An Eye on "The Mitochondria Man" : Robert Naviaux and Chronic Fatigue Syndrome (ME/CFS)

Cort

Founder of Health Rising and Phoenix Rising
Staff member
This is the start of an "Eye On" series focusing on researchers new to the chronic fatigue syndrome/fibromyalgia research fields. Few researchers present more exciting possibilities for ME/CFS than Dr. Robert Naviaux at UC San Diego (UCSD).

[fright]
Keeping-eye-on.jpg
[/fright]Naviaux recently joined the Scientific Advisory Board of the Open Medicine Foundation (OMF) and he's believed to have co-authored a paper that is under review. Early reports suggest the Severe Patient Big Data study may, in its early stages, uncovered significant about the mitochondria in ME/CFS

In some ways Naviaux seems tailor-made for ME/CFS. Naviaux runs the Robert Naviaux Laboratory at UC San Diego, is the founder/ co-director of UCSD's Mitochondrial and Metabolic Disease Center, and co-founder and a former president of the Mitochondrial Medicine Society. This man is clearly a pioneer in the relatively new and emerging field of mitochondrial research but he has an interesting immune side as well.

Naviaux trained at the NIH in tumor immunology and natural killer cell biology, and at the Salk Institute in virology and gene therapy. If ME/CFS or FM turns out to have a viral/inflammation/mitochondrial connection it's hard to imagine someone better placed to take advantage of that.

[fleft]
Animal-studies.jpg
[/fleft]Naviaux gained some renown in 2013 when he was able to reverse autism in a mouse model using a hypothesis that could help explain chronic fatigue syndrome and fibromyalgia as well. He proposed that a sustained "cell danger response" is causing the cells in autism to essentially to shut down, stop communicating with other cells and go into hibernation.

Naviaux believes that cells damaged by viruses, or toxins react defensively causing their membranes stiffen and the

“When cells are exposed to classical forms of dangers, such as a virus, infection or toxic environmental substance, a defense mechanism is activated. This results in changes to metabolism and gene expression, and reduces the communication between neighboring cells. Simply put, when cells stop talking to each other, children stop talking.” Naviaux

(That's an intriguing idea given the evidence of "immune exhaustion" in ME/CFS and FM, and the rather massive alterations of immune cell networks Gordon Broderick and Dr. Klimas have found in ME/CFS. Could immune cell shut downs be behind those network alterations? )

Everybody seems to believe that the innate or early immune response which causes inflammation is involved in ME/CFS but Naviaux has taken the conversation a step further by tying in the mitochondria. Naviaux knew the mitochondria were involved in inflammation - they can be huge emitters of free radicals - and looked for ways in which they interacted with the immune system. He found them in substances called "mitokines" such as ATP and adenosine that cells with distressed mitochondrial emit.

The purines and pyrimidines ( ATP, ADP, UTP, and UDP), produced by these damaged cells can effect everything from inflammation, neurotransmission, pain production, and autonomic nervous system activity. They bind to purinergic and other receptors on cells found from the circulatory to digestive to immune systems to the brain.

Sleeping Sickness Drug

Naviaux used a drug called suramin that battled sleeping sickness to reverse autism in his mouse model. An anti-purinergic signaling drug, suramin, Naviaux believes, stops the cell danger signal in its tracks. In two studies he's been able to show that the drug rebuilt the mouse's brain synapses, re -enabled stalled cell-to-cell signaling, improved its social behavior and motor coordination and normalized it's mitochondrial metabolism. The drug is now being tested in a small trial of autistic children.

[fright]
Cascade-stop.jpg
[/fright]Suramin is more of use for what it reveals than as a treatment possibility than a full-flung treatment. It can only be taken for couple of months but newer antipurinergic medicines might be able to be taken for longer or might just need to be taken intermittently.

As Naviaux developed his hypothesis that damaged cells are triggering purinergic signaling cascades in autism, Donald Staines in Australia was proposing vasoactive neuropeptides were doing much the same thing in ME/CFS. Staines also proposed that ATP and adenosine releases from cells with mitochondrial problems may be causing the purinergic signaling to go bananas in ME/CFS.

Meanwhile Alan Light's examination of physiological pathways linked to stress and distress in ME/CFS was uncovering issues with purinergic signaling as well. Light found that increased purinergic receptor activity was highly associated with post exertional fatigue after exercise in ME/CFS (but not MS). He, too, suggested that purinergic receptors in ME/CFS patients were reacting to ATP molecules emanating from stressed cells. Back in 2012 he proposed that purinergic receptor upregulation in ME/CFS was turning the microglia in the brain on and producing pain and fatigue in ME/CFS.

Naviaux and other ME/CFS researchers, then, may be coming from different directions and ending up in much the same place.

We don't know what Naviaux has found in ME/CFS - we're waiting on his publication for that; it could be something entirely different but his past research alone suggests that he is someone to watch.

[fleft]
Mitochondrial-schema.jpg
[/fleft]A member of the Health Rising Forums, Rachel Riggs, knows this first hand. After visiting Dr. Naviaux's lab she described a researcher who was very enthusiastic about ME/CFS, who mentioned linkages between autism and the disease - a disease, he thought, which put ME/CFS bodies in a kind of hibernation. Dr. Naviaux said his paper on ME/CFS will, if and when it is published, surprise a lot of people. Rachel had a palpable sense that the lab was on the cusp of something big.

Naviaux's got some big accomplishments behind him and some big toys to play with. His lab developed two advanced technologies; biocavity laser spectroscopy and mtDNA mutation detection by mass spectrometry, and recently created new bioinformatic methods that allow them to better analyze genetic data. Put all that together and Naviaux says he has the ability to "dissect the metabolic and molecular features of virtually any disease".

Naviaux appears to be all in ME/CFS. His biggest hurdle may be finding the money to fully study it. Hopefully the new approach by the NIH or the growing ability of ME/CFS donors to support exciting research will be enough.

Naviaux is part of an increasing focus on the mitochondria in ME/CFS research circles. The Chronic Fatigue Initiative has engaged Maureen Hanson to do a series of ME/CFS mitochondrial studies. Richard Deth, a mitochondrial expert, is working with Dr. Klimas at the Institute for Neuroimmune Institute in Florida. Dr. Saligan, a P2P report participant, and member of the NIH Intramural study is a bit of a wild card. His work on the stress response and catastrophizing has raised concerns, but his main research interest is focused on the physiological aspects of cancer fatigue.

Saligan has done studies on murine models of radiation induced fatigue, gene expression and cancer fatigue, prostate cancer and fatigue, inflammation and cancer fatigue, BDNF and fatigue, immunogenomic markers and fatigue, mitochondria and prostate fatigue, biomarkers and cancer fatigue and on and on and he's done one review on catastrophizing and fatigue.
 
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Rachel Riggs

Well-Known Member
Dr. Naviaux is indeed one to watch - I have an enormous amount of confidence in his work - but he needs support from this community and the research dollars required to make that happen! During my visit with him, he shared with me that he has personally contributed $700k of his own money to keep his lab going - and his wife who is an MD/PhD and former clinician, also works alongside him for FREE. That's dedication!
 
Last edited:

Mark C

New Member
This is the start of an "Eye On" series focusing on researchers new to the chronic fatigue syndrome/fibromyalgia research fields. Few researchers present more exciting possibilities for ME/CFS than Dr. Robert Naviaux at UC San Diego (UCSD).

[fright]View attachment 1343 [/fright]Naviaux recently joined the Scientific Advisory Board of the Open Medicine Foundation (OMF) and he's believed to have co-authored a paper that is under review. Early reports suggest the Severe Patient Big Data study may, in its early stages, uncovered significant about the mitochondria in ME/CFS

In some ways Naviaux seems tailor-made for ME/CFS. Naviaux runs the Robert Naviaux Laboratory at UC San Diego, is the founder/ co-director of UCSD's Mitochondrial and Metabolic Disease Center, and co-founder and a former president of the Mitochondrial Medicine Society. This man is clearly a pioneer in the relatively new and emerging field of mitochondrial research but he has an interesting immune side as well.

Naviaux trained at the NIH in tumor immunology and natural killer cell biology, and at the Salk Institute in virology and gene therapy. If ME/CFS or FM turns out to have a viral/inflammation/mitochondrial connection it's hard to imagine someone better placed to take advantage of that.

[fleft]View attachment 1344 [/fleft]Naviaux gained some renown in 2013 when he was able to reverse autism in a mouse model using a hypothesis that could help explain chronic fatigue syndrome and fibromyalgia as well. He proposed that a sustained "cell danger response" is causing the cells in autism to essentially to shut down, stop communicating with other cells and go into hibernation.

Naviaux believes that cells damaged by viruses, or toxins react defensively causing their membranes stiffen and the



(That's an intriguing idea given the evidence of "immune exhaustion" in ME/CFS and FM, and the rather massive alterations of immune cell networks Gordon Broderick and Dr. Klimas have found in ME/CFS. Could immune cell shut downs be behind those network alterations? )

Everybody seems to believe that the innate or early immune response which causes inflammation is involved in ME/CFS but Naviaux has taken the conversation a step further by tying in the mitochondria. Naviaux knew the mitochondria were involved in inflammation - they can be huge emitters of free radicals - and looked for ways in which they interacted with the immune system. He found them in substances called "mitokines" such as ATP and adenosine that cells with distressed mitochondrial emit.

The purines and pyrimidines ( ATP, ADP, UTP, and UDP), produced by these damaged cells can effect everything from inflammation, neurotransmission, pain production, and autonomic nervous system activity. They bind to purinergic and other receptors on cells found from the circulatory to digestive to immune systems to the brain.

Sleeping Sickness Drug

Naviaux used a drug called Surinam that battled sleeping sickness to reverse autism in his mouse model. An anti-purinergic signaling drug, Surinam, Naviaux believes, stops the cell danger signal in its tracks. In two studies he's been able to show that the drug rebuilt the mouse's brain synapses, re -enabled stalled cell-to-cell signaling, improved its social behavior and motor coordination and normalized it's mitochondrial metabolism. The drug is now being tested in a small trial of autistic children.

[fright]View attachment 1345 [/fright]Surinam is more of use for what it reveals than as a treatment possibility than a full-flung treatment. It can only be taken for couple of months but newer antipurinergic medicines might be able to be taken for longer or might just need to be taken intermittently.

As Naviaux developed his hypothesis that damaged cells are triggering purinergic signaling cascades in autism, Donald Staines in Australia was proposing vasoactive neuropeptides were doing much the same thing in ME/CFS. Staines also proposed that ATP and adenosine releases from cells with mitochondrial problems may be causing the purinergic signaling to go bananas in ME/CFS.

Meanwhile Alan Light's examination of physiological pathways linked to stress and distress in ME/CFS was uncovering issues with purinergic signaling as well. Light found that increased purinergic receptor activity was highly associated with post exertional fatigue after exercise in ME/CFS (but not MS). He, too, suggested that purinergic receptors in ME/CFS patients were reacting to ATP molecules emanating from stressed cells. Back in 2012 he proposed that purinergic receptor upregulation in ME/CFS was turning the microglia in the brain on and producing pain and fatigue in ME/CFS.

Naviaux and other ME/CFS researchers, then, may be coming from different directions and ending up in much the same place.

We don't know what Naviaux has found in ME/CFS - we're waiting on his publication for that; it could be something entirely different but his past research alone suggests that he is someone to watch.

[fleft]View attachment 1347 [/fleft]A member of the Health Rising Forums, Rachel Riggs, knows this first hand. After visiting Dr. Naviaux's lab she described a researcher who was very enthusiastic about ME/CFS, who mentioned linkages between autism and the disease - a disease, he thought, which put ME/CFS bodies in a kind of hibernation. Dr. Naviaux said his paper on ME/CFS will, if and when it is published, surprise a lot of people. Rachel had a palpable sense that the lab was on the cusp of something big.

Naviaux's got some big accomplishments behind him and some big toys to play with. His lab developed two advanced technologies; biocavity laser spectroscopy and mtDNA mutation detection by mass spectrometry, and recently created new bioinformatic methods that allow them to better analyze genetic data. Put all that together and Naviaux says he has the ability to "dissect the metabolic and molecular features of virtually any disease".

Naviaux appears to be all in ME/CFS. His biggest hurdle may be finding the money to fully study it. Hopefully the new approach by the NIH or the growing ability of ME/CFS donors to support exciting research will be enough.

Naviaux is part of an increasing focus on the mitochondria in ME/CFS research circles. The Chronic Fatigue Initiative has engaged Maureen Hanson to do a series of ME/CFS mitochondrial studies. Richard Deth, a mitochondrial expert, is working with Dr. Klimas at the Institute for Neuroimmune Institute in Florida. Dr. Saligan, a P2P report participant, and member of the NIH Intramural study is a bit of a wild card. His work on the stress response and catastrophizing has raised concerns, but his main research interest is focused on the physiological aspects of cancer fatigue.

Saligan has done studies on murine models of radiation induced fatigue, gene expression and cancer fatigue, prostate cancer and fatigue, inflammation and cancer fatigue, BDNF and fatigue, immunogenomic markers and fatigue, mitochondria and prostate fatigue, biomarkers and cancer fatigue and on and on and he's done one review on catastrophizing and fatigue.

To get more ME/CFS R&D funding, we need to get millions missing and invisible and not funded, "out of the closet" and onto www.diseasemaps.org where we can be seen, and can coordinate regionally, to get in front of public and politicians who will then fund, when it is obvious to all that Feds have grossly discriminated against M.E. for decades, and since more common in women, also grossly discriminating against She!

We need to first get visible, then get political, then train 100 senators and every congressman about how male centric disease gets $3B NIH budget per year, but female centric ME/CFS gets $6M NIH in 2015, so this is gross sex discrimination by Govt.

They are sworn to provide equal justice for all, and must do so. Once they understand the facts and discrimination, we need to put everyone to a litmus test, will they support greatly expanded funding for ME/CFS to $250M per year, and it not, vote them out since they do not deserved to be in office if they let gross discrimination. Some goes for Obama.

If he can throw billions overnight at Ebola or Zika viral diseases almost overnight, he can invest $250M, why not overnight, to help cure 2,000,000 affected Americans get back to work, make American stronger, cut healthcare costs, save up to $50B CDC estimated cost of ME/CFS to US economy.

Hope everyone can support these researchers directly or via non-profits now, and get NIH to have funding at $250M, and election platform for all parties, all incumbents and candidates - or vote them OUT!
 
Last edited by a moderator:

Rachel Riggs

Well-Known Member
@Mark C Agreed - seems like Millions Missing is our best opportunity for greater visibility at the mo - but it is difficult to make a lot of noise when we are such a sick population. Trust me, if I wasn't as sick as I am I'd be out there kicking some arse...
 

h3ro

Active Member
As soon as I saw this:

“When cells are exposed to classical forms of dangers, such as a virus, infection or toxic environmental substance, a defense mechanism is activated. This results in changes to metabolism and gene expression, and reduces the communication between neighboring cells. Simply put, when cells stop talking to each other, children stop talking.” Naviau
I thought of recent research into TRP channels by NCNED in Australia and of course you seem to have confirmed the link between these 2 hypotheses further down.


Aberrant TRP channels seem to explain all my symptoms really well and my immunologist (he collaborates with NCNED) seems to agree.

This makes me really happy that this line of research is getting pursued by more researchers.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Dr. Naviaux is indeed one to watch - I have an enormous amount of confidence in his work - but he needs support from this community and the research dollars required to make that happen! During my visit with him, he shared with me that he has personally contributed $700k of his own money to keep his lab going - and his wife who is an MD/PhD and former clinician, also works alongside him for FREE. That's dedication!
That is indeed! That's also a man that believes he's found answers! It's going to be interesting.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
As soon as I saw this:

“When cells are exposed to classical forms of dangers, such as a virus, infection or toxic environmental substance, a defense mechanism is activated. This results in changes to metabolism and gene expression, and reduces the communication between neighboring cells. Simply put, when cells stop talking to each other, children stop talking.” Naviau
I thought of recent research into TRP channels by NCNED in Australia and of course you seem to have confirmed the link between these 2 hypotheses further down.


Aberrant TRP channels seem to explain all my symptoms really well and my immunologist (he collaborates with NCNED) seems to agree.

This makes me really happy that this line of research is getting pursued by more researchers.
It's great to see some of this stuff come together...Maybe the elephant - remember the elephant looked at by the blind men - each of which thought it was something else - is starting to emerge as an elephant - a neuro-immune disorder with ion channel and mitochondrial problems (???)
 

Sharonann

New Member
This is the start of an "Eye On" series focusing on researchers new to the chronic fatigue syndrome/fibromyalgia research fields. Few researchers present more exciting possibilities for ME/CFS than Dr. Robert Naviaux at UC San Diego (UCSD).

[fright]View attachment 1343 [/fright]Naviaux recently joined the Scientific Advisory Board of the Open Medicine Foundation (OMF) and he's believed to have co-authored a paper that is under review. Early reports suggest the Severe Patient Big Data study may, in its early stages, uncovered significant about the mitochondria in ME/CFS

In some ways Naviaux seems tailor-made for ME/CFS. Naviaux runs the Robert Naviaux Laboratory at UC San Diego, is the founder/ co-director of UCSD's Mitochondrial and Metabolic Disease Center, and co-founder and a former president of the Mitochondrial Medicine Society. This man is clearly a pioneer in the relatively new and emerging field of mitochondrial research but he has an interesting immune side as well.

Naviaux trained at the NIH in tumor immunology and natural killer cell biology, and at the Salk Institute in virology and gene therapy. If ME/CFS or FM turns out to have a viral/inflammation/mitochondrial connection it's hard to imagine someone better placed to take advantage of that.

[fleft]View attachment 1344 [/fleft]Naviaux gained some renown in 2013 when he was able to reverse autism in a mouse model using a hypothesis that could help explain chronic fatigue syndrome and fibromyalgia as well. He proposed that a sustained "cell danger response" is causing the cells in autism to essentially to shut down, stop communicating with other cells and go into hibernation.

Naviaux believes that cells damaged by viruses, or toxins react defensively causing their membranes stiffen and the



(That's an intriguing idea given the evidence of "immune exhaustion" in ME/CFS and FM, and the rather massive alterations of immune cell networks Gordon Broderick and Dr. Klimas have found in ME/CFS. Could immune cell shut downs be behind those network alterations? )

Everybody seems to believe that the innate or early immune response which causes inflammation is involved in ME/CFS but Naviaux has taken the conversation a step further by tying in the mitochondria. Naviaux knew the mitochondria were involved in inflammation - they can be huge emitters of free radicals - and looked for ways in which they interacted with the immune system. He found them in substances called "mitokines" such as ATP and adenosine that cells with distressed mitochondrial emit.

The purines and pyrimidines ( ATP, ADP, UTP, and UDP), produced by these damaged cells can effect everything from inflammation, neurotransmission, pain production, and autonomic nervous system activity. They bind to purinergic and other receptors on cells found from the circulatory to digestive to immune systems to the brain.

Sleeping Sickness Drug

Naviaux used a drug called Surinam that battled sleeping sickness to reverse autism in his mouse model. An anti-purinergic signaling drug, Surinam, Naviaux believes, stops the cell danger signal in its tracks. In two studies he's been able to show that the drug rebuilt the mouse's brain synapses, re -enabled stalled cell-to-cell signaling, improved its social behavior and motor coordination and normalized it's mitochondrial metabolism. The drug is now being tested in a small trial of autistic children.

[fright]View attachment 1345 [/fright]Surinam is more of use for what it reveals than as a treatment possibility than a full-flung treatment. It can only be taken for couple of months but newer antipurinergic medicines might be able to be taken for longer or might just need to be taken intermittently.

As Naviaux developed his hypothesis that damaged cells are triggering purinergic signaling cascades in autism, Donald Staines in Australia was proposing vasoactive neuropeptides were doing much the same thing in ME/CFS. Staines also proposed that ATP and adenosine releases from cells with mitochondrial problems may be causing the purinergic signaling to go bananas in ME/CFS.

Meanwhile Alan Light's examination of physiological pathways linked to stress and distress in ME/CFS was uncovering issues with purinergic signaling as well. Light found that increased purinergic receptor activity was highly associated with post exertional fatigue after exercise in ME/CFS (but not MS). He, too, suggested that purinergic receptors in ME/CFS patients were reacting to ATP molecules emanating from stressed cells. Back in 2012 he proposed that purinergic receptor upregulation in ME/CFS was turning the microglia in the brain on and producing pain and fatigue in ME/CFS.

Naviaux and other ME/CFS researchers, then, may be coming from different directions and ending up in much the same place.

We don't know what Naviaux has found in ME/CFS - we're waiting on his publication for that; it could be something entirely different but his past research alone suggests that he is someone to watch.

[fleft]View attachment 1347 [/fleft]A member of the Health Rising Forums, Rachel Riggs, knows this first hand. After visiting Dr. Naviaux's lab she described a researcher who was very enthusiastic about ME/CFS, who mentioned linkages between autism and the disease - a disease, he thought, which put ME/CFS bodies in a kind of hibernation. Dr. Naviaux said his paper on ME/CFS will, if and when it is published, surprise a lot of people. Rachel had a palpable sense that the lab was on the cusp of something big.

Naviaux's got some big accomplishments behind him and some big toys to play with. His lab developed two advanced technologies; biocavity laser spectroscopy and mtDNA mutation detection by mass spectrometry, and recently created new bioinformatic methods that allow them to better analyze genetic data. Put all that together and Naviaux says he has the ability to "dissect the metabolic and molecular features of virtually any disease".

Naviaux appears to be all in ME/CFS. His biggest hurdle may be finding the money to fully study it. Hopefully the new approach by the NIH or the growing ability of ME/CFS donors to support exciting research will be enough.

Naviaux is part of an increasing focus on the mitochondria in ME/CFS research circles. The Chronic Fatigue Initiative has engaged Maureen Hanson to do a series of ME/CFS mitochondrial studies. Richard Deth, a mitochondrial expert, is working with Dr. Klimas at the Institute for Neuroimmune Institute in Florida. Dr. Saligan, a P2P report participant, and member of the NIH Intramural study is a bit of a wild card. His work on the stress response and catastrophizing has raised concerns, but his main research interest is focused on the physiological aspects of cancer fatigue.

Saligan has done studies on murine models of radiation induced fatigue, gene expression and cancer fatigue, prostate cancer and fatigue, inflammation and cancer fatigue, BDNF and fatigue, immunogenomic markers and fatigue, mitochondria and prostate fatigue, biomarkers and cancer fatigue and on and on and he's done one review on catastrophizing and fatigue.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
@Mark C Agreed - seems like Millions Missing is our best opportunity for greater visibility at the mo - but it is difficult to make a lot of noise when we are such a sick population. Trust me, if I wasn't as sick as I am I'd be out there kicking some arse...
You're already kicking arse pretty Rachel :playful::playful:

Thanks for getting in to see Dr. Naviaux - that was what inspired this blog.
 

SueS

Active Member
'Put all that together and Naviaux says he has the ability to "dissect the metabolic and molecular features of virtually any disease".'

This really jumped out at me. For some time I've been feeling that unravelling ME will also mean unravelling a whole lot of other illnesses as well. I do think that somehow we are virgin territory, that solving our puzzle involves people on the edge of not just new testing but also a new scientific paradigm, and that's why we've fallen through the cracks.

This is exciting.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
'Put all that together and Naviaux says he has the ability to "dissect the metabolic and molecular features of virtually any disease".'

This really jumped out at me. For some time I've been feeling that unravelling ME will also mean unravelling a whole lot of other illnesses as well. I do think that somehow we are virgin territory, that solving our puzzle involves people on the edge of not just new testing but also a new scientific paradigm, and that's why we've fallen through the cracks.

This is exciting.
It's definitely a new scientific paradigm and I think you're right - the way medicine understands disease now has allowed us to slip through the cracks.

Technology is going to lead the way I think, which is why its great to have cutting-edge researchers like Naviaux interested.
 

Victor Maalouf

Active Member
Similarities between Autism and CFS/ME? Nooooooo.... really? YOU DON'T SAY!?

Hah!

But yeah. Turning off the cells' "danger response" sounds about right. I'm willing to bet that Autism study will work.
 

Katherine Autry

Active Member
To get more ME/CFS R&D funding, we need to get millions missing and invisible and not funded, "out of the closet" and onto www.diseasemaps.org where we can be seen, and can coordinate regionally, to get in front of public and politicians who will then fund, when it is obvious to all that Feds have grossly discriminated against M.E. for decades, and since more common in women, also grossly discriminating against She!

We need to first get visible, then get political, then train 100 senators and every congressman about how male centric disease gets $3B NIH budget per year, but female centric ME/CFS gets $6M NIH in 2015, so this is gross sex discrimination by Govt.

They are sworn to provide equal justice for all, and must do so. Once they understand the facts and discrimination, we need to put everyone to a litmus test, will they support greatly expanded funding for ME/CFS to $250M per year, and it not, vote them out since they do not deserved to be in office if they let gross discrimination. Some goes for Obama.

If he can throw billions overnight at Ebola or Zika viral diseases almost overnight, he can invest $250M, why not overnight, to help cure 2,000,000 affected Americans get back to work, make American stronger, cut healthcare costs, save up to $50B CDC estimated cost of ME/CFS to US economy.

Hope everyone can support these researchers directly or via non-profits now, and get NIH to have funding at $250M, and election platform for all parties, all incumbents and candidates - or vote them OUT!

A class action lawsuit for gender discrimination would do the trick.
 
Hi,
this looks very interesting, among other elements the day night (circadian rhythm) disruption rings a bell. Also, the fact that he's applied mass spectrometry is interesting (see below).

Presumably disruption of the mitochondria would result in changes in proteins and/or lipids etc. i.e. potential biomarkers. Cort, you wrote about Jonas Bergquist presentation at the Invest in ME conference last year; from memory he suggested that analysis of proteins and lipids in a cerebrospinal fluid study of Swedish ME/CFS patients suggested a possible metabolic disorder (the study used LCMSMS i.e. mass spectrometry) . Therefore, there may be opportunities to diagnose ME/CFS from proteins, and/or lipids, using mass spectrometry. Perhaps understanding the disease mechanism will prompt further research into biomarkers.

Re funding.
I've tried - locally (Northern Ireland Assembly - regional government) i.e. use of Government science laboratories to apply the technique used by Jonas Bergquist (LCMSMS - mass spectrometry) to diagnose ME/CFS. Government science laboratories use this technique to measure antibiotic/growth promoter residues in food; cost per sample is approximately £200 pounds. FDA in America, and numerous other countries, also use this technique to test food imports/exports. No success with Northern Ireland Assembly. Good to know where ME/CFS patients rank relative to concerns about residues in imported chicken meat! Then again, I'm a voter i.e. I'm part of this outcome.
I've tried - Nationally (all party parliamentary group on ME - UK Westminster government) - No success. Apparently investigating the application of Government science laboratories mass spectrometry resources, to the diagnosis of ME/CFS, is not the sort of thing they're interested in (whatever it is there interested in -- getting elected?). Comments above re how patients rank relative to concerns over food safety etc refer.
I've tried - European level (European commission funded research) - seeking approximately 30,000 euros to fund the testing of blood samples from the Swedish ME/CFS patients. Guess what - yes - three in a row - not interested. There may be approximately 1 million Europeans with ME/CFS but I was advised that "your request related to the development of a diagnostic test seems to be hardly in line with the kind of actions listed in the [Health] work plan priorities. Furthermore, most of the actions are multi beneficiaries and should cover at least 3 Member States.".
Comments above re how patients rank relative to concerns over food safety etc refer.


Hopefully, we'll see this research (Naviaux) published in the near future and this will help to build a case to fund diagnostic testing and treatment.

PS - Governments do deliver certain things (e.g. testing imported foods - concerns over food safety). However, getting them to fund health research (e.g. to diagnose ME/CFS) appears to be more difficult. A quote comes to mind "they [Governments] work for you"!
 

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