Monday, December 30, 2013

NIH: Brain may flush out toxins during sleep

Editor's note:  Unrefreshing sleep and memory loss have been frequently reported Gulf War Illness symptoms.  Now, and NIH-funded study shows an even greater interrelationship between sleep and memory.  

Perhaps even more important for Gulf War Illness is the discovery that the brain appears to be cleansing itself of toxic molecules during sleep.

Gulf War Illness researchers and those who follow GWI research may find value in these important recent findings.




Brain may flush out toxins during sleep

NIH-funded study suggests sleep clears brain of damaging molecules associated with neurodegeneration
A good night’s rest may literally clear the mind. Using mice, researchers showed for the first time that the space between brain cells may increase during sleep, allowing the brain to flush out toxins that build up during waking hours. These results suggest a new role for sleep in health and disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the NIH.
“Sleep changes the cellular structure of the brain. It appears to be a completely different state,” said Maiken Nedergaard, M.D., D.M.Sc., co-director of the Center for Translational Neuromedicine at the University of Rochester Medical Center in New York, and a leader of the study.
For centuries, scientists and philosophers have wondered why people sleep and how it affects the brain. Only recently have scientists shown that sleep is important for storing memories. In this study, Dr. Nedergaard and her colleagues unexpectedly found that sleep may be also be the period when the brain cleanses itself of toxic molecules.
Their results, published in Science, show that during sleep a plumbing system called the glymphatic system may open, letting fluid flow rapidly through the brain. Dr. Nedergaard’s lab recently discovered the glymphatic system helps control the flow of cerebrospinal fluid (CSF), a clear liquid surrounding the brain and spinal cord.
Image of a mouse brain
Scientists watched dye flow through the brain of a sleeping mouse.Courtesy of Nedergaard Lab, University of Rochester Medical Center.
“It’s as if Dr. Nedergaard and her colleagues have uncovered a network of hidden caves and these exciting results highlight the potential importance of the network in normal brain function,” said Roderick Corriveau, Ph.D., a program director at NINDS.
Initially the researchers studied the system by injecting dye into the CSF of mice and watching it flow through their brains while simultaneously monitoring electrical brain activity. The dye flowed rapidly when the mice were unconscious, either asleep or anesthetized. In contrast, the dye barely flowed when the same mice were awake.
“We were surprised by how little flow there was into the brain when the mice were awake,” said Dr. Nedergaard. “It suggested that the space between brain cells changed greatly between conscious and unconscious states.”
To test this idea, the researchers inserted electrodes into the brain to directly measure the space between brain cells. They found that the space inside the brains increased by 60 percent when the mice were asleep or anesthetized.
“These are some dramatic changes in extracellular space,” said Charles Nicholson, Ph.D., a professor at New York University’s Langone Medical Center and an expert in measuring the dynamics of brain fluid flow and how it influences nerve cell communication.
Certain brain cells, called glia, control flow through the glymphatic system by shrinking or swelling. Noradrenaline is an arousing hormone that is also known to control cell volume. Similar to using anesthesia, treating awake mice with drugs that block noradrenaline induced unconsciousness and increased brain fluid flow and the space between cells, further supporting the link between the glymphatic system and consciousness.
Previous studies suggest that toxic molecules involved in neurodegenerative disorders accumulate in the space between brain cells. In this study, the researchers tested whether the glymphatic system controls this by injecting mice with labeled beta-amyloid, a protein associated with Alzheimer’s disease, and measuring how long it lasted in their brains when they were asleep or awake. Beta-amyloid disappeared faster in mice brains when the mice were asleep, suggesting sleep normally clears toxic molecules from the brain.
“These results may have broad implications for multiple neurological disorders,” said Jim Koenig, Ph.D., a program director at NINDS. “This means the cells regulating the glymphatic system may be new targets for treating a range of disorders.”
The results may also highlight the importance of sleep.
“We need sleep. It cleans up the brain,” said Dr. Nedergaard.
This work was supported by grants from the NINDS (NS078167, NS07830, NS028642).
For more information about neurological disorders and the latest neuroscience research:
NINDS is the nation’s leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease – a burden borne by every age group, by every segment of society, by people all over the world.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs,
NIH...Turning Discovery Into Health®


Xie et al “Sleep initiated fluid flux drives metabolite clearance from the adult brain.” Science, October 18, 2013. DOI: 10.1126/science.1241224

Sunday, December 22, 2013

DAVID WINNETT: "Persian Gulf Warriors - Left for Dead"

"Persian Gulf Warriors - Left for Dead"

For two decades and more their government continually said;
"This illness is all in their heads,”
The Veterans who served were not being heard,
Their lives, their livelihoods, their families as well; their greatest dreams were literally going to hell,
Unbearable pain from toe to head,
Profound fatigue, their legs feeling like lead,
Eventually these Veterans began to understand,
They'd been abandoned and left for dead,
Beyond the pain and misery their illness brought to every waking hour,
By far the most pain derived was coming to grips with the emotional hurt inside,
To have lived and believed in the warrior creed that no one is left behind,
When the warrior finally understands the emptiness that's hidden behind often quoted slogans meant to entice new recruits,
"Semper Fi", "The Few, the Proud", "An Army of One", and "No One Left Behind",
When the truth emerges, when they're finished and have no further use for you,
It's out the gate you go,
"We wish you the best, you passed the test, a farewell and a hearty goodbye",
But woe is the warrior who later dares to connect unusual illness to wartime exposures; all manner of toxins, chemical and biological weaponry, medicines unapproved for human use and more,
How dare that warrior complain too loud,
Why doesn't the warrior follow procedure; suck up the pain, and die obediently proud,
Act like a warrior, be loyal and true, deal with your pain, your government is truly counting on you,
Don't give up hope, but above all else, don't you dare rock the boat,
It's all in your head, your imagination gone wild, we've seen this before,
Be a good little warrior, accept the consequence of going to war,
Whatever you do, never believe what they said; that your government doesn't care; that we've left you for dead,
We'll always be there, to you ‘til the end we'll always be true,
Just follow procedure; don't call us, we'll call you......

David K. Winnett, Jr. 


Friday, December 20, 2013

Gutted Research Advisory Committee to Meet in January: Public Call-In Information Provided

( - The Congressionally chartered Research Advisory Committee on Gulf War Veterans' Illnesses (RAC) has released public call-in information for its upcoming meetings in Washington, DC, on January 7-8, 2014.

The call-in number for the RAC meeting is 800-767-1750, and the Participant Code is 35378 followed by the # key.

According to the RAC's agenda, most of the January meetings will be taken up by committee discussion on its upcoming report.  

There will also be two medical research updates by the research team of Dr. Nancy Klimas, based at Nova Southeastern University in Ft. Lauderdale, Fla.  The treatment-focused Florida Gulf War Illness research consortia was funded through a substantial grant from the GWI Congressionally Directed Medical Research Program (CDMRP).  A second GWI CDMRP-funded research consortia, based at Boston University, is headed by Dr. Kim Sullivan, who also serves as the RAC's assistant scientific director (though is not presenting at the upcoming meeting).  Dr.'s Klimas and Gordon Broderick are scheduled to present their updates on Jan. 7.  

Recent staff-driven changes retaliating against RAC's outspoken advocacy for ill Gulf War veterans included VA's gutting of the treatment-focused mission, scope, structure, and composition of the RAC, and narrowing the RAC's focus to VA-only research.  However, Dr. Melissa Forsythe, COL (Ret.), program director for the GWI CDMRP, housed under the U.S. Army's Material and Medical Research Command (USAMMRC), has been scheduled by the RAC to provide a CDMRP update to the RAC, also on Jan. 7.  

The VA is also scheduled to provide a research update on its own "Gulf War" research portfolio.  The VA has been under fire in recent years for dramatically cutting its Gulf War research budget, improperly bulking up its "Gulf War research" portfolio with millions of dollars of non-GWI research, and gutting and whitewashing a first-ever Gulf War Illness Research Strategic Plan developed by a consensus of three VA advisory committees.  

In June, all the Gulf War veterans on the panel walked out of the last RAC meeting in protest of VA's  mishandling of Gulf War Illness research and sweeping changes to the RAC.  VA inaction on those concerns led veteran panel members Marguerite Knox (LTC, ARNG) and Anthony Hardie to resign in protest, "rather than continuing to serve on a  VA committee that VA continues to ignore."  

Among the VA-selected replacements is Jim Bunker, a lighting rod of controversy in the Gulf War veteran community and who is unopposed to VA's sweeping changes to the RAC.   

-Anthony Hardie,

Monday, December 16, 2013

Georgetown University to Study Post-Exertional Malaise using NIH Funding

SOURCE:  ProHealth

Georgetown University to Study Post-Exertional Malaise

  [ 11 votes ]   [ Post a Comment ] • December 15, 2013
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Georgetown University to Study Post-Exertional Malaise. Dr. James Baraniuk
Dr. James Baraniuk
Editor's Comment: James Baraniuk made headlines last March when he discovered the first physical evidence of Gulf War Illness. (Read about it HERE.) He found that in Gulf War vets the nerve fibers that connect brain areas involved in the processing and perception of pain and fatigue were not working properly. Further research revealed atrophy in the brain stems of some vets, causing irregular heartbeat. Another group showed atrophy in the regions of the brain controlling pain perception. (Read more HERE.)
Dr. Baraniuk believes that patients with ME/CFS have similar brain anomalies, and that these can be demonstrated using functional MRIs (fMRI), a brain scanning technique that measures brain activity by detecting changes in blood flow. In this study, he plans to use fMRIs to measure brain changes in ME/CFS patients after exercise, thereby pinpointing the precise areas of the brain that produce post-exertional malaise (PEM) and providing an objective means of identifying subgroups.

Dr. Baraniuk's project was awarded $335,300 by the NIH. The study began in September 2013, and will end in July 2018.


Fatigue, widespread pain and tenderness are common findings in Chronic Fatigue Syndrome (CFS) and allied disorders such as Gulf War Illness (GWI) and Fibromyalgia (FM). In addition, they share sleep alterations, diverse nociceptive complaints, migraine, and systemic hyperalgesia. This overlap suggests that these syndromes share specific mechanisms of neural pathophysiology.

Central sensitization is a logical explanation for their pain complaints but has been difficult to explain at the neuronal level. One of the cardinal clinical features of FM, GWI and CFS is "exertional exhaustion". Exercise, cognitive or other stressors induce a relapse of symptoms that may be immediate or can be delayed up to 24 hours. Although studies have found changes associated with exercise in CFS, the causal relationship between the brain and the aberrant response to exercise are unknown. Furthermore, changes that predict the transition to exertional exhaustion have not yet been identified.

We developed a novel exercise stress test, fMRI, neurocognitive testing strategy to study this phenomenon in GWI subjects who met 1994 CFS criteria. We believe the outcomes can be generalized to CFS, and form the basis for a new understanding of this disease.

Hypothesis: Exercise induces cognitive, somatosensory and autonomic dysfunction that are common features of CFS, GWI, & FM. Axonal alterations may be responsible for the neuropathology
  • (SPECIFIC AIM 1). The exercise stressor disrupts vulnerable compensatory neural mechanisms to reveal two autonomic and cognitive phenotypes via fMRI
  • (SPECIFIC AIM 2). Axonal dysfunction in FM can be identified from functional connectivity studies linked to specific dysregulated neurotransmitters of the brain
  • (SPECIFIC AIM 3). Corollary: CFS neuropathology can be modeled based on exercise-induced outcomes of GWI subjects.
Our integrated exercise & fMRI protocol identified the novel finding of significantly increased axial diffusivity (AD) in specific white matter tracts by diffusion tensor imaging (DTI) that was predictive of GWI status compared to controls. GWI groups also met CFS criteria.

Next, we found that exercise perturbs neurophysiological brain networks that led to 2 GWI phenotypes that were associated with exercise induced changes in autonomic control, white matter integrity, cortical and brainstem atrophy, and brain blood flow dynamics. Baseline studies showed limited cross-sectional "static" differences, but the exercise stressor revealed causal and significant "dynamic" alterations of neural processes.

We propose that CFS subjects will display a comparable dichotomy of objective findings. Identification of CFS subgroups would begin the process of defining objective neuropathological mechanisms in CFS. These objective outcomes may define specific CFS phenotypes and help explain the heterogeneous presentation of this illness. Conversely, identification of other coherent patterns may provide new objectively defined criteria for CFS. These mechanisms can lead to objective diagnostic tests and identification of new targets for treatment.

Public Health Relevance Statement
An exercise challenge - fMRI study in subjects who met criteria for both Chronic Fatigue Syndrome and Gulf War Illness revealed:
  • (A) significant differences in white matter integrity in specific brain tracts that distinguished CFS/GWI from control subjects, and
  • (B) two potential illness phenotypes based on significant differences in autonomic, neurocognitive, brain blood flow, and other purely objective outcomes.
These exercise-induced alterations reveal mechanisms of CFS neuropathology, and provide opportunities for a new diagnostic test and insights into targets for development of drugs and other treatments.

SourceNIH Project Reporter, Project Number:1R01NS085131-01
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