the brain’s activity while awake. REM periods generally occur every 90 minutes, and are longest during the second half of the night. REM sleep normally makes up 20% to 25% of sleep time.

How does sleep change with age?

Sleep time and sleep stages naturally change as we age. Total sleep time decreases by 10 minutes every decade until age 60, when it stops decreasing. Time in N3 sleep, the deepest sleep stage, also shortens with age; time in N1 and N2 tends to increase. As a result, people wake more easily from sleep as they age. The percentage of REM sleep also naturally decreases; thus, reduced time spent in REM may be a marker of aging.

The circadian rhythm is a 24-hour internal clock that governs numerous body functions including body temperature, release of hormones, and sleep time. The internal clock “advances” with age, so older adults tend to fall asleep earlier and wake earlier. Adapting to jet lag and shift work becomes more difficult. Daytime napping also increases as the strength of the circadian rhythm and the drive to sleep at night decrease.

Studies have also shown that older adults who are healthy may not perceive problems with sleep when it is actually impaired, or may assume that certain disruptions are part of aging when they have treatable conditions.

Why would less sleep increase my risk of death?

In the short term, sleep deprivation increases cortisol levels, causes increased blood pressure, decreases glucose tolerance, and increases the activity of the body’s fight-or-flight system, all of which are linked to increased risk of diabetes, heart attacks, and strokes. Daytime cognitive performance is also reduced, resulting in more accidents. Twenty-four hours of sustained wakefulness impairs driving ability to the same degree as a blood alcohol concentration of 0.10%, which is above the legal limit.

In the long term, both short and long sleep (less than five hours or more than nine hours) have been associated with earlier death. People who sleep less than four hours dramatically increase their risk of dying early, possibly through heart disease, diabetes, high blood pressure, chronic stress, lower immunity, and overall more rapid aging.

Less dream-stage sleep makes a difference

We know that short sleep is associated with increased mortality, but until now it has been unclear if shorter sleep in a particular sleep stage makes a difference in the health risks associated with sleep deprivation. A new study published in JAMA Neurology looked at the relationship between REM sleep and earlier death in two large study groups, one consisting of 2,675 older men and the other of 1,386 middle-aged men and women. They followed both groups over time and looked at the relationship between sleep stages and causes of death.

Both groups showed increased mortality rates related to a decrease in REM sleep, with a 13% higher mortality rate for every 5% reduction in REM sleep. REM sleep was the most important sleep stage for predicting survival.

Putting new research into context: What does this mean for me?

This study showed an association between reduced REM and increased mortality, but it did not demonstrate the cause of the association. REM deprivation could independently contribute to the development of numerous other diseases. The results apply more clearly to older adults, given that the age groups studied averaged in the 50s and 70s. Short REM may also be a marker of a sick or aging brain; less REM sleep has already been tied to a greater risk of dementia. Overall, ensuring adequate REM sleep is important to protecting your long-term health.

Getting better sleep in middle age and beyond

Maintaining good sleep should remain a priority throughout your life. Everyone can make healthy choices to maximize restorative sleep. Dr. Suzanne Bertisch has written previously about recommendations(NOT PROTOCOLS) for improving sleep hygiene, and even more suggestions(NOT PROTOCOLS) are available in the Harvard Health Publishing Special Health Report Improving Sleep: Getting a Good Night’s Rest.

Some fundamental steps to improve your sleep and health include:

• Get at least seven hours of sleep each night. If you still feel tired, sleep a little more; some people need eight or nine hours of sleep to feel rested.
• Keep a consistent bedtime and wake time. This will make falling asleep easier, and will keep your circadian rhythm aligned with your sleep and wake time.
• Try to sleep when your body naturally wants to fall asleep and wake up. This can differ from sleep and wake times required for work schedules, which also has negative consequences. A sleep doctor can help you realign your circadian clock with your schedule.
• Depression or other mood disorders can cause disrupted sleep. Talk to your doctor if you are feeling low, no longer enjoy your hobbies, or are struggling with anxiety or sadness.
• If you can’t fall asleep, stay asleep, or feel sleepy all the time, you may need evaluation from a doctor for a sleep disorder such as sleep apnea or insomnia. Treating these disorders can make a major difference in overall sleep quality and health.

Related Information: Improving Sleep: A guide to a good night’s rest

Sleep disruption after brain injury is associated with worse motor outcomes and slower functional recovery

Useless. Describes a problem, OFFERS NO SOLUTION.

Absolutely nothing here is going to help with 30% of survivors having sleep problems. Damn it all, solve stroke problems, don't just do useless research.

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now.

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 The latest here:

 Sleep disruption after brain injury is associated with worse motor outcomes and slower functional recovery

Neurorehabilitation and Neural Repair (NNR) , Volume 34(7) , Pgs. 661-671.

NARIC Accession Number: J84095.  What's this?
ISSN: 1545-9683.
Author(s): Fleming, Melanie K. ; Smejk, Tom ; Slater, David H.; van Gils, Veerle ; Garratt, Emma ; Kara, Ece Y.; Johansen-Berg, Heidi.
Publication Year: 2020.
Number of Pages: 9.

Abstract: 

Study investigated the relationship between sleep quality and motor recovery in 59 patients with brain injury patients receiving inpatient rehabilitation. Sleep quality was assessed (up to 3 times) objectively using actigraphy (7 nights) and subjectively using the Sleep Condition Indicator. Motor outcome assessments included Action Research Arm test (upper-limb function), Fugl-Meyer Assessment (motor impairment), and the Rivermead Mobility Index. The Functional Independence Measure (FIM) was assessed at admission and discharge by the clinical team. Fifty-five age- and gender-matched healthy controls completed one assessment. Inpatients demonstrated lower self-reported sleep quality and more fragmented sleep than controls. For inpatients, sleep fragmentation explained significant additional variance in motor outcomes, over and above that explained by admission FIM score such that more disrupted sleep was associated with poorer motor outcomes. Using stepwise linear regression, sleep fragmentation was the only variable found to explain variance in rate of change in FIM, whereby more disrupted sleep was associated with slower recovery. Results suggest that inpatients with brain injury demonstrate impaired sleep quality, and this is associated with poorer motor outcomes and slower functional recovery. Further investigation is needed to determine how sleep quality can be improved and whether this affects outcome.
Descriptor Terms: BRAIN INJURIES, LIMBS, MOBILITY IMPAIRMENTS, MOTOR SKILLS, REHABILITATION, SLEEP DISORDERS.


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Get this Document: https://journals.sagepub.com/doi/full/10.1177/1545968320929669.

Citation: Fleming, Melanie K. , Smejk, Tom , Slater, David H., van Gils, Veerle , Garratt, Emma , Kara, Ece Y., Johansen-Berg, Heidi. (2020). Sleep disruption after brain injury is associated with worse motor outcomes and slower functional recovery.  Neurorehabilitation and Neural Repair (NNR) , 34(7), Pgs. 661-671. Retrieved 8/19/2020, from REHABDATA database.
 

Sleep Problems Adversely Impact Recovery Following Stroke

Useless. Describes a problem, OFFERS NO SOLUTION.

Absolutely nothing here is going to help with 30% of survivors having sleep problems. Damn it all, solve stroke problems, don't just do useless research.

 

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now.

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 

The latest here:

Sleep Problems Adversely Impact Recovery Following Stroke

Amit Akirov, MD

Sleep problems may adversely impact health-related quality of life, function, and participation during the first 12 months of stroke rehabilitation, according to study results published in Clinical Rehabilitation.

Previous studies reported that sleep has a major role in the acquisition of motor skills after stroke and that poor sleep quality is associated with worse outcomes. The goal of the current study was to assess the impact of self-reported sleep problems on recovery following stroke.

The researchers performed a secondary analysis of sleep-related data collected at 2, 6, and 12 months post-stroke from the Locomotor Experience Applied Post-Stroke (ClinicalTrials.gov Identifier: NCT00243919)  study. This was a phase III, single blind, randomized-controlled clinical trial of adult patients during the first year following stroke.

The participants reported sleep problems at each point and the impact of sleep on their function. In addition, they completed the Stroke Impact Scale to assess health-related quality of life after stroke.

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Data collected from 408 subjects (mean age 62.0 years; 55% men) was used for the study, including 327 (80%) patients with a history of ischemic stroke and 76 (19%) patients with that of a hemorrhagic stroke. Data was available from 380 participants at 6 months and from 360 subjects at 12 months.

A total of 98 participants (24%) reported the presence of sleep problems at 2 months, and this rate remained steady at 6 months (94 subjects, 25%) and at 12 months (83 subjects, 23%). Additionally, 10% of participants with sleep problems reported a moderate-to-quite-a-bit-of-impact on function at 2, 6 and 12 months.

Participants who reported having a “sleep problem such as insomnia” that impacted their function had worse function in limb strength, memory and thinking, mood and ability to control emotions, communication, activities of daily living ability, mobility, hand function, and participation during the first year after stroke. However, there was no difference in full recovery.

The study had several limitations, including those associated with the use of self-reported data and lack of objective evidence for sleep disorder. Researchers had not determined whether patients who reported sleep problems were subsequently assessed, diagnosed, or if they received treatment during the study. Other limitations included the study’s cross-sectional design and missing data on sleep disorder diagnoses preceding stroke.

“Our findings here,” concluded the researchers, “indicate that sleep problems may degrade health-related quality of life, function, and participation during the subacute and chronic stages of post stroke recovery.”

Reference

Fulk G, Duncan P, Klingman KJ. Sleep problems worsen health-related quality of life and participation during the first 12 months of stroke rehabilitation [published online, June 30, 2020]. Clin Rehabil. doi:10.1177/0269215520935940

‘A Rinsing of the Brain.’ New Research Shows How Sleep Could Ward Off Alzheimer's Disease

But is wine better? How come your doctor doesn't know the answer to that fuckingly simple question? 

Wine Cleans Alzheimer's Plaque January 2020

 Useless. Describes a problem, OFFERS NO PROTOCOL.

Absolutely nothing here is going to help with 30% of survivors having sleep problems. Damn it all, solve stroke problems, don't just do useless research.

Is your doctor suggesting either of these? Never mind, way too soon for your doctor to read, understand and implement these interventions. Maybe 50 years from now, you'll be dead.

Effects of saffron on sleep quality in healthy adults with self-reported poor sleep: A randomized, double-blind, placebo-controlled trial June 2020

Pink Noise Machines Improve Sleep & Fight Dementia  June 2020

 The latest here:

‘A Rinsing of the Brain.’ New Research Shows How Sleep Could Ward Off Alzheimer's Disease

Alice Park

August 6, 2020, 6:38 AM

Each of us carts around a 3-lb. universe that orchestrates everything we do: directing our conscious actions of moving, thinking and sensing, while also managing body functions we take for granted, like breathing, keeping our hearts beating and digesting our food. It makes sense that such a bustling world of activity would need rest. Which is what, for decades, doctors thought sleep was all about. Slumber was when all the intricate connections and signals involved in the business of shuttling critical brain chemicals around went off duty, taking time to recharge. We’re all familiar with this restorative role of sleep for the brain–pulling an all-nighter or staying awake during a red-eye flight can not only change our mood, but also affect our ability to think clearly until, at some point, it practically shuts down on its own. When we don’t get enough sleep, we’re simply not ourselves.

Yet exactly what goes on in the sleeping brain has been a biological black box. Do neurons stop functioning altogether, putting up the cellular equivalent of a Do Not Disturb sign? And what if a sleeping brain is not just taking some well-deserved time off but also using the downtime to make sense of the world, by storing away memories and captured emotions? And how, precisely, is it doing that?

In the past five years, brain researchers have begun to expose a hidden world of chemical reactions, fluids flowing into and out of the brain, and the busy work of neurons that reveal the sleeping brain is as industrious as the waking one. Without good-quality sleep, those critical activities don’t take place, and as a consequence, we don’t just feel tired and cranky, but the processes that lead to certain diseases may even get seeded. One of the reasons we sleep, it now seems, might be to keep a range of illnesses–including cognitive diseases like Alzheimer’s and other dementias–at bay. As Adam Spira, a professor in the department of mental health at the Johns Hopkins Bloomberg School of Public Health, puts it, “Sleep really should not be seen as a luxury or waste of time. People joke that they’ll sleep when they’re dead, but they might end up dead sooner if they don’t sleep.”

Blame Polymath Benjamin Franklin, who averred, “There will be sleeping enough in the grave”; ever since, a culture of industry has rooted itself in the human psyche–embedding the idea that activity, even well into the night, is valued far more than daily rest.

In part that’s because while medical experts have long recommended seven to eight hours of sleep a night–including some time spent in deep, or non-REM, sleep–exactly what our bodies are doing during that time is less clear. Now, thanks to newer technologies for measuring and tracking brain activity, scientists have defined the biological processes that occur during good-quality sleep. That they seem to be essential for lowering the risk of brain disorders, from the forgetfulness of senior moments to the more serious memory loss and cognitive decline of dementia and Alzheimer’s disease, may convince the Franklins of the world that sleep is not for the lazy.

Experts in the field of Alzheimer’s are especially excited, since there are currently no treatments for the neurodegenerative disease, and sleep-based strategies might open new ways to slow its progression in some and even prevent it in others.

“There has been a real renaissance in research around the connection between sleep, sleep quality, sleep disturbance and dementia, especially Alzheimer’s dementia,” says Dr. Kristine Yaffe, professor of psychiatry, neurology and epidemiology at the University of California, San Francisco. The National Institutes of Health is currently funding at least half a dozen new studies exploring how sleep may impact dementia, and the Alzheimer’s Association created a committee to promote more research in the area.

For decades, researchers thought sleep disturbances were a symptom or a consequence of Alzheimer’s. They assumed that as clumps of amyloid proteins built up, then started to strangle and kill nerve cells–particularly in the memory regions of the brain–changes in sleep followed. Even older people without Alzheimer’s can experience changes in their sleep patterns, sleeping less and more lightly as they age. So experts didn’t initially take these shorter and more fragmented sleep cycles seriously.

But in the 1980s and 1990s, scientists began studying whether there was any causal relationship between sleep patterns and cognitive-test performance among older people without Alzheimer’s by studying them over longer periods of time. Those studies suggested that people with poor sleep habits tended to perform worse on cognitive tests over time. “That got people thinking about the possibility that sleep could be a risk factor in dementia,” says Spira.

Yaffe’s recent research, which focused on a group of healthy older women, supported the idea that what seemed to matter, in terms of dementia risk, was the quality as opposed to the quantity of sleep. Those who reported spending less time in bed actually sleeping, and more time tossing and turning and waking up throughout the night, were more likely to develop any type of dementia five to 10 years later than those who got better-quality sleep.

Others focused on explaining the biology behind the sleep-dementia connection. At this point, Alzheimer’s researchers knew that a buildup in the brain of amyloid and another protein called tau were key features of the disease. At Washington University School of Medicine in St. Louis, David Holtzman, chair of the department of neurology, launched studies to track exactly where in the brain this amyloid originated. His search led him to nerve cells, which release fragments of the protein as they go about their normal business. Typically, these protein by-products (sometimes called amyloid beta) are released into the circulatory system, where they float around without causing problems, but in some cases they remain in the brain, where they morph into a sort of molecular Velcro, sticking together to form amyloid plaques, which in turn damage neurons.

But what controls the production of amyloid beta? In a 2009 study on mice, Holtzman found that while the animals were awake, levels of the protein fragments circulating in their brains surged. When the mice slept, the levels dropped dramatically–especially during the deeper stages of non-REM sleep. And when he and his team deprived the mice of non-REM sleep, more amyloid built up in their brains over time than in mice who got regular nightly rest. He saw similar changes when he compared amyloid in the spinal fluid of people who were well rested vs. sleep-deprived.

It was a revelation for Alzheimer’s experts. “That showed experimentally for the first time that there was an effect of sleep deprivation on Alzheimer’s disease pathology,” says Spira. “That’s what really flipped everything on its head.” In 2013, to test whether the same effect occurred in people, Spira studied brain scans of 70 healthy adults with an average age of 76. Indeed, the scans of those who reported less or compromised sleep showed higher levels of amyloid plaques than the scans of those who slept better.

A year later, a biological explanation for why poor sleep might be linked to Alzheimer’s emerged. Dr. Maiken Nedergaard, co-director of the Center for Translational Neuromedicine at the University of Rochester, identified a previously ignored army of cells that is called to duty during sleep in the brains of mice and acts as a massive pump for sloshing fluid into and out of the brain. This plumbing system, which she dubbed the “glymphatic system” (it works in parallel to the lymph system that drains fluid from other tissues in the body), seemed to perform a neural rinsing of the brain, swishing out the toxic proteins generated by active neurons (including those amyloid fragments) and clearing the way for another busy daily cycle of connecting and networking.

Taken together with Spira’s discovery that levels of amyloid spiked during the day and dropped during sleep, Nedergaard’s findings gave further credence to the theory that sleep might perform a housekeeping function critical for warding off diseases like Alzheimer’s. “These results very much support the notion that one of the roles of sleep is to actually accelerate the clearance of beta amyloid from the brain,” says Nora Volkow, director of the U.S. National Institute on Drug Abuse.

Late last year, Laura Lewis, assistant professor of biomedical engineering at Boston University, built on Nedergaard’s work by matching up the ebb and flow of cerebrospinal fluid in the brain with brain-wave activity, which indicates different stages of sleep. She showed that in healthy adults, during the day when the brain is active, there is less fluid bathing neurons and tissues in the organ. During sleep–and especially during deeper sleep–this solution saturates the brain in a cleansing flood. The finding reinforced Nedergaard’s theory that sleeping may help clear the brain of toxic proteins that can eventually cause disease.

Still, while all these discoveries are strongly suggestive, they are not what scientists would call definitive. For that, researchers need two additional pieces of evidence: first, a clear correlation between disrupted sleep patterns and a higher risk for Alzheimer’s; and second, evidence that if these high-risk people improve their sleep, that risk falls.

They are currently working to build those data sets, and already the results are promising. For example, Volkow measured baseline amyloid levels in the brains of 20 healthy people ages 22 to 72 years, then scanned their brains again after each had a good night’s sleep and yet again after each was kept awake for about 31 hours straight. After a loss of sleep, levels of amyloid were 5% more than after adequate sleep; the spikes were concentrated in parts of the brain involved in memory and higher thinking, which are typically affected in Alzheimer’s.

But seeing levels of amyloid change with more or less sleep doesn’t necessarily mean sleep habits are contributing to Alzheimer’s. To make that case, researchers are studying people with disorders like sleep apnea, or those who work night shifts or keep irregular working hours, such as first responders, pilots and flight attendants. Studies already suggest that all of these groups are more vulnerable to Alzheimer’s. The next step is to see if treatment, or changes in sleep habits, matters. For people with sleep apnea, for example, doctors can prescribe devices to wear during sleep to keep oxygen flowing more consistently to the brain so they don’t wake up. In shift workers, researchers want to test the impact of resetting their biological clocks to a standard day-night schedule. If these efforts lower their likelihood of developing Alzheimer’s, that would make a strong case for a connection between lifelong sleep patterns and risk of dementia.

Researchers also need to better understand how sleep medications and treatments like melatonin affect the dementia process. While some sleep aids promote the deeper sleep that seems to be protective against brain decline, it’s not clear yet whether long-term dependence on such medications can maintain the benefit.

Even while these studies are being done, many experts believe the data are already strong enough to start educating at least older people, especially those at higher risk of developing Alzheimer’s, about improving their sleep habits. Yaffe, for one, already does that with her patients. “Even practical sleep-hygiene tips, where we teach people best practices like avoiding caffeine in the evening and darkening their room and staying off their phones, could help them sleep better,” she says. “I would love to see whether this low-cost and pragmatic approach could improve cognition or prevent decline in Alzheimer’s patients.”

She and others don’t believe sleep alone can fully prevent Alzheimer’s or halt its progression. But together with other therapies that could emerge to treat the disease, sleep may be a powerful way to help people lower their risk even further. It’s even possible that sleep could play an important role in keeping our brains healthy in other ways: by controlling metabolism and other cellular functions behind diseases like diabetes, hypertension and even cancer. As the latest research shows, a good night’s sleep isn’t a luxury–it’s critical for keeping the brain healthy.