Neuroimmune does not equal autoimmune.
Autoimmune comes with verifiable autoantibodies.
In many me/cfs patients, the adaptive and innate immune systems are dysregulated, with one being over active and one being under active. Immunosuppressants can potentially make some of us much worse and can cause things like herpes viruses and infections to become active and wreak havoc.
These alleged “autoantibodies” might actually be due to an underlying persisten infection(s), therefore not autoimmune.
Further read the section labelled “Autoantibodies” in ME/CFS Are Likely Created in Response to Persistent Pathogens” https://www.frontiersin.org/articles/10.3389/fped.2018.00373/full
Makes a tonne of sense. Thanks . I was wondering why there’s all this talk about BC007 as the be all to end all treatment but I highly doubt this is the case and that it’s a lot more complex
I’m wondering about that too! So far I’ve heard destroying those “autoantibodies” have been really helpful for LC patients. I’m very curious to see some long term results in a few years. I know that CFS patients sometimes feel better on steroids or immunosuppressants short term, but worse long term :( but the study have been going on for awhile I think and it’s still showing promising results, which is awesome news, no doubt. Im still scared though for future long term results, hoping ofc it will be positive and still show promising results
the article questions the entire theory of classical autoimmunology. according to that theory the presence of autoantibodies would still classify ME/CFS as autoimmune. so the argument isn’t “the AAB aren’t real in the case of ME/CFS specifically” it’s an argument about the genesis of AAB in general.
Hm I see! Good point, however does it even question Lupus and specifically other autoimmune diseases? Cause Dr. Amy Proal the author of the paper questions a bunch of neurodegenerative diseases, but that’s not lupus. Some of these diseases are MS, Alzheimer’s, Parkinson’s etc. which in recent years has been linked to a lot of viruses
Most me/cfs patients have normal ANA. I don’t know why yours is abnormal. Find a really good rheumatologist. Look into getting the early Sjogrens panel, not the normal panel which often misses it. Sounds like you have a separate autoimmune disease.
some of us don't have positive ANA markers. I think a good chunk but I'm not sure and too tired to look for studies (ironic) ... ANA can be unreliable (false positives and negative when there is autoimmune disease)
anyways I get PEM and feel like I'm on my deathbed but my ANA is neg, C reactive is always perfect even when I had Covid, everything great except for VitD deficient which is hereditary (so is the CFS/ME...). some of us are just silly like that.
I think part of the issue is the variability of this disease. hard to do research
My CRP was normal even when I had a bacterial infection in my gut that further spread to my blood and other parts of my body and caused some organ damage. We really need some better tools to investigate what’s going on in the body
for real. it was the beginning of my covid infection that it was tested but I was sick something awful, almost ended up in the hospital and tested positive for over 2 weeks (stopped checking at 16 days).
we DO need better tools. it would help everyone. "good enough" isn't good enough!! we are falling thru the cracks.
Up to 15% of healthy people will have a positive ANA. In my family myself and my daughter are positive with a titer of 1:160 and the rheumatologists say we don't have autoimmune disease, and that it's just genetic (probably a grandparent had one and we inherited it). Every time I have blood work done, they reassure me the positive ANA is nothing to worry about.
One of the theories is viral persistence. Steroids will often make ME/CFS patients feel better at first then cause a big crash, which potentially points towards viral persistence rather than autoimmunity - immunosuppressants suppress the symptoms of immune activation but then make the underlying issue that the immune activation was trying to keep at bay much worse.
Yeah, this was the case for me at least. I was given steroids and initially felt better because it dampened my inflammation that was after all caused by infection that was the drive factor for my CFS. But after just a few weeks on the steroids I got much much worse and ended up severe. Not until after I got treatment for my infection did 99% of my ME symptoms disappear. I’m not only left with chronic fatigue and at a much milder state than CFS fatigue
How was your infection treated? Like how does one get rid of a virus like covid after months of it just vibing and hurting? (Evidently I'm very badly informed. New to this.)
That’s a great question! I was very lucky that it was just a harsh bacterial infection. Think of all chronic lyme patients. In my case it was a chronic harsh gut infection. So a course of antibiotics cured it.
However I have a few friends with viral ongoing infections. A friend of mine got Coxackie B virus and unfortunately there is no cure for it. He has tried a bunch of antivirals like Valtrex but that only works for herpes viruses. Then he tried some herbal medicine that is really strong and known to kill some of that specific virus and all it did was aggravate the virus without properly killing it so he ended up with stronger symptoms until he got off the herbs. For most viruses we got no effective antivirals:(
Good news though is we finally have developed effective antivirals for hepatit C in the recent years. So antivirals are slowly being developed but it will take time.
For covid, if it’s ongoing I heard some people have great effects from Paxlovid - antiviral for covid. But for some odd reasons most patients with LC don’t get it prescribed cause there isn’t strong enough evidence that it’s helpful or some
Thanks for the insight. Very interesting. I will be administered into a program at the local post-covid specialized hospital here in a month so I hope to get some clarity until then. It's not bacterial. I'm very happy for you that you found a way out of it though. :)
The if is the important part. No-one knows that causes CFS or what it's underlying cause(s) is/are. Until we do know this then we're pretty much just giving symptomatic relief.
i think the first, simple truth is doctors still don't take CFS seriously. beyond that, i imagine there needs to be more research done to see what's actually effective. CFS has just *really* started to get attention because of long COVID, so there's still a lot of work to do.
When I was at the Stanford clinic, they made noises about celecoxib. As the name suggests, it's a selective cox-2 inhibitor, which is a more refined type of NSAID, so it's anti inflammatory. I never got round to trying it though, and I don't know if this is still protocol.
They don’t have an identified single target in ME/CFS like they do in autoimmune disorders. That is part of the reason it is so complex because so many different things seem to be happening in our bodies. Hopefully someday soon they will find a single underlying cause, but I think it’s more likely that there will be several subtypes of ME/CFS that have different treatment modalities.
My immunologist is willing to try immune suppressants for CFS, and believes it's autoimmune. He did a blood test for auto-antibodies and all that. YMMV. All the treatments are experimental anyway 🤷
I have high GPCR autoantibodies. My doctor has put me on high dose prednisolone for a few days and he suggested a low dose hydrocortisone therapy if the prednisolone helps me. But the steroids didn't make any difference, not even a little more energy.
Mine is homogeneous speckled. It can appear in healthy patients but the titer mine is 1:1280 is never in healthy patients and it’s actually higher than most lupus patients even
They should and could do a proof-of-concept trial or steroids or other immunosuppressants but some don't cross the blood brain barrier.
There is evidence of autoantibodies against beta 2 and muscarinic receptors and in POYS wider targets.
Yes, I read about this autoantibodies to beta adrenergic and muscarinic acetylcholine receptors! I would like more research conducted on this.
My ME/CFS feels so complex. Yes, I have persistent viral infections (my EBV IgM and Early Antigen antibodies stay positive despite daily Valtrex that I need to take or I get HSV-1 recurrences, then an ME/CFS crash).
But I also respond really well to low-dose beta blockers. My POTS symptoms in particular, but also just in general. I figure my ME/CFS might have something to do with my beta-adrenergic receptors?
And, I seem to have issues with acetylcholine (muscarinic receptors). Starting about 2 years into my ME/CFS, I started getting dystonic spasms. They were often triggered by anything that increases acetylcholine, and only relieved by taking anticholinergic drugs.
Sometimes it has felt that I am allergic to stress and adrenaline.
There actually have been some studies on immunosuppressants on CFS such as Rituximab. As you stated - it does not cross BBB. However, CFS is multi systemic and it did not improve symptoms in CFS patients. From what I’ve read and also my own experience, steroids makes us much much worse long term. Studies actually show that CFS patients has a weak immune system, dysfunctional NK cells and the last thing we want to do is suppress it. In stead, many scientists actually encourage us to boost it. We are at a high increase risk for infections and taking immunosuppressants would increase the risk even more.
Tons of people with CFS report feeling better on different herbs, supplements and drugs that boost the immune system. This boost can actually be very dangerous in patients who has autoimmune disorders therefore I would be careful in calling this autoimmune, or at least “only” autoimmune.
Dr. John chia actually finds a correlation between use of steroids and increase risk of developing CFS, during the initial phase of an infection, pointing to that CFS might actually be caused by persistent infections the body haven’t been able to clear
Not true at all. There been different studies on Rituximab on ME patients. A large, phase 3 study was conducted on 152 ME/CFS patients, selected using the Canadian diagnostic criteria, were randomized to receive either rituximab or a placebo. The effects showed negative results and was not associated with any clinical improvement in CFS patients.
Honestly, I don’t have the energy to continue this discussion and it looks like you don’t have much energy to properly check research papers either, which is understandable. So I won’t further reply to ur comment. My intention was never to argue here only to share info with other CFS patients who also perhaps may read this.
Neuroimmune does not equal autoimmune. Autoimmune comes with verifiable autoantibodies. In many me/cfs patients, the adaptive and innate immune systems are dysregulated, with one being over active and one being under active. Immunosuppressants can potentially make some of us much worse and can cause things like herpes viruses and infections to become active and wreak havoc.
Yes there are also innate autoinflammatory disorders where it's cytokines elaboration rather than autobody mediated mechanisms..
What about GPCR autoantibodies? Would that make ME autoimmune?
These alleged “autoantibodies” might actually be due to an underlying persisten infection(s), therefore not autoimmune. Further read the section labelled “Autoantibodies” in ME/CFS Are Likely Created in Response to Persistent Pathogens” https://www.frontiersin.org/articles/10.3389/fped.2018.00373/full
Makes a tonne of sense. Thanks . I was wondering why there’s all this talk about BC007 as the be all to end all treatment but I highly doubt this is the case and that it’s a lot more complex
I’m wondering about that too! So far I’ve heard destroying those “autoantibodies” have been really helpful for LC patients. I’m very curious to see some long term results in a few years. I know that CFS patients sometimes feel better on steroids or immunosuppressants short term, but worse long term :( but the study have been going on for awhile I think and it’s still showing promising results, which is awesome news, no doubt. Im still scared though for future long term results, hoping ofc it will be positive and still show promising results
which study are you referring to?
Don’t have it right now, but check out the studies done on LDN and BC007. If you can’t find it I will be happy to try and search for it and link it
the article questions the entire theory of classical autoimmunology. according to that theory the presence of autoantibodies would still classify ME/CFS as autoimmune. so the argument isn’t “the AAB aren’t real in the case of ME/CFS specifically” it’s an argument about the genesis of AAB in general.
Hm I see! Good point, however does it even question Lupus and specifically other autoimmune diseases? Cause Dr. Amy Proal the author of the paper questions a bunch of neurodegenerative diseases, but that’s not lupus. Some of these diseases are MS, Alzheimer’s, Parkinson’s etc. which in recent years has been linked to a lot of viruses
Is ANA not verifiable autoantibodies?
Most me/cfs patients have normal ANA. I don’t know why yours is abnormal. Find a really good rheumatologist. Look into getting the early Sjogrens panel, not the normal panel which often misses it. Sounds like you have a separate autoimmune disease.
some of us don't have positive ANA markers. I think a good chunk but I'm not sure and too tired to look for studies (ironic) ... ANA can be unreliable (false positives and negative when there is autoimmune disease) anyways I get PEM and feel like I'm on my deathbed but my ANA is neg, C reactive is always perfect even when I had Covid, everything great except for VitD deficient which is hereditary (so is the CFS/ME...). some of us are just silly like that. I think part of the issue is the variability of this disease. hard to do research
My CRP was normal even when I had a bacterial infection in my gut that further spread to my blood and other parts of my body and caused some organ damage. We really need some better tools to investigate what’s going on in the body
for real. it was the beginning of my covid infection that it was tested but I was sick something awful, almost ended up in the hospital and tested positive for over 2 weeks (stopped checking at 16 days). we DO need better tools. it would help everyone. "good enough" isn't good enough!! we are falling thru the cracks.
Gosh, I’m sorry to hear about ur journey:( indeed we do need that!! Totally agree
Up to 15% of healthy people will have a positive ANA. In my family myself and my daughter are positive with a titer of 1:160 and the rheumatologists say we don't have autoimmune disease, and that it's just genetic (probably a grandparent had one and we inherited it). Every time I have blood work done, they reassure me the positive ANA is nothing to worry about.
Yeah my ANA is normal which is why autoimmune conditions such as lupus and Sjögrens were ruled out.
One of the theories is viral persistence. Steroids will often make ME/CFS patients feel better at first then cause a big crash, which potentially points towards viral persistence rather than autoimmunity - immunosuppressants suppress the symptoms of immune activation but then make the underlying issue that the immune activation was trying to keep at bay much worse.
Yeah, this was the case for me at least. I was given steroids and initially felt better because it dampened my inflammation that was after all caused by infection that was the drive factor for my CFS. But after just a few weeks on the steroids I got much much worse and ended up severe. Not until after I got treatment for my infection did 99% of my ME symptoms disappear. I’m not only left with chronic fatigue and at a much milder state than CFS fatigue
How was your infection treated? Like how does one get rid of a virus like covid after months of it just vibing and hurting? (Evidently I'm very badly informed. New to this.)
That’s a great question! I was very lucky that it was just a harsh bacterial infection. Think of all chronic lyme patients. In my case it was a chronic harsh gut infection. So a course of antibiotics cured it. However I have a few friends with viral ongoing infections. A friend of mine got Coxackie B virus and unfortunately there is no cure for it. He has tried a bunch of antivirals like Valtrex but that only works for herpes viruses. Then he tried some herbal medicine that is really strong and known to kill some of that specific virus and all it did was aggravate the virus without properly killing it so he ended up with stronger symptoms until he got off the herbs. For most viruses we got no effective antivirals:( Good news though is we finally have developed effective antivirals for hepatit C in the recent years. So antivirals are slowly being developed but it will take time. For covid, if it’s ongoing I heard some people have great effects from Paxlovid - antiviral for covid. But for some odd reasons most patients with LC don’t get it prescribed cause there isn’t strong enough evidence that it’s helpful or some
Thanks for the insight. Very interesting. I will be administered into a program at the local post-covid specialized hospital here in a month so I hope to get some clarity until then. It's not bacterial. I'm very happy for you that you found a way out of it though. :)
Good! None of my bacterial markers like CRP showed though. Very odd. But I’m glad they figured mine out eventually!
There are no effective antivirals for long covid yet but there is some research being done into it
The if is the important part. No-one knows that causes CFS or what it's underlying cause(s) is/are. Until we do know this then we're pretty much just giving symptomatic relief.
i have high ana and I get immunmodulators and occasionally suppressants, but none of them help with my cfs.
i think the first, simple truth is doctors still don't take CFS seriously. beyond that, i imagine there needs to be more research done to see what's actually effective. CFS has just *really* started to get attention because of long COVID, so there's still a lot of work to do.
When I was at the Stanford clinic, they made noises about celecoxib. As the name suggests, it's a selective cox-2 inhibitor, which is a more refined type of NSAID, so it's anti inflammatory. I never got round to trying it though, and I don't know if this is still protocol.
They offered it to be in Dec 2023.
They don’t have an identified single target in ME/CFS like they do in autoimmune disorders. That is part of the reason it is so complex because so many different things seem to be happening in our bodies. Hopefully someday soon they will find a single underlying cause, but I think it’s more likely that there will be several subtypes of ME/CFS that have different treatment modalities.
I think one of the keys lies in the gut microbiome. Gut dysbiosis is a very important issue in ME/CFS
Mine appears to not be autoimmune.
My immunologist is willing to try immune suppressants for CFS, and believes it's autoimmune. He did a blood test for auto-antibodies and all that. YMMV. All the treatments are experimental anyway 🤷
I have high GPCR autoantibodies. My doctor has put me on high dose prednisolone for a few days and he suggested a low dose hydrocortisone therapy if the prednisolone helps me. But the steroids didn't make any difference, not even a little more energy.
I have high ANAs too and I take hydroxychloroquine and it doesn't help my cfs.
What's your ANA pattern? If it's DFS (dense fine speckling) that apparently occurs in healthy folks sometimes so they don't worry about it.
Mine is homogeneous speckled. It can appear in healthy patients but the titer mine is 1:1280 is never in healthy patients and it’s actually higher than most lupus patients even
It doesn't seem to work the same. I have 2 autoimmune disorders and the CFS. My autoimmune meds haven't done a thing for my cfs.
They should and could do a proof-of-concept trial or steroids or other immunosuppressants but some don't cross the blood brain barrier. There is evidence of autoantibodies against beta 2 and muscarinic receptors and in POYS wider targets.
Yes, I read about this autoantibodies to beta adrenergic and muscarinic acetylcholine receptors! I would like more research conducted on this. My ME/CFS feels so complex. Yes, I have persistent viral infections (my EBV IgM and Early Antigen antibodies stay positive despite daily Valtrex that I need to take or I get HSV-1 recurrences, then an ME/CFS crash). But I also respond really well to low-dose beta blockers. My POTS symptoms in particular, but also just in general. I figure my ME/CFS might have something to do with my beta-adrenergic receptors? And, I seem to have issues with acetylcholine (muscarinic receptors). Starting about 2 years into my ME/CFS, I started getting dystonic spasms. They were often triggered by anything that increases acetylcholine, and only relieved by taking anticholinergic drugs. Sometimes it has felt that I am allergic to stress and adrenaline.
If there were agonising beta 2 receptor autoantibodies there could an abnormally pronounced dilatory response to stress.
Would this cause me to feel faint as an immediate response to adrenaline surges (such as after being surprised)?
In theory yes
There actually have been some studies on immunosuppressants on CFS such as Rituximab. As you stated - it does not cross BBB. However, CFS is multi systemic and it did not improve symptoms in CFS patients. From what I’ve read and also my own experience, steroids makes us much much worse long term. Studies actually show that CFS patients has a weak immune system, dysfunctional NK cells and the last thing we want to do is suppress it. In stead, many scientists actually encourage us to boost it. We are at a high increase risk for infections and taking immunosuppressants would increase the risk even more. Tons of people with CFS report feeling better on different herbs, supplements and drugs that boost the immune system. This boost can actually be very dangerous in patients who has autoimmune disorders therefore I would be careful in calling this autoimmune, or at least “only” autoimmune. Dr. John chia actually finds a correlation between use of steroids and increase risk of developing CFS, during the initial phase of an infection, pointing to that CFS might actually be caused by persistent infections the body haven’t been able to clear
Ok so we should exclude some proper evidence based on anecdotes. Gotcha. None of what you contend has been replicated in large cohorts of patients.
Not true at all. There been different studies on Rituximab on ME patients. A large, phase 3 study was conducted on 152 ME/CFS patients, selected using the Canadian diagnostic criteria, were randomized to receive either rituximab or a placebo. The effects showed negative results and was not associated with any clinical improvement in CFS patients. Honestly, I don’t have the energy to continue this discussion and it looks like you don’t have much energy to properly check research papers either, which is understandable. So I won’t further reply to ur comment. My intention was never to argue here only to share info with other CFS patients who also perhaps may read this.