The low energy state, the inflammation, the oxidative stress – all the bad stuff that has shown up in ME/CFS – does it all come together in the brain? Andrew Lloyd asserted a decade ago that the symptoms in ME/CFS are all brain symptoms. If the brain findings from the IACFS/ME conference are any clue he could be right.
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Regarding Natelson’s theory that ME/CFS starts in the brain and travels through the body – I came across research which found something different – the term “experimental autoimmune encephalomyeletis” which researchers termed what looked to them something like MS but which looks (to us) a lot like CFS/ME. These researchers found mast cells were releasing cytokines in the body which are crossing the blood brain barrier and finding their way to the brain “… which allows inflammatory cells to infiltrate into the central nervous system (CNS) and destruct myelin and oligodendrocytes [30]. CD4+ T cells, including IFN-γ-secreting T helper 1 cells (Th1), IL-17-producing T helper 17 cells (Th17), and IL-9-producing T helper 9 cells (Th9), contribute to the pathogenic autoimmune response in EAE [43]. However, the roles of these cells in MS are still unclear [44]…” The research quoted on this webpage finds elevated levels of tryptase in the cerebral spinal fluid.
Has anyone seen NIH’s news release of Oct 17th “NIH Scientists Uncover Genetic Explanation for Frustrating Syndrome”? https://www.nih.gov/news-events/news-releases/nih-scientists-uncover-genetic-explanation-frustrating-syndrome
NIH found genes that elevate levels of tryptase in the blood of what sounds like ME/CFS and definitely EDS patients. But they’re not saying the words of our diseases – they’re applying their findings to vaguely “four to six percent of the general public” and the research is being done at their National Institute of Allergy and Infectious Diseases. An EDS patients speaks of sending blood for this study here: http://ohtwist.com/what-is-mcad/
I’m wondering if Ron Davis, Robert Naviaux, etc. are being informed of the NIH genetic studies into CFS/ME/EDS under the umbrella of different diseases like MS and anaphylactic allergic reactions. There’s more than one study that’s been done. https://www.ncbi.nlm.nih.gov/pubmed/25169217 IF NIH refuses to admit they’re looking into ME/CFS/EDS per se, we’ll never have a compiled body of research into our disease, just what we have now: scattered studies of symptoms and genes under a myriad of different names which doctor’s won’t know to apply to us.
Some Rituxan studies, if I understand correctly, have focused on patients who lack acetylcholine due to what they call “Acetylcholine Receptor Autoantibody Myasthenia Gravis”. http://www.neurology.org/content/82/10_Supplement/S36.009 They found that some patients have intolerable reaction to Rituxan. 3 drugs are given just before Rituxan injections. http://www.nmouk.nhs.uk/downloads/Rituximab-protocol.pdf One is an antihistamine, which decreases acetylcholine in the body. Another I think increases acetylcholine and the last is an acetaminophen. Acetaminophen is listed at Drugs.com as “often having anticholinergic activity”, that is, it can block acetylcholine.
I have no idea of whether all these things could be linked to one type of ME/EDS/CFS patient. I just wonder how aware researchers are of each others work when they’re looking at what they think are different diseases/conditions.
Hi Laura, what you’ve written is very relevant, and very interesting. Here’s something on EAE that looks promising too … but it’s from almost 7 years ago!
That is interesting too, Stan, thanks! I think that the problem is that NIH is funding only researchers who are treating/researching patients who they feel contracted CFS/ME after a virus. Hence, probiotics. Which are great for everyone. Histamine production is a normal response to injury, whether that’s physical, viral, bacterial, or chemical. If there isn’t enough acetylcholine in the body, the vagus nerve can’t signal temper the histamine so it keeps showing up. The problem isn’t that the histamines were properly produced in response to injury, which is why they show up when researching cytokines, mast cells etc. It’s that they didn’t stop being produced. No brakes on the car.
You have several fibro and CFS articles suggesting that these diseases may link to neuroinflammation. The Natelson and Shungu study showing lactate in the brain stands out for me as evidence of that.
My question is do you know of any practitioners who are using advanced imaging techniques to find lactate levels in the brain? To be honest, I find a lot of use of MRS and other advanced MRI techniques in the research literature, but literally zero doctors use these technologies in clinical practice. The use of lactate levels in the brain seems to be a great way to measure progress against the disease, as well as a tool for diagnosis.
I’m afraid I have no ideas if any practitioners are doing this (aside from Natelson, if he is). Lots of time research techniques don’t show up in doctor’s offices unless insurance companies will pay for them.
I have severe ME and am likely to die of it.
However what really needs addressing is the Myalgic Encephalomyrlitis is not the same disease as Chronic Fatigue.
Chronic fatigue is just a symptom found in many diseases. It so wrong and insulting to say ” its just CFS “.
It certainly is NOT and is an invention by the USA to cover their private, very expensive health insurance industry. If its called Fatigue , the they get away without paying up if some poor person happens to catch it. ME is life long.
ME is certainly a Disease of the BRAIN, that reeks havoc with your body and organs and if left would soon lead to death
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The low energy state, the inflammation, the oxidative stress – all the bad stuff that has shown up in ME/CFS – does it all come together in the brain? Andrew Lloyd asserted a decade ago that the symptoms in ME/CFS are all brain symptoms. If the brain findings from the IACFS/ME conference are any clue he could be right.
Health Rising’s Quickie Summer Donation Drive is On!
Thanks for this great writeup Cort!
Regarding Natelson’s theory that ME/CFS starts in the brain and travels through the body – I came across research which found something different – the term “experimental autoimmune encephalomyeletis” which researchers termed what looked to them something like MS but which looks (to us) a lot like CFS/ME. These researchers found mast cells were releasing cytokines in the body which are crossing the blood brain barrier and finding their way to the brain “… which allows inflammatory cells to infiltrate into the central nervous system (CNS) and destruct myelin and oligodendrocytes [30]. CD4+ T cells, including IFN-γ-secreting T helper 1 cells (Th1), IL-17-producing T helper 17 cells (Th17), and IL-9-producing T helper 9 cells (Th9), contribute to the pathogenic autoimmune response in EAE [43]. However, the roles of these cells in MS are still unclear [44]…” The research quoted on this webpage finds elevated levels of tryptase in the cerebral spinal fluid.
Has anyone seen NIH’s news release of Oct 17th “NIH Scientists Uncover Genetic Explanation for Frustrating Syndrome”? https://www.nih.gov/news-events/news-releases/nih-scientists-uncover-genetic-explanation-frustrating-syndrome
NIH found genes that elevate levels of tryptase in the blood of what sounds like ME/CFS and definitely EDS patients. But they’re not saying the words of our diseases – they’re applying their findings to vaguely “four to six percent of the general public” and the research is being done at their National Institute of Allergy and Infectious Diseases. An EDS patients speaks of sending blood for this study here: http://ohtwist.com/what-is-mcad/
I’m wondering if Ron Davis, Robert Naviaux, etc. are being informed of the NIH genetic studies into CFS/ME/EDS under the umbrella of different diseases like MS and anaphylactic allergic reactions. There’s more than one study that’s been done. https://www.ncbi.nlm.nih.gov/pubmed/25169217 IF NIH refuses to admit they’re looking into ME/CFS/EDS per se, we’ll never have a compiled body of research into our disease, just what we have now: scattered studies of symptoms and genes under a myriad of different names which doctor’s won’t know to apply to us.
Just wanted to add one more comment here regarding Dr. Natelson’s research into brain signalling:
A study was just posted a few days ago at NCBI regarding acetylcholine and brain signalling: https://www.ncbi.nlm.nih.gov/gene/43
Some Rituxan studies, if I understand correctly, have focused on patients who lack acetylcholine due to what they call “Acetylcholine Receptor Autoantibody Myasthenia Gravis”. http://www.neurology.org/content/82/10_Supplement/S36.009 They found that some patients have intolerable reaction to Rituxan. 3 drugs are given just before Rituxan injections. http://www.nmouk.nhs.uk/downloads/Rituximab-protocol.pdf One is an antihistamine, which decreases acetylcholine in the body. Another I think increases acetylcholine and the last is an acetaminophen. Acetaminophen is listed at Drugs.com as “often having anticholinergic activity”, that is, it can block acetylcholine.
We know that EDS patients have a problem with not enough collagen. There seems to be a connection with collagen and acetylcholine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2150590/ and https://www.ncbi.nlm.nih.gov/pubmed/26785775
I have no idea of whether all these things could be linked to one type of ME/EDS/CFS patient. I just wonder how aware researchers are of each others work when they’re looking at what they think are different diseases/conditions.
Hi Laura, what you’ve written is very relevant, and very interesting. Here’s something on EAE that looks promising too … but it’s from almost 7 years ago!
http://www.prohealth.com/me-cfs/library/showarticle.cfm?libid=15148
That is interesting too, Stan, thanks! I think that the problem is that NIH is funding only researchers who are treating/researching patients who they feel contracted CFS/ME after a virus. Hence, probiotics. Which are great for everyone. Histamine production is a normal response to injury, whether that’s physical, viral, bacterial, or chemical. If there isn’t enough acetylcholine in the body, the vagus nerve can’t signal temper the histamine so it keeps showing up. The problem isn’t that the histamines were properly produced in response to injury, which is why they show up when researching cytokines, mast cells etc. It’s that they didn’t stop being produced. No brakes on the car.
You have several fibro and CFS articles suggesting that these diseases may link to neuroinflammation. The Natelson and Shungu study showing lactate in the brain stands out for me as evidence of that.
My question is do you know of any practitioners who are using advanced imaging techniques to find lactate levels in the brain? To be honest, I find a lot of use of MRS and other advanced MRI techniques in the research literature, but literally zero doctors use these technologies in clinical practice. The use of lactate levels in the brain seems to be a great way to measure progress against the disease, as well as a tool for diagnosis.
I’m afraid I have no ideas if any practitioners are doing this (aside from Natelson, if he is). Lots of time research techniques don’t show up in doctor’s offices unless insurance companies will pay for them.
I have severe ME and am likely to die of it.
However what really needs addressing is the Myalgic Encephalomyrlitis is not the same disease as Chronic Fatigue.
Chronic fatigue is just a symptom found in many diseases. It so wrong and insulting to say ” its just CFS “.
It certainly is NOT and is an invention by the USA to cover their private, very expensive health insurance industry. If its called Fatigue , the they get away without paying up if some poor person happens to catch it. ME is life long.
ME is certainly a Disease of the BRAIN, that reeks havoc with your body and organs and if left would soon lead to death
Thanks for your post. I agree. I have EDS and ME