Study about infection-triggered autoimmune disease, Multiple Sclerosis, EBV and Theiler’s murine encephalomyelitis virus

Annikki

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Sorry for the cumbersome title, but the following study is definitely worth looking at. I love it because it reflects my idea that an external trigger, i.e. an entity with different DNA (or RNA) from your own triggers ME. Many of us got ME after having a "run of the mill" viral infection. I never thought that just a coincidence. I probably never will.

This study I'm sharing looks at MS and other autoimmune diseases of the brain. It doesn't mention CFS/ME, but I cannot help think it relates in a critical way. LOL, I found it down a winding path which began with reading about the structure of coronavirus from a great article in the Washington Post. Somehow I wound up looking up glycoproteins and autoimmunity after this and found this gem of a study:
Virus infection, antiviral immunity, and autoimmunity
Daniel R. Getts,1 Emily M. L. Chastain,1 Rachael L. Terry,1 and Stephen D. Miller1
Author information Copyright and License information Disclaimer

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3971377/

The publisher's final edited version of this article is available at Immunol Rev
See other articles in PMC that cite the published article.

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Summary
As a group of disorders, autoimmunity ranks as the third most prevalent cause of morbidity and mortality in the Western World. However, the etiology of most autoimmune diseases remains unknown. Although genetic linkage studies support a critical underlying role for genetics, the geographic distribution of these disorders as well as the low concordance rates in monozygotic twins suggest that a combination of other factors including environmental ones are involved. Virus infection is a primary factor that has been implicated in the initiation of autoimmune disease. Infection triggers a robust and usually well-coordinated immune response that is critical for viral clearance. However, in some instances, immune regulatory mechanisms may falter, culminating in the breakdown of self-tolerance, resulting in immune-mediated attack directed against both viral and self-antigens. Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as bystander T-cell activation, culminating in epitope spreading, have been the predominant mechanisms elucidated through which infection may culminate in an T-cell-mediated autoimmune response. However, other hypotheses including virus-induced decoy of the immune system also warrant discussion in regard to their potential for triggering autoimmunity. In this review, we discuss the mechanisms by which virus infection and antiviral immunity contribute to the development of autoimmunity.
Keywords: autoimmune disease, molecular mimicry, epitope spreading, bystander activation, T-cell receptor affinity, microbial superantigens
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Introduction
The ability to recognize self and non-self is a pillar of the adaptive immune response, with deficiencies in these mechanisms leading to increased susceptibility to infection and cancer, or conversely, aberrant immune responses resulting in immunopathology and autoimmunity (14). Genome-wide association studies have identified polymorphisms in numerous genes associated with immune activation and regulation predisposing to development of autoimmune disease (5, 6); however, manifestation of autoimmunity may only occur after infection with certain pathogens (7). A precise set of pathogens as well as distinct autoimmune-associated immune responses remain to be elucidated (8). To the contrary, data suggest that autoimmunity may result from numerous immune pathways triggered by a plethora of microorganisms (9). In the case of multiple sclerosis (MS), viruses such as Epstein–Barr virus (EBV) and measles virus (MV) have been implicated in humans; however, a precise causal relationship between these ubiquitous viruses and MS has yet to be elucidated (10, 11). On the other hand, there are clear examples of rodent neurotropic viruses, such as Theiler’s murine encephalomyelitis virus (TMEV) and mouse hepatitis virus (MHV), which infect neurons and other cells within the central nervous system (CNS) resulting in deregulation of antiviral immune mechanisms and culminate in development of autoimmunity (1214). It remains to be confirmed whether exposure of the brain parenchyma to pathogenic infection is critical for autoimmune induction in humans, or whether infection of the periphery is a sufficient trigger. However, following TMEV infection, viral persistence in the CNS is an essential requirement for autoimmunity induction (15). Using such surrogate virus-induced rodent MS models, numerous aberrant innate and adaptive immune responses that are associated with or support the breakdown of self-tolerance and subsequent propagation of autoimmunity have been discovered. These pathways, including how pathogens circumvent or trigger certain innate immune system functions, as well as the intricate interplay between professional antigen-presenting cells (APC) and elements of the cellular immune response, are discussed in this review. Based on our experience and that of others, it is clear that infection-triggered autoimmune disease is the result of dynamic, interrelated, and non-mutually exclusive mechanisms. Understanding how viral infection results in autoimmunity must be viewed as a process that can occur through numerous simultaneous and/or sequential pathways, which depend on the nature of the pathogen as well as the genetics and the immune response of the host.
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Viruses associated with CNS autoimmunity
While this review focuses on viruses associated with triggering CNS autoimmune disorders, there are a number of bacteria and other microbes that have been associated with peripheral autoimmune disease, for example the Group A Streptococcus family can cause heart, joint, or brain autoimmunity (16). A significant amount of our current understanding of how self-tolerance is overcome comes from viral models of CNS infection and other rodent models of MS.
Infection of the CNS represents the failure of critical immune surveillance mechanisms and is most common in immune-compromised individuals, often times leading to morbidity in survivors (1719). Numerous highly pathogenic viruses, including those from the paramyxoviridae, flaviviridae, and herpesviridae families are known to infect cells within the brain (Table 1); however, only a handful including EBV, MV, and HTLV-1 have been linked with MS or other demyelinating disorders (10, 11, 20).
Table 1
Select viruses associated with central nervous system autoimmune diseases
Virus Species Family Associated with autoimmune disease Mechanism Reference(s) Measles virusHumanParamyxoviridaeYes – multiple sclerosis (MS)Bystander activation*
 Molecular mimicry*(11, 31)Epstein–Barr virusHumanHerpesviridaeYes – MSBystander activation*
 Molecular mimicry*(56, 134)HTLV-1HumanRetroviridaeYes – HTLV-1-associated myelopathy/tropical spastic paraparesisBystander activation*
 Molecular mimicry*(20)Theiler’s murine encephalomyelitis virus (TMEV)MousePicornoviridaeYes – TMEV-induced demyelinating diseaseMolecular mimicry
 Epitope spreading bystander activation(35, 37, 116)Japenese encephalitis virus (JEV)MouseFlaviviridaeYesMolecular mimicry(43)Sindbis virusMouseFlaviviridaeYesMolecular mimicry(163)Semliki Forest virusMouseFlaviviridaeYesMolecular mimicry(41, 42)WNVHuman/MouseFlaviviridaeYesImmune decoy*
 Bystander activation*(57, 158)
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*Suggested or proposed mechanism.
The association of EBV with MS remains controversial. EBV is a double-stranded DNA human herpes virus that primarily not only infects B cells (21) but can also infect endothelial cells (22). Approximately 95% of the general population is infected with EBV, and EBV remains latent within B cells for the life of the individual (23, 24). The incidence of MS is increased in those who are seropositive for EBV compared to those who are seronegative (25, 26). Also, there is evidence supporting a potential role for molecular mimicry in activation of myelin-specific T cells in MS patients (27). However, considering the large number of seropositive patients that do not have MS and the difficulty in isolating infected B cells from the CNS, the link is arguably weak (25, 2830).
In addition to EBV, MS patients generally have higher titers of MV, an RNA virus (31). Unlike EBV, a cause-and-effect relationship for MV has been shown, with 1 in 1000 patients likely to suffer a myelin basic protein (MBP)-specific postinfectious encephalomyelitis (32).
While HTLV-1 is not directly associated with MS, infection can result in a very similar disease, known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/ TSP) (20). Autoimmunity and molecular mimicry are believed to play a role in the pathogenesis of HAM/TSP, as antibodies cross-reactive to both HTLV-1 and neurons have been found in HAM/TSP patients (33).
Although direct evidence linking certain CNS infections with autoimmune disease in humans is correlative and non-definitive, strong support for virus-triggered CNS autoimmunity is derived from animal models. This includes infection with TMEV, Semliki Forest virus (SFV), Sindbis virus (SV), and MHV (34). Furthermore, using such tools as tetramers and transgenic mice, it has been elegantly shown that TMEV infection of the brain, as an example, is a critical step in the initiation of full-blown T-cell-mediated autoimmunity (13, 35)
While RNA viruses have been primarily used to investigate CNS infection and the development of autoimmunity, they represent a group of diverse pathogens, which are capable of eliciting an array of innate and adaptive immune responses. Using TMEV, we and others have unearthed numerous mechanisms through which viral infection of the CNS can initiate autoimmunity (3537). TMEV is a single strand RNA virus of the picornovirdae family. A number of strains of TMEV have been characterized and differ in infectivity and pathogenicity. The GDVII strain is extremely neurovirulent and causes acute encephalitis typically resulting in mortality (38). The BeAn and DA strains, however, are able to persist in the CNS after their initial acute encephalitis and cause chronic immune-mediated demyelinating disease (39).
The ability of TMEV to chronically persist is evidently required for the eventual induction of CNS autoimmunity. A natural murine pathogen, TMEV is transmitted via the fecal-oral route (40). In laboratory models, the virus is usually injected into the CNS via intracranial injection. In many strains of mice, including C57BL/6, the innate immune and adaptive immune responses adequately resolve the infection with no lasting sequelae. However, in other strains that are deficient in certain elements of the immune response, such as SJL/J mice that lack natural killer dendritic cells (E. M. L. Chastain, D. R. Getts, S. D. Miller, unpublished observation), the virus establishes a long-term persistent infection within the CNS. In such situations, the infection leads to a chronic antiviral immune response, which at some point moves from a centrally focused antiviral response, to one that also targets myelinated axons. At this point, a fulminant autoimmune disorder characterized by CNS-infiltrating myelin specific CD4+ T cells develops and is referred to as TMEV-induced demyelinating disease (TMEV-IDD).
In addition to TMEV, the positive-stranded RNA alphavirus SFV results in acute encephalitic disease that lasts 7 days, after which time the virus is cleared. Interestingly, a week to several weeks later, cytotoxic CD8+ T cells as well as antibodies reactive to MBP and MOG epitopes are found in the brain and periphery. Together these cause CNS demyelination that is observed clinically with symptoms such as aberrant gate, reduced activity, and even death (41, 42). Similarly to SFV virus, in which autoimmunity appears secondary to the primary infectious process, SV infection results in rapid paralysis within 6 days post infection. In the case of this positive-stranded RNA alphavirus, the initial immune responses are specific for SV; however, auto-specific immunity arises via epitope spreading (34).
JEV is a positive-sense strand RNA flavivirus that is closely related to WNV and St. Louis encephalitis virus. JEV spreads to the CNS after amplification in peripheral lymph nodes and can infect both neurons and astrocytes. Clinical symptoms in mice occur within the first week of infection and results in abnormal gait and hind limb paralysis (43, 44). Autoimmunity may contribute to disease progression as both MPB-specific antibodies and T cells were observed in infected mice (43). In addition to experimental models of JEV infection, clinical myasthenia gravis development has been described in patients previously exposed to WNV. Together the data show that there are a number of viruses that may increase, if not directly trigger autoimmunity in humans.
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General pathogenesis of viral infection of the brain
Although plastic and physiologically well supported, the neuron, the central player in the organization of the CNS, is not readily replenished after development early in life (45). Thus, it is not surprising that infection of CNS, especially the brain, represents a potentially life-threatening event. The outcome of CNS infection is dependent on the interaction of the immune system, the nervous system, and the invading pathogen. A battle driven by the primal evolutionary need for survival of both virus and host, ultimately determines the fate of the challenged host. In many cases, this interaction has been optimized over time by coevolution of virus and host, resulting in the survival of both at the population level. However, in individual cases, the outcome may be dire, with, at best survival with severe neurological sequelae, and at worst, significant neurochemical disturbance leading to coma and death (46, 47). Historically, the CNS has been described as an immune privileged organ; however, it is now well known that the brain is more than capable of eliciting an internal immune response, as well as calling upon peripheral immune elements as needed.
The development of autoimmunity as result of CNS infection requires a significant number of events to occur (Fig. 1). The mechanisms by which viruses gain access to the CNS, directly/indirectly cause cell damage and death, activate the immune response, and initiate autoreactive responses are discussed here.

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Fig. 1
Schematic outlining the potential pathway(s) through which infection may trigger autoimmunity.
See text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3971377/
 
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@Annikki
Like you apparently, everything, or almost everything, of value that I've discovered has come from falling down the rabbit hole, or as you put it, the long and winding road, that starts with one thing, has a link to another, mentions something that seems worth following up on with research, whcih leads to aother link, and so on and so on and so on .....

I'm a little brain challenged today, so I'm going to read the full article more closely when I'm better focused and cog'ed, but on a cursory speed-thru, it looks really, really interesting, and thank you for posting it !!!
 

lenora

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Whoa, that is a lot of research to take in. Good for you! I wanted to say that I have 3 close friends who not only have MS but cancer in addition to it. All were hard working, hard driving women and I was often amazed at the similarities they shared. I can remember being tested for these illnesses and was told then that the likelihood of getting one after the other was greater. That was over 34 or so years ago!

Today, one of the women and her hubby pay $80,000/yr. (yes, you read that right), for her medication to keep her MS at bay. Unfortunately, it's well known that the same drug causes cancer in some women. She happens to be one of them. Still, she finds the MS far more limiting, the cancer easier to treat and she has made her decision. These things don't just affect unknown subjects, but real people in real life. After a certain time, you learn to accept and truly live one day at a time. What's the point of going to 8 doctors looking for the one who will tell you what you want to hear (or at least think so)....that yes, you're at great risk for lupus or another type of illness? If it happens, it happens, but we do, with the passage of time, learn to accept what we have and just move on from there. I've seen it happen not just to me, but to others who also have some pretty big problems. There is so much to be learned from these illnesses, so many people to help. I believe my ME began after severe stress b/c of other neurological diseases (that all ended with the word "death"....but I'm still here, had surgery to stop the progression, etc.) Thanks for putting that latest research on here....it must have taken you a very long time. Yours, Lenora.
 

Annikki

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@Annikki
Like you apparently, everything, or almost everything, of value that I've discovered has come from falling down the rabbit hole, or as you put it, the long and winding road, that starts with one thing, has a link to another, mentions something that seems worth following up on with research, whcih leads to aother link, and so on and so on and so on .....


I'm a little brain challenged today, so I'm going to read the full article more closely when I'm better focused and cog'ed, but on a cursory speed-thru, it looks really, really interesting, and thank you for posting it !!!
Feel better, I think we are all worn out right now. I know stress never helps me. Take care of yourself, especially now. I just get through what articles I can and then rest.
 

Annikki

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Whoa, that is a lot of research to take in. Good for you! I wanted to say that I have 3 close friends who not only have MS but cancer in addition to it. All were hard working, hard driving women and I was often amazed at the similarities they shared. I can remember being tested for these illnesses and was told then that the likelihood of getting one after the other was greater. That was over 34 or so years ago!
Thanks for sharing that. I knew someone with MS. To my horror, I learned recently that people who treat their MS (or other autoimmune conditions) with immunosuppressants are being advised to be careful not to get exposed to Covid-19. I think the warning implied these patients could protect themselves from Covid-19 by stopping their immunosuppressant use. Which is to say, they treat these illnesses like they're trivial as they always did. Most people with MS direly need treatment, stopping treatment isn't an option.

Speaking of bad news, Lupus patients are unable to get the one medication that helps Lupus. The problem is pharmacies are running out of the medication because many people believe falsely this drug treats Covid-19. No studies show it has any effect on Covid-19. Trump said it does, but he's full of it.

Now paranoid healthy people are hoarding the drug and Lupus patients can't get it. Even the local news here mentioned it. There are no studies which prove this drug, hydroxychloroquine, does anything to treat Covid-19. As usual, those of us in the autoimmune community are being trampled on.

The panic buying of this Lupus drug ironically reflects how Covid-19 may have come into being. Covid-19 originated in a bat species whose habitat is 800 miles away from Wuhan. Researchers speculate that it could have made another "jump" into another species before infecting humans, which would help explain how it wound up in a Wuhan wet market.

They say it the virus could have jumped from a bat to a pangolin and then to humans.

I had no idea what a pangolin was, so I watched a documentary about them on Youtube. Pangolins are mammals with scaly plates on their backs:
1585720079512.png

It was a depressing documentary. Pangolins are becoming an endangered species because the Chinese believe falsely that their scales are medicinal and cure all sorts of ailments. That's highly unlikely because those scales are just made of keratin, like human fingernails.

Fingernails don't cure anything. Still, there is a huge black market for pangolin scales to make this "medicine." They are making Asian pangolin species go instinct to make this product. Now the black market traders are going to Africa to collect pangolins, endangering also African pangolins. There's huge money in the endeavor so African nations are struggling futily to curb this illegal animal trade.

Pangolins are also a culinary delicacy. Not only has the problem put pangolin species at risk, we also have a lethal virus which may have found a temporary home in the creatures before infecting us.

what if NHS was evil enough to claim cognitive behavioral therapy cured Covid-19? Personally, I have more faith in pangolin scales curing ME that CBT.
 
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lenora

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Yes, I've seen (or had) many drugs stripped away from me over the years b/c it had some other use. Now I don't trust any drug that I'm given. I know it may be stopped at any time, dislike the feeling, but all I can do is complain to the right department (which isn't even acknowledged) and well, we're stuck. That's a terrible shame about people with lupus, not a great disease itself. I thought I read where the govt. is going to do something to help them get the drugs ASAP. Of course we hear so many things we don't know what to believe. Personally, I don't believe anything and, like I said, I consider any drug or treatment as something that could be taken away.

No, I'd never heard of a pangolin, either. The photo almost looks like a huge pine cone, the scales are so precisely affixed. I wish people would stop eating delicacies that are in effect, wildlife. Exactly how much meat can one get off a bat for heaven's sake? It's true that we have to respect other cultures, but when the world's safety is in effect, isn't it time to think another way? I don't know...I have mixed feelings about that. Those folks may consider a plum pudding rather disgusting...I know I do and so does everyone in our family. My poor mother used to take 2 days, grind her own suet and make those puddings....and every single one of us hated them! Sorry, memory breakthrough there. Have you ever had a British christmas or wedding cake? Those things are like fruitcakes and let me tell you, they last forever. Yuck!

Most flus and viruses jump from the animal to the human population. This is something that we have to live with...but why has there been so much more of it in the past few years. It's also true that we're overdue for a mass pandemic, so what's it doing? Just holding its breath waiting for next December? I hope our President is right when he thinks the end of April will be the end of this virus. I don't think so...especially when you look at other countries and how it's lingering. Yours, Lenora
 
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I hope our President is right when he thinks the end of April will be the end of this virus. I don't think so...especially when you look at other countries and how it's lingering. Yours, Lenora
Personally, I have more faith in pangolin scales curing ME that CBT.
My guess is that we're looking at sometime in early June, if we're really, really lucky and follow all the rules.....
It's also true that we're overdue for a mass pandemic, so what's it doing? Just holding its breath waiting for next December?
I'm not sure I'm following you ...... we're no longer overdue for a major pandemic, we're right in the middle of the first half of one. So the good news is that we dont have to wait til December. The bad news is that ..... it's already here
 
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NUMBER OF COVID CASES IN THE US, AS OF 1159 PM: 216,000
NUMBER OF DEATHS: 5, 100
GLOBAL DEATHS: 42,898
GUN SALES IN CALIF, AZ, TX: OFF THE CHARTS FOR LAST WEEK OR 10 DAYS …


By the time I posted this, those numbers were already obsolete, this thing is moving so fast.
 
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Bi @bertiedog
It looks like we're the only two people on-line here right now ..... which feels, uh, spooky :nervous::nervous::nervous:. I really didn't expect COVID to hit this site so severely, but the 'Members on-line' box on the home page is virtually empty ....like a ghost town :wide-eyed::wide-eyed::jaw-drop::aghhh::aghhh: ....

Shudder ....
 

lenora

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Still, I'll be quite interested in what happens to this virus by next fall. Actually, it worries me sick....that means that even people who aren't at risk are going to be, and people still don't take it seriously. Believe it or not, I'm not crazed with worry about it, but having it attack someone else in my family can upset me. Also, it occurred to me that everyone's antennae should have gone up when China said it was building hospitals....immediately and fast! Now exactly why would we think they'd be doing that unless they were absolutely 100% necessary...and for what reason? Yours, Lenora P.S. Well, did you give up & go to bed, or fall asleep over your keyboard? Not sleeping's the pits, although I'm so used to it that I actually look better when I don't!
 
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Annikki

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Bi @bertiedog
It looks like we're the only two people on-line here right now ..... which feels, uh, spooky :nervous::nervous::nervous:. I really didn't expect COVID to hit this site so severely, but the 'Members on-line' box on the home page is virtually empty ....like a ghost town :wide-eyed::wide-eyed::jaw-drop::aghhh::aghhh: ....


Shudder ....
I imagine people here are feeling worse from all the stress. Stress has been triggering fatigue, and IC symptoms in me the past week or so . I take breaks and try to limit news consumption when I feel bad. Self care and pacing yourself is so important.

I pay if I get too anxious about all this and overdose on news. Comedy is a good thing, I give myself a daily dose of it to keep my spirits up and my body healthy. I've watching news bloopers on youtube, reading The Onion, and watching both The Golden Girls and Are You Being Served. It helps.
 

bertiedog

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Yes felt very shit yesterday till late afternoon after a good sleep and a nice mug of tea.

Keep having a good day followed by a sh.. day. Wonder if its to do with my taking some NAC daily and Glutathione with alpha lipoic acid. Its an awful lot of sulphur and I think I have got a SNP regarding the processing of sulphur so wondering if it could be due to this. So today haven't taken any but added in some carnitine to help with my bad muscle issues this week which have accompanied massive fatigue.

Pam
 

bertiedog

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Comedy is a good thing,
You are so right and last night I watched the free You Tube video of the National Theatre production with James Cordon and some other well known actors. It was hilarious, quite stupid really but just what I needed. It lasted nearly 3 hours because in the middle of it I had a large food delivery from Tesco! Had to give up with that though because it made me very dizzy but so good to settle down and watch the rest of the play. I think the National Theatre is going to be putting on several plays like this to cheer everybody up and well worth looking out for.

Pam
 

Booble

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My grandmother had MS that started in what must have been the early 1930s. They didn't have much medication options back then. Her legs were numb and she could not walk. She was a proud woman and didn't want anyone to know she was in a wheel chair. She was determined to overcome it. She was able to get some kind of experimental treatment in Boston. They attached electrodes to her legs. I kid you not. She went regularly for treatment. She told a story of how she was at an appointment and she was able to stand and walk. She looked out the window of the doctor's office and there was a phone booth on the street corner. She told the doctor she wanted to go down to the phone and call her husband, my grandfather. Supposedly the doctor let her do this or went down with her and she called him and told him she had walked! When I was born 30 years later, she was active. She could walk and play golf. She said her legs felt like pins and needles at all times but she could use them. I don't know why that electrode treatment never got further study. My grandmother went on to live until age 103!
 

bertiedog

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NAC and ALA both boost glutathione. Glutathione is a very powerful detoxifier. You might have been experiencing symptoms of detoxification.
It didn't feel like that I just had exhaustion and very bad muscle pain, especially sciatica. Anyway haven't had any today and more energy and also had a good treatment and the massage therapist said my body really needed it as so many of the muscles were in huge knots. My legs are aching now from the treatment and I am resting lots, just had one short walk.

BTW I am waiting for the results of my Genova G I Effects test done 2 weeks ago. They have reformatted the report which should make it much easier to understand and to action.

Pam
 
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Its an awful lot of sulphur and I think I have got a SNP regarding the processing of sulphur so wondering if it could be due to this
I've never had any genetic testing, so hae no idea where I have SNPs or what other genetic challenges may exist, but I do know that when the ME started getting really bad, my ability to tolerate ANY sulfur, from garlic to glutathione and on, was reduced to zip. I had to cut out everything from B-Complex to selenomethionine, and still haven't added them all back in.

Maybe you're dealing with something like this, and it overwhelms your system from time to time. What you describe doesn't sound like a herx.
 

bertiedog

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Maybe you're dealing with something like this, and it overwhelms your system from time to time. What you describe doesn't sound like a herx.
Yes I think so cos only started the combination this Tuesday which was very good and then the following days have been the exact opposite with my muscles severely affected. Maybe it builds up and affects the electrolytes in a negative way. it does feel like when I have had low sodium previously (I am a salt waster and need occasional fludrocortisone when it gets warm due to a Congenital Adrenal Hyperplasia). Hopefully I will find out fairly quickly. At least my energy in general was better today even though my muscles were rubbish.

Pam