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Autoimmune Model Proposes Chronic Fatigue Syndrome (ME/CFS) Begins in the Gut

Jonas Blomberg’s paper “Infection Elicited Autoimmunity and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: An Explanatory Model” was published in “Frontiers in Immunology”, an apt journal for a paper featuring an “explanatory model” of chronic fatigue syndrome (ME/CFS). Autoimmunity is definitely a new “frontier”; as Blomberg points out, it’s possibility not a reality yet, but like other frontiers it evokes new vistas – new opportunities and some new challenges.

European ME/CFS reseachers

Jonas Blomberg headed up a European group which produced an autoimmune model of ME/CFS

Blomberg has recently been immersed in a study designed to validate (or not) Dr. Scheibenbogen’s autoantibody findings in chronic fatigue syndrome (ME/CFS). The lead role the Europeans are taking on in exploring autoimmunity in ME/CFS is evident: Blomberg and Gottfries are Swedish, Scheibenbogen is German, and Mella and Fluge – of the Rituximab trial – are Norwegian.

(Carl-Gerhard Gottfries’ story is so unusual that it warrants a short retelling. Gottfries, a Swedish psychiatrist, recovered from ME/CFS using, of all things, a staphylococcus vaccine.  Gottfries opened an ME/CFS clinic, published his findings and treated patients with the vaccine for several decades until it was withdrawn from the market. Find out more about Gottfries’ fascinating story here.)

There are so many ideas floating around concerning the cause ME/CFS that one is tempted to throw up one’s hands. Is cellular energy production in the dumps? Are the autonomic nervous system problems keeping people wired and exhausted at the same time? Is an autoimmune process pummeling the body? Are hidden infections tormenting ME/CFS patients with never ending flu-like symptoms? Or as Cortene suggests, are problems in the HPA axis wreaking havoc on the rest of the body.

We could go on and on (ion channel dysfunction (Griffiths University); whacked out basal ganglia (Miller/Japanese); microbiome dysregulation (Lipkin & Hornig, Unutmaz, Lombardi), “traveling genes”  (RCCX – Meglathery); atypical sepsis (Bell); neuroinflammation (Younger), (mast cell activation in the hypothalamus – Theoharides. ).

The fact that so many people have proposed so many interesting hypotheses is encouraging, but the downside to such a munificence of possibilities is a kind of inertia. Until the ME/CFS field settles on one or a few models of disease, this small field is inevitably going to progress more slowly that we would wish.

In fact, the two Davises at Stanford (Ron and Mark – not related) have questioned whether the field should devote time and money to chasing down hypotheses at all.  Better, they have suggested, to gather more and more data and see what emerges. That said, something has been emerging – an explanatory model in which autoimmunity plays a key role.

An Autoimmune Model of Chronic Fatigue Syndrome 

Basically, the authors propose that it all starts with your genes and your leaky gut. Not the leaky gut you necessarily associate with ME/CFS but the leaky gut you had before, perhaps long before you came down with ME/CFS.

A Genetic Predisposition

Autoimmune diseases typically feature a strong genetic component and run in families. It’s not that rheumatoid arthritis shows up in family member after family member. It’s that a range of other autoimmune diseases do. Blomberg picks out three intriguing autoimmune diseases – thyroid disease, Sjogren’s Syndrome (SS) and lupus – which studies suggest run in ME/CFS families.

genetic predisposition to chronic fatigue syndrome

Evidence of a genetic predisposition is one of several factors suggesting ME/CFS could be an autoimmune disease.

ME/CFS itself is also associated with diseases Blomberg considers to be emerging autoimmune diseases including hypothyroidism, fibromyalgia and POTS, each of which has been associated with increased levels of autoantibodies. Blomberg clearly believes an autoimmune cluster containing many of the diseases associated with ME/CFS is emerging before our eyes.

High rates of two of those diseases (thyroid, SS) also recently showed up in a postural orthostatic tachycardia syndrome (POTS) study (along with antiphospholipid syndrome).

Blomberg then ploughed through genetic, immune and epigenetic data in ME/CFS, highlighting some findings suggesting autoimmunity might be present.

For instance, autoimmune diseases often occur when HLA molecules improperly display self-antigens to cytotoxic or helper T-cells.  T-cells, it turns out, are often huge drivers of autoimmunity, and when they produce autoimmunity, HLA issues are often prominent. Guess what: an HLA issue has been found in ME/CFS. (Ron Davis is studying HLA genes in ME/CFS.) Another study found that increased prevalence of genetic alteration (a SNP) in a T-cell receptor gene known to play a role in autoimmunity suggested that a T-cell based autoimmune process could be present.

Infections, EBV, Autoimmunity and ME/CFS

Infections often trigger autoimmunity. In fact, the infectious trigger that has sparked ME/CFS for many is one big clue that an autoimmune process may be present. With regard to autoimmunity, the more severe the infection, the better, and several studies show that deficiencies in IgG subclasses may have left people with ME/CFS more vulnerable to a severe infection.

Several gene expression studies showing alterations in T-cell and innate immune response genes suggested that ME/CFS patients’ immune systems could be fighting off an infection.

The Autoimmune Virus

EBV is especially interesting as a facilitator of autoreactivity. Blomberg et. al.

If you’re unlucky enough to first meet up with the Epstein-Barr virus (a common trigger of ME/CFS) during adolescence, it’s likely to trigger your immune system to produce a massive number of antibodies, including autoantibodies.  EBV also produces antigens with highly repetitive structures (e.g., Gly–Ala–Gly–Ala repeats in EBNA1) which tend to confuse the immune system and trigger the production of autoantibodies.

It’s no wonder, then, that infectious mononucleosis (glandular fever) significantly increases the risk of later coming down with at least two autoimmune diseases: multiple sclerosis (MS) and lupus. That’s an interesting enough intersection for Blomberg to assert that the immune responses that ME/CFS, MS and lupus have to EBV should be compared.

The Key Organ – the Gut

Anyone have gut symptoms (cramping, bloating, loose bowels, constipation) prior to ME/CFS?  I did – they weren’t major, but if one area of my body was a little bit off back then, it was my gut.

Blomberg believes your leaky gut may be the key to your illness. Not the leaky gut you necessarily have now, but the leaky gut you had before you got ME/CFS.

gut chronic fatigue syndrome

Blomberg believes a genetic predisposition and a leaky gut set the stage for ME/CFS

The gut is such a potential hotspot for autoimmunity because it contains so much foreign material. In fact the gut has been posited as something of a training ground for the immune system- it provides the immune system with the foreign materials it needs to learn how to distinguish self from non-self.

Gut disturbances are fairly common in autoimmune diseases, and the idea that alterations in gut flora are touching off autoimmune processes is being examined in a host of autoimmune diseases (multiple sclerosis, type 1 diabetes, RA, ankylosing spondylitis). The common occurrence of irritable bowel syndrome (IBS) – and the leaky gut that often comes with it – in ME/CFS presents a potential pathway for autoimmunity.

Blomberg proposes that the breach of your gut barrier created a state of low level chronic inflammation prior to you getting ME/CFS. The gut barrier is important because it’s a place in the body where tolerance (the ability to distinguish between self and non-self antigens) is more difficult to maintain. Given the extraordinary diversity and sheer number of gut bacteria, it’s easy to see how the immune system could be overwhelmed and lose it’s way.

Blomberg believes that slow leakage from the gut created a population of auto-reactive B-cells that remained mostly inactive or quiescent (in a state of anergy), almost like undercover agents infiltrating a city, waiting for the signal to pounce.  At some point a “decisive” immune event flipped them into action, and an autoimmune disease – ME/CFS – was born.

He bases his hypothesis of pathogenic autoantibody creation in ME/CFS on a process that appears to be occurring in lupus. The first step occurs when a genetically predisposed person meets up with bad gut bacteria. First, abnormal but not pathogenic B-cells, which have a “weak autospecificity”, appear. These weakly targeted B-cells are not strongly directed against a specific antigen or part of the cell and don’t appear to be particularly dangerous at first, but the body should still eliminate them. Blomberg proposes that it doesn’t.

Over time exposure to the bad gut bacteria causes the specificity of the B-cells to change – making them more targeted and dangerous. At some point an infection turns them on and they start producing clones of themselves which begin attacking the body. ME/CFS is born.

One possible sign that tolerance – the ability of the body to remove autoantibody-producing cells  – has been breached in ME/CFS are the TFG-B (and IL-10) findings. IL-10 and TGF-B, in particular, are the rare cytokines that are more or less consistently found dysregulated in ME/CFS cytokine studies. It turns out that T-helper cells use both these cytokines to regulate tolerance and anergy at the gut mucosa – the very place Blomberg believes the process of autoimmunity in ME/CFS begins.

Ian Lipkin’s recent study found a significant difference in gut composition between ME/CFS patients with IBS and those without. Some of those differences appeared to affect energy production.

Autoantibodies

It turns out that autoantibodies by themselves are not necessarily indicative of autoimmunity. Some “natural autoantibodies – (mostly IgM antibodies) are simply designed to rid the body of dead/apoptotic, damaged and infected cells and rarely cause autoimmune diseases. Other more dangerous autoantibodies need to be turned on by “cell danger” signals before they do harm. (This is why autoantibodies can often be found in healthy people.)

Autoantibodies have, of course, been found in ME/CFS and related diseases like POTS. At the Montreal conference Blomberg reported that his team was validating Scheibenbogen’s autoantibody findings in ME/CFS. They are one clue that autoimmunity is happening in ME/CFS but they provide, Blomberg reported, only circumstantial evidence of autoimmunity.

It’s the “erroneously activated” B-cells, he reported, that are “the root of the evil”, and it’s these cells that need more focus. Blomberg asserts that an in-depth sequencing of these deranged B-cells is needed. By sequencing the variable immunoglobulin chains found in them it should be possible to trace back to how they turned bad.

Other Possible Evidence of Autoimmunity

As noted earlier, Carl-Gerhard Gottfries successfully used a staphylococcal vaccine for years to treat himself and others with chronic fatigue syndrome (ME/CFS). That approach may have worked because the immune stimulation it provoked may have been able to induce tolerance; i.e. induce the body to remove the bad B-cells.

Since Rituximab knocks down B-cells, thereby removing misbehaving ones, it would seem to fit into Blomberg’s hypothesis. Unfortunately, the Rituximab trial failed, and if anecdotal reports are correct, more completely than we could have imagined.

Another possible indication that autoimmunity is present in ME/CFS are studies suggesting the incidence of Hodgkin’s lymphoma is increased in ME/CFS as it is in other autoimmune diseases.

In the end, though, Blomberg reports that the evidence that autoimmunity is at work in ME/CFS is circumstantial. It relies on the fact that people with ME/CFS often have other autoimmune diseases such as thyroiditis or diseases suspected of involving autoimmunity such as POTS, FM and IBS, that autoantibodies are present, and that immunostimulation (IVIG, staphyloccocus vaccine) may work.

Most of the work, though, needed to fulfill the Witebsky–Rose criteria for autoimmunity, remains to be done.

Primary Biliary Cirrhosis – An Autoimmune Roadmap for Chronic Fatigue Syndrome (ME/CFS)?

At the start of their paper, Blomberg et. al. proposed that their model could explain many of the facets of ME/CFS that have emerged – the most prominent of which are the energy production problems.

An autoimmune disease exists in which an attack on the energy producing processes in the body produces symptoms and findings similar to those found in ME/CFS.  In primary biliary cirrhosis  (PBC) antibodies attack a small fatty acid molecule (lipoic acid) that’s part of the energy producing machinery on the surface of the mitochondria.

pyruvate dehydrogenase

Pyruvate Dehydrogenase -By Jonathanmott09 – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18520937

The antibodies in PBC attack the pyruvate dehydrogenase (PDH) enzyme complex which regulates the transition from glycolysis (anaerobic energy metabolism) to the tricarboxylic acid cycle (aerobic energy metabolism). The same issue -the transition from glycolysis to aerobic metabolism – has shown up repeatedly in ME/CFS studies.

Even though PBC is considered a liver disease, it produces enormous amounts of fatigue as well as cognitive problems, orthostatic intolerance and sympathetic nervous system hyperactivity. In fact, Julia Newton, who studied PBC before she studied ME/CFS and started a Rituximab trial in PBC two years ago, stated back in 2013 that,

“…at this stage the muscle and cardiac abnormalities that we have seen in patients with ME/CFS are exactly the same as those that we have seen in patients with PBC.”

Another fascinating aspect of PBC is that the autoantibodies are attacking a molecule, lipoic acid, which is added to the PDH enzyme using a rare process called lipoylation. Because some gut bacteria (Novosphingobium) also use lipoylation, it’s possible that bacterial leakage initiated the autoimmune process causing PBC.

Blomberg suggested that pathogenic, as yet unidentified immunoglobulins directed against mitochondrial proteins could be the source of ME/CFS and exhorted researchers to compare the post-exertional malaise in ME/CFS to other diseases such as fibromyalgia, PBC, etc.

Autoimmunity or Oxidative Stress? 

Finally Blomberg et. al. suggested that oxidative stress could be producing the same energy depleting issues as autoimmunity. That’s an intriguing idea given the comforting consistency oxidative stress study results have had in ME/CFS.  The authors noted that it was recently shown that the oxidation of a critical part of the pyruvate kinase enzyme can effectively block the transition of glycolysis to aerobic metabolism.

Dr. Shungu believes the lactate accumulations and glutathione reductions his studies have validated in the ventricles of the brains of ME/CFS patients are associated with oxidative stress.

Conclusion

Blomberg’s autoimmune model proposes that the seeds for ME/CFS were lain possibly long before the disease appeared and only “sprouted” once a decisive immune event occurred. He believes that a genetic predisposition plus a leaky gut laid the groundwork over time for what eventually became an autoimmune disease.

Autoantibodies provide circumstantial evidence of autoimmunity in ME/CFS but are not nearly enough to validate it.  Blomberg asserted that an intensive study of the abnormal B-cells in ME/CFS could both help to validate that diagnosis and identify the precipitating event which triggered this illness.

If ME/CFS is an autoimmune disease targeting the mitochondria it may have a close cousin called primary biliary cirrhosis (PBC) which produces similar symptoms including enormous fatigue. In PBC autoantibodies disrupt the transition from anaerobic to aerobic energy production – the same process, interestingly enough, that appears to be affected in ME/CFS.

While autoimmune processes could produce the energy problems in ME/CFS, oxidative stress – which studies have found to be consistently high in this disease – could produce the same result.

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35 Comments

  • Terrie Williams

    September 3, 2018 at 11:16 pm - Reply

    This is interesting. I had a bout dysentery in my early 20s that took years to go completely away. Years later, maybe 10, I developed the beginning symptoms of ME/CFS.

    • Cort Johnson

      September 4, 2018 at 5:28 pm - Reply

      I had Giardia about 5 years before I got ill. Plus my bowels tended to be messy. I actually wondered if something was wrong with me despite the fact that generally I was as healthy as a horse.

      • Terrie

        September 4, 2018 at 6:34 pm - Reply

        Interesting. I always thought that there could be a connection because i also have ibs and celiac disease.

  • konijn

    September 3, 2018 at 11:23 pm - Reply

    I am a severelly ill me/cfs patient. yes, possible what they say, but what are they doing about it. There are so many hypothesis, that I am to ill to follow them all.
    help i what I need, urgent help.

    • Cort Johnson

      September 4, 2018 at 5:31 pm - Reply

      All they can do is come up with ideas and follow their leads. Blomberg suggests doing in depth study of B-cells. If he’s right and they find something then we have possibilities. I don’t know how that fits, though, with the failed Rituximab trial since it is a B-cell blocker. I don’t believe it effects all B-cells, though.

      Another idea is to look for autoantibodies that effect the mitochondria and energy production with the idea that ME/CFS is a close cousin to PBC.

    • Anne

      September 9, 2018 at 6:58 am - Reply

      If you’re bedbound, try shaking your body now and again for approx 5 -10 mins, concentrating this movement in your abdominal area. It’ll aid gut waste transit and in turn will help keep harmful gut bacteria in check. I believe it is the imbalance of gut biome that’s fuelling/triggering the ME/CFS symptoms and keeping a less blocked (hence heathier) gut system is half the battle. PS: it’s harder for women than men to maintain a healthy gut as we have longer transverse sections which in turn are more prone to prolapse/waste blockage. Sorry for grossness but I’m sure my advice is sound (besides, shaking your body won’t do any harm). Hope this helps but don’t expect a quick fix (with this disease that’d be a very tall order indeed, wouldn’t it?!).

      • Francis Martin

        September 10, 2018 at 7:37 am - Reply

        Hi Anne. Maureen Hanson’s doing a faecal transplant study (i.e. to try to reset the microbiome), along with a Norwegian group [Invest in ME Conference June 2018]. Don’t know if Maureen is presenting at the OMF Community Symposium (in a few weeks) but we might hear more then. It’s jarring to hear how people with ME/CFS are. All the best.

  • Aidan

    September 4, 2018 at 12:58 am - Reply

    Autoimmune Alpha-Gal IGE Allergy is likely something hitting Genetic people with EDS born traits & it can be sudden onset or a gradual onset & another thing that does come up are 2 types of Headaches the Silent Migraine & Narcolepsy involvement but Alpa Gal once it is

    removed from diets & environmental surroundings people tend to get better & the worse off patients are likely the ones on these numerous Alpha Gal ingredient…I react to everything even Gum Tylenol Ibuprofen Vitamins smells I never reacted like this before becoming Sick & the

    Floxie patients all have something in common so do the Gulf War Vets they all took Alpha Gal ingredient products then became worse of during & after treatments, there could also be 2 types here & I have seen countless now get violently ill hours after meals even pills can trigger

    Alpha-Gal & also malabsorption issues like fruits & IBS so does Sugar-containing Alpha Gal factory cross-contamination from bone char products…I know one Man now he is 3 months out on a very strict Vegan protocol & he swears he will not ever eat Meats ever again he is

    symptom-free & well, countless say they stopped Gluten, it also contains Milk Sugar…Is it in everyone maybe not but it is there in numerous now

  • Issie

    September 4, 2018 at 5:35 am - Reply

    Since so much of the immune system is in the gut, makes sense that we have issues there. Whether or not it’s a microbiome imbalance, an allergy etc. Makes sense that it plays a part. I’ve got 2 microbiolome test that we are playing around with results on Ken Lassesens site. Both test came back very different despite them being from same fecal matter at same time. We are trying to sort differences. But it’s really interesting how off my ecology is. I know this is a new exploration and we really don’t know proper ratios – but we do know what the different organisms do and what results happen with too high and too low. Also the test can tell about vitamins, enzymes etc. Based on your results it can tell you what medicines could potentially throw things off more. (Interesting that nearly everything I take could.) Foods I had discovered I reacted adversely too, are also on target there. I’m really impressed with Kens work and what he is trying to do. Very enlightening.

    I’ve thought all along that all these “illnesses” may be manifestations of same underlying issues. I’m of the opinion it’s our immune dysfunction and inflammation. We just have to figure out “WHY” and “What” we need to do about it. If we can’t “fix” it maybe we can find a good “purple bandaid”.

    Issie

    • Cort Johnson

      September 4, 2018 at 5:34 pm - Reply

      Ha…were the results from the same lab?

      Someone just gave me a link to a paper on the gut and IBS – a central nervous system disorder. It appears that the gut has the power to effect just about everything.

    • Christine Pickett

      September 5, 2018 at 1:10 am - Reply

      Issue
      Tell me more about Ken Lassesens. I Google but didn’t find him.
      I’m interested in the testing you mentioned. Was it a basic stool analysis or something more specialized ?
      Thanks for the information.

      • Issie

        September 5, 2018 at 4:02 pm - Reply

        It is a fecal sample that you stir into a vial and mail off to a lab that does gut microbiome testing. The lab that Ken has most samples from is Ubiome. (But others will also work.) They will submit it to insurance for you.

        Kens program is what you load that data into to get suggestions for imbalances. It’s still a work in progress. He is still tweaking it. But it is comprehensive and amazing. He has put a lot of time and work into it.

        Issie

        • Christine Pickett

          September 5, 2018 at 4:39 pm - Reply

          Issue
          Thank you for your prompt reply and all that information. Does your Dr. Support you in doing this ? Any thoughts on how to present this to a Dr who may not buy in initially ? Am dealing with him because he took over the practice when my DO retired. Ugh. So hard to deal with newbies when there’s a huge history and the label I hear most is “complicated case”. Am searching for the next Dr to support me on this life W/CFIDS + + + more diagnosis than I care to list. Or think about most days. Didn’t mean to ramble. Thanks for listening.

          • Issie

            September 5, 2018 at 6:01 pm -

            For it to be billed to insurance, your doc has to order test. It can be done without going to insurance and be paid by you with no doctors orders. Yes, my doc is on board. She approves of the things I look into. Very fortunate to have her – though she doesn’t take insurance. But will look at alternative solutions first.

            Issie

  • Francis Martin

    September 4, 2018 at 7:59 am - Reply

    Need to look more closely at this.

    Cort, if Fluge and Mella used rituximab to wiped out CD20+ B cells then are there surviving CD20+ B cells/other B cells? If so then are these surviving B cells producing the auto-antibodies?

    • Cort Johnson

      September 4, 2018 at 5:37 pm - Reply

      If I remember correctly Rituximab doesn’t wipe out all B-cells but I don’t know which ones are left. How ironic it would be if we tried a drug that just missed the right B-cells. First, though, Blomberg et. al. need to validate which, if any, B-cells are the problems.

      • Francis Martin

        September 4, 2018 at 6:54 pm - Reply

        Excellent article Cort. Thank you for your reply.
        I’m guessing here:
        the compound which is responsible for altered cellular metabolism, in ME/CFS, is in the blood plasma. Fluge and Mella found altered cellular energy metabolism (which tracked with the plasma i.e. not cells) and Ron Davis worked out the approximate weight of the component responsible for this. Possibly if you could identify that compound/s (autoimmune antibody?) then it would help to understand the underlying disease process.

  • konijn

    September 4, 2018 at 11:29 am - Reply

    Hi Cort,

    do you maybe know a really reliable laboratory for microbioom reseach/analysis for personal use?
    I live in Belgium, tryd to find one on the internet but do not come verry far with it, found nothing reliable.
    thanks!

    • Francis Martin

      September 4, 2018 at 1:15 pm - Reply

      Hi hope you mind me replying. Maureen Hanson (Cornell) is working with a Norwegian group on faecal transplants. I was hoping the study would be complete by now; not sure why there’s been a delay. You could contact Hanson/Norwegian group and ask. Big problem is that even if you have shift in microbiome (i.e. to a more pathogenic state) how can you/can you reverse same? Faecal transplant study might just come up with something.

      • konijn

        September 4, 2018 at 3:39 pm - Reply

        thank you Francis! 🙂 I can hopefully indead contact Maureen Hanson. Or the Norwegian group.

  • konij n

    September 4, 2018 at 11:30 am - Reply

    Hi Cort,

    do you maybe know a really reliable laboratory for microbioom reseach/analysis for personal use?
    I live in Belgium, tryd to find one on the internet but do not come verry far with it, found nothing reliable.
    thanks!

  • Cindy Downey

    September 4, 2018 at 7:10 pm - Reply

    Dr. Bruce Carruthers, lead author of both the CCC, and the ICC said IBS often predates ME by many years. The gut theories seem to hold a lot of promise.

    • Cort Johnson

      September 4, 2018 at 9:49 pm - Reply

      Interesting. Thanks for passing that on.

      I think something “underground” must have been going on in many of us. How else to explain such tremendous declines in health in such short times? It was if the system was primed to collapse. I think the researchers are uncovering the biological changes that occur PRIOR to CRPS. I wish more models would focus on this aspect of ME/CFS.

  • dejurgen

    September 6, 2018 at 9:41 pm - Reply

    “The authors noted that it was recently shown that the oxidation of a critical part of the pyruvate kinase enzyme can effectively block the transition of glycolysis to aerobic metabolism.”

    I’ve been looking into the relation massive oxidative stress, glutathione, NADPH and ATP production recently. The idea is, when oxidative stress is massive, so is glutathione consumption. Glutathione needs to be recycled and massive consumption of glutathione requires massive amounts of NADPH. The “better” way to produce massive amounts of NADPH (on a non-keto diet) is to turn down both glycolysis (both anaerobic and aerobic metabolism) and the NADP producing parts of the Krebbs cycle (aerobic metabolism) in favor of the pentose phosphor pathway and the NADPH producing parts of the Krebbs cycle.

    An enzyme essential for the transition from glycolysis to the Krebbs cycle that is blocked by oxidants could prove useful in helping to achieve this. It kinda looks like it (a key enzyme that falters due to oxidation) may not be a fault but an evolutionary advantage in human evolution.

    Also: “Epstein-Barr virus induces an oxidative stress during the early stages of infection in B lymphocytes, epithelial, and lymphoblastoid cell lines” (link not provided, many digits gets usually blocked by wordpress, easy to search for).

    I also made a potential link between my ME, food sensitivities and IBS and H2S producing gut bacteria (in topic #21 in https://www.healthrising.org/forums/threads/eating-papaya-with-protein-rich-meals-gave-me-a-significant-improvement-in-health.5980/page-2#post-34252). I’ll have to experiment further but it seems to fit my case quite well.

    Now there is “She had written a paper proposing that the excessive production of hydrogen sulfide gas had put ME/CFS patients into a kind of hibernation like state.” in https://phoenixrising.me/research-2/hydrogen-sulfide-a-breakthrough-in-mecfs/hydrogen-sulfide-and-chronic-fatigue-syndrome-the-originator-speaks

    From https://en.wikipedia.org/wiki/Hydrogen_sulfide : “Hydrogen sulfide is a broad-spectrum poison, meaning that it can poison several different systems in the body, although the nervous system is most affected. The toxicity of H2S is comparable with that of carbon monoxide.[26] It binds with iron in the mitochondrial cytochrome enzymes, thus preventing cellular respiration.”

    https://www.sciencedirect.com/science/article/pii/B9780128010280002531 : “The most intensively studied is the cardiovascular system, where H2S elicits identical effects to hypoxia in both pulmonary and systemic blood vessels from a wide range of vertebrates, and participates in cytoprotection from oxidative damage…”

    So it kinda “compounds” with hypoxia but it protects against oxidative damage at the same time. Could that explain why many (not all!) of us are overwhelmed by oxidative stress, are depleted in glutathione but somehow show no clear markers of permanent oxidative damage?

  • Dave

    September 9, 2018 at 7:58 pm - Reply

    If staphylococcal vaccine cured CFS/ME, then why haven’t more researchers zeroed in on that and continued to experiment and investigate it, or is that approach too simple? Many discoveries have happened by accident, which in no way diminishes their importance.

    • Aidan

      September 10, 2018 at 10:24 am - Reply

      He never Cured himself with this vaccine he was still symptomatic & was later blocked using it in patients…

      • Dave

        September 11, 2018 at 12:30 am - Reply

        Okay, but the above refers to some success with it. It may be due to the same effect that poison ivy has in distracting the immune system and reducing CFS/ME symptoms, while replacing them with something worse – I’ve experienced it myself. It’s just temporary.

    • Francis Martin

      September 11, 2018 at 7:15 am - Reply

      Check out Ron Davis’s presentation at the 2018 Invest in ME Conference. He presented data which related to a patient who had a bacterial infection; Ron pointed out that they improved and that this was due to the infection.
      Cort (here) has also highlighted this effect (in previous articles); it also turns up in Autism. The possible similar improvement in symptoms in Autism and ME/CFS i.e. during periods of infection may support Naviaux’s theory that Autism and ME/CFS are related diseases.

    • Francis Martin

      September 11, 2018 at 7:18 am - Reply

      Ron Davis presented data, at the 2018 Invest in ME Conference, which related to a patient who had a bacterial infection. Ron pointed out that they improved and that this was due to the infection.
      Cort (here) has also highlighted this effect (in previous articles); it also turns up in Autism. The possible similar improvement in symptoms in Autism and ME/CFS i.e. during periods of infection may support Naviaux’s theory that Autism and ME/CFS are related diseases.

  • deboruth

    September 15, 2018 at 9:09 pm - Reply

    Excellent, fascinatine piece Cort.I showed ANA on a rheumatologist’s testing perhaps 10 years ago.

  • Francis Martin

    September 15, 2018 at 9:48 pm - Reply

    Regarding the possible mitochondrial problems in ME/CFS; this study would appear to support that theory https://pubs.rsc.org/en/content/articlelanding/2018/an/c8an01437j#!divAbstract.

  • Francis Martin

    September 15, 2018 at 9:50 pm - Reply

    Regarding the possible involvement of mitochondria in ME/CFS; this study would appear to support that theory https://pubs.rsc.org/en/content/articlelanding/2018/an/c8an01437j#!divAbstract.

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