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Could “Junk DNA” Be Causing Chronic Fatigue Syndrome / Myalgic Encephalomyelitis?

Carmen Scheibenbogen

Dr. Scheibenbogen continues to successfully plough new ground

It seems like every time you turn around another part of the genome pops up. It’s amazing how far our knowledge of the human genome has progressed since the Human Genome Project was completed just 15 years ago. Thankfully the small band of researchers involved in chronic fatigue syndrome / myalgic encephalomyelitis (ME/CFS) seem to be keeping up with the latest findings.

Dr. Scheibenbogen seems intent on ploughing new ground. First she re-energized the search for autoantibodies in ME/CFS. Then she examined the effectiveness of a promising treatment called immunoadsorption. With her latest study she and her colleagues at Institute for Medical Immunology, Charité-Universitätsmedizin in Berlin became the first in this disease to examine a peculiar part of our genome called long non-coding RNA’s.

Hope for an ME/CFS Autoimmune Subset: A German Researcher Steps Forward

When most people think of RNA they’re probably thinking of the messenger RNA (mRNA) which carries the genetic code from the DNA in the nucleus of our cells to ribosomes. The ribosomes then translate the mRNA into proteins – which then do the work of our cells.

pre mRNA

pre-mRNA -(Wikipedia—httpsupload.wikimedia.orgwikipediacommonsthumbaa4Pre-mRNA-1ysv-tubes)

Not all RNA produces proteins, however. Formerly termed “junk DNA“, non-coding RNA’s – RNA’s which do not encode proteins –  make up a substantial part of our genome.  (They lack the “reading frames” necessary for the process of translation from RNA to protein to begin). Long non-coding RNA’s (lncRNA) are particularly long pieces of RNA (>200 nucleotides long) which do not encode proteins.

While their presence has been known for decades, it wasn’t until the 1990’s that the first hint of the role they play in regulating gene expression and epigenetics  appeared. Research since then has shown that lncRNA’s play an important role modulating the activity of transcription factors which turn the expression of our genes on and off.

Epigenetics –  heritable changes in gene expression that do not involve changes in the underlying DNA sequence – is all the rage now. The ability of infections and other stressors to turn genes on or off via epigenetics presents an intriguing explanation for how an infection could result in ME/CFS. Because lncRNA’s can regulate the epigenetic process, they could provide even more basic insights into how ME/CFS began.

LncRNA’s can also catalyze biological reactions and respond to cellular signals. Their extreme flexibility allows them to interact with proteins, DNA and RNA to affect many physiological processes. One review stated they, “can impact almost all physiological functions.” Another review called them, “a new and crucial layer of biological regulation”.

They’re certainly providing a fresh look at complex diseases. Search for long non-coding RNA’s in PubMed and you’ll get a long list of diseases they may be implicated in. A recent review of the role lncRNA’s may play in cancer called them, “new players in the old battle against cancer”. Some regulate mitochondrial synthesis and energy production.  Pathogens can induce the production of lncRNA’s in humans that then promote viral survival.

It’s become increasing apparent that they can play a role in fundamental developmental processes that can produce chronic disease states. One review called them “arguably the hottest area of RNA research” today.  Still much remains to be learned about the roles they play.

“Remarkable” Finding

The expression signature of very long non‑coding RNA in myalgic encephalomyelitis/chronic fatigue syndrome. Chin‑An Yang1,2,3,4 , Sandra Bauer5, Yu‑Chen Ho3, Franziska Sotzny5, Jan‑Gowth Chang1,3,4† and Carmen Scheibenbogen. Transl Med (2018) 16:231 https://doi.org/10.1186/s12967-018-1600-x

In this study – the first of its kind in ME/CFS – Dr. Scheibenbogen examined the expression of ten very large lncRNAs (> 5 kb) involved in immune regulation, or which influence genes involved in the stress response and/or metabolic and neurologic processes.

The authors were clearly surprised by their findings.  After all, they’d simply taken ten lncRNA’s that they thought, based on findings in other diseases, might play a role in ME/CFS.

In a finding they called “remarkable”, the expression of those ten lncRNA’s was enough to distinguish ME/CFS patients from healthy controls. In fact, the expression of any two of three of these lncRNA’s (NTT, MIAT and EMX2OS) was all that was needed to pick out most ME/CFS patients.

Diagnositic accuracy

The elevated expression of just three lncRNA’s was enough to identify most ME/CFS patients

Then seeking to understand if the chronic illness state present in ME/CFS could be turning these lncRNA’s on by exposing them to biological stressors known to be present in ME/CFS. They found that punishing cell lines with oxidative stress did, in fact, increase the expression of the lncRNA’s. Subjecting the cell lines to a viral stressor also increased expression of one of them. Doing it increased the expression of a gene associated with chronic inflammation and blood vessel dysfunction – two problems that are believed to be present in ME/CFS.

ME/CFS seems to revel in producing findings that baffle researchers and this study was no expression. The enhanced expression of one lncRNA (EMX2OS) was something of a mystery as it is rarely found in the cells (peripheral blood mononuclear cells) they examined. It is, however, increased in brain hypoxia; i.e. low oxygen levels in the brain – which Dr. Shungu’s studies suggest may be present in ME/CFS.

Study Suggests “Bad Energy” is Core Problem in Fibromyalgia and Chronic Fatigue Syndrome (ME/CFS)

Finally, the authors noted that it took just three lncRNA’s (NTT, MIAT, and EMX20s) to do what it took Kerr 88 genes and Naviaux 8-13 metabolites to do – differentiate ME/CFS patients from healthy controls. One wonders if Scheibenbogen’s examination of lncRNA’s is getting at some basic components of ME/CFS.

Treatment Implications

No direct treatment implications were mentioned. In the short-term they’re viewed more as providing excellent diagnostic biomarkers. For instance, lncRNA’s are now being used to one of most difficult diagnostic scenarios of all – prostate cancer. They’re now being used in men with high PSA levels and negative biopsy results.

Direct treatments based on lncRNA’s are probably years away but should be noted that lncRNA’s are a very active area of research for a good reason: turning down their expression could turn off basic processes that cause disease. The author of a recent study which found that LncRNA’s play a role regulate fat metabolism reported:

“We are still in the early stages of figuring out how lincRNAs function in human disease, but what used to be considered ‘junk’ in the genome may actually point us towards the jackpot of developing effective therapeutic approaches for cardiometabolic diseases,” Jennie Lin, MD, MTR

This new exploration of ME/CFS patient’s genomes further substantiates the notion that ME/CFS is a disease of immune dysregulation. Given the study’s strong results surely more lncRNA study in ME/CFS is on the way.

 

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32 Comments

  • David

    November 23, 2018 at 4:19 pm - Reply

    My head reels from all these hypothesis! What does this finding mean in terms of treatments? Or is it possible to treat us?

    • Cort Johnson

      November 23, 2018 at 4:54 pm - Reply

      My mind does too! What struck me was how many different things researchers are finding. It seems like every study finds some abnormality – which is encouraging.

      What was really encouraging for me about this study was that it seemed to integrate the genes, the immune system and metabolism…Perhaps the immune system and metabolism will be the major theme that eventually ends up explaining ME/CFS.

    • Alex Young aka alex3619

      November 23, 2018 at 9:07 pm - Reply

      If and only if its correct, it means there WILL be a treatment, but tells us nothing about WHEN. Very soon after we start to understand the processes we will start to be treated better, by better informed doctors. Early treatments will most likely be about modifying factors.

      If an existing drug has some effect then after five to ten years we might have a therapy. This is because a phase 3 study, if not several, will be needed.

      For a totally new drug its more like 20 years.

      Effective diagnostics are the most likely scenario in the short to medium term. However the change in attitude from formerly ill informed doctors, and insurance companies in denial, will improve our lives long before we have a cure.

      The reason why we keep getting new findings is simple. We are looking for needles in a paddock full of haystacks. Its easier to search the ones near the barn door, but having found nothing most conclude nothing is to be found. Now we know we keep finding needles in haystacks at the far end of the paddock, and so the search has moved to those haystacks. Knowing which haystacks get results changes the game.

      Please note my comment starts with an “if”. Most new findings turn out to be wrong, limited, or misinterpreted. It is however very hopeful.

  • Aidan

    November 23, 2018 at 4:22 pm - Reply

    This Woman is very smart she knows her business well I have a lot of confidence & she & her Team are what is needed to move forward I also think she should Team up with Dr. Ron Davis & his Teams as well…

    • Cort Johnson

      November 23, 2018 at 6:20 pm - Reply

      I look at this, Dr. Hanson and Dr. Marshall and their exosome studies and the nanoneedle Ron Davis is using and the Bateman Horne Center and their antibody study and I think this field is small but very creative!

  • Gail

    November 23, 2018 at 4:33 pm - Reply

    Cort, as always thank you for the excellent article. It sounds like Dr. Scheibenbogen is getting to the root of the problem. The question that’s always on my mind when I read ME articles is “How does this get fixed?” Any ideas?

    • Cort Johnson

      November 23, 2018 at 5:21 pm - Reply

      I don’t know about specific treatments but the research has really amped up as researchers learn how important they are. Cancer is a particularly active field. Because they regulate basic processes turning them off may be able to get at the heart of some disease processes.

      In the short term, though, they’re more likely to be used as effective biomarkers for drug testing – something ME/CFS vitally needs. In the longer term they could be directly targeted. I amended the blog to report that.

  • Eimear Forde

    November 23, 2018 at 4:52 pm - Reply

    Thank you Cort but what does this mean in terms of treatments if anything? My mind is boggling

  • nila

    November 23, 2018 at 5:53 pm - Reply

    I have had this illness since I can remember.. bad onset when 29 years old and I’m 79 now. I am so grateful for all the researchers and persons who have a deep interest in finding cures. I have known since the beginning that Oxygen plays a Great Role in the illness. Being a competitive National swim champ and then swimming with the Olympic Women’s coach in the late Fifty’s has given some of my own answers..Inflammation has been poo-pooed for many years.. I know that my brain gets inflamed and swells in the frontal lobes, I CAN FEE THE PRESSURE IN KINDA a LIKE HEADACHE. The limbic system and very concerning Basilganil.
    ( Parkinson’s trigger and diagnosed so called for now– mental illnesses..THIS IS A FOR SURE CAUSE THEY DID A SPECT SCAN ON MY BRAIN WITH NUCLEAR CONTRAST. think ABOUT IT!!! bLOOD fLOW AND OXYGEN TRANSIENTLY STARVING INFLAMMED BRAIN IN “sOME” FLARE UP’S i HAD IN THE 80.S.. I am very in EXCITED with this new hypo.research. that talks about too missing hormones that stop working ( transiently) ACTH and normal corticosteroids stop working ..limbic systems in the Brain..WHICH DOMIATES YOUR WHOLE aUTO NOMIC BRAIN FUNCTION. Now I ask you to put together the exercise intolerance and the autonomic brain controls..connect the dots.. oxygen and blood flow swelling the brain after exercise..BRAIN FOG AND MANY OTHER ISSUES THAT ARE DOWNRIGHT SCARY.Can not read or Think Straight..talking is very hard..ALL THIS HAPPENED TO ME WHEN I WOULD HAVE A REALLY BAD FLARE UP.. Then there WAS

    anxiety and panic disorders!! Stick with me here..Klonopin freed me up..so much. Now what happened in my swimming days fits in also… I was well known over the; Southeast USA and Florida as THE one who could win over the speciaty swimmers..THEN TRAGDY HIT ME.. i was far in front of the swimmer’s in severl events.. I would lose all my energy/ I could feel it flee through my body. I was stopped dead in my lane..only few yards to go// I had symtoms of Polio BUT TRAINSEANT.. This due to anrmria and depletin of oxygen// three years ago I was Tested/ i do not make B12!! I have seen Jay Glodstein many yrs/ ago/ I have a very high Q..My life has been a Testament to Human endurance.NOW THEY TELL ME THAT ePSTEIN bARR CAUSES INFLAMATION aND SO DOES hERPE sIX B. i”VE had all those titers taken over and Properly read as POSITIVE// i KNOW which one is doing it’s damage BECAUSE THEY HAVE dIfferent symptoms. I also can’t take some vaccines! So I could Write alot more..I hope to write an inspirationaI booK..ANY BODY WANT me to help you with a study/// MY BAGS are packed.

    • Paula

      November 24, 2018 at 5:44 am - Reply

      Hi Nila…I really enjoyed your reply to the article…
      I also have had this condition for a long time..I also was a swimmer and diver. I also felt the total drain
      When I was training or competing….I wasn’t as advanced as you mind.
      You have inspired me to keep up with the research your amazing that you haven’t given up..I am now 63, and when my brain is behaving I feel in my 30s….which of course in these times I over do it and crash….thank you…you have helped with your own knowledge…

    • Susan

      November 30, 2018 at 12:40 am - Reply

      You may want to read the bestseller ‘Medical Medium’ by health guru Anthony William. It is all about the long history of EBV, why and how it causes the fatigue, and how to reverse it by rebuilding the natural immune system and taking certain supplements.

      Chinese Medicine has long been familiar with treating similar diseases, if one correlates the body’s “energy” with it’s “immune system strength”. Although the author never mentions TCM, there is a huge correlation that anyone who has ever studied both Western and Eastern medicine can see.
      I had my most severe ME/CFS/FM episode 4 years ago, where I was bedridden for months and could no longer comprehend more than 2 pages in a book; My FM is now gone, I can bicycle 40 (flat) miles, and the brain fog is slowly going away, thanks to Medical Medium …and a lot of green blueberry-banana smoothies. It still takes 3+ days to recover from a bike ride, but I am slowly returning to ‘normal’.
      Hope you can too!

      Yes, Almost ALL the chronic health issues are caused by a HHV virus. The virus, like most pathogens, hates oxygen. The EBV virus lives in our body’s mucus and causes epigenetic changes to reduce the oxygen in it’s surroundings. It eats and excretes neurotoxins. Hence the inflammation and occasional rashes.

      99.9% of adults carry EBV, and it constantly mutates. So in the next 20-30 years, there will never be a long term cure for ME/CFS through a magic pill, just like there is no cure for a cold or the flu. Not feeding the virus (it loves mucus causing foods & eggs) and rebuilding the immune system is your best bet.

  • Bottsie

    November 23, 2018 at 5:56 pm - Reply

    As always, excellent article, Cort! On 12/21, I will mark 11 years with this disease. For most of those years, I have said that when they find the answer it will be relatively simple and will have been staring them in the face the entire time. They’re expecting the answer to be as complicated and diverse as the symptoms, so they can’t ‘see the tree for the forest’. While reading this article, I couldn’t help but compare the IncRNA to maintenance workers who so often go unnoticed, but who are vital in keeping things clean and up-and-running.

  • dejurgen

    November 23, 2018 at 6:09 pm - Reply

    “Dr. Scheibenbogen examined the expression of…”

    When diagonally reading the paper I asked myself the questions:
    * What about the healthy controls who might develop later on ME: would they be outliers in the healthy group?
    * What about the ME patients, would they have been outliers in the healthy group a few years before disease onset?

    Then I realized the study is about the expression of this lncRNA. Nowhere it states that this lncRNA has any sort of mutations. So far there is no evidence that these genes are different in patients. Let us suppose they are not:
    A) Then they would not be the initial cause of our disease.

    That would remain three options:
    B) They are “observers” reacting to a problematic state, but there reaction is not problematic. Then they do neither cause nor maintain this disease. Think about lncRNA that initiates “curing” mechanisms and is either somewhat effective or at least not counter effective.
    C) They are “poor aid” reacting to a problematic state, but there reaction is making the situation worse. Then they do maintain this disease but only do so as long as the original trigger is present to some extent.
    D) They are “terrible aid” reacting to a problematic state, but there reaction is making the situation worse. Then they do maintain this disease all on their own even if the original trigger is completely gone.

    If it would only be the expression that is different in ME and not the actual genes that were mutated that would be a wonderful research tool:
    * Take an identical twin with one healthy and one ill member (looking at you Cort;-)
    * Put ill members genes in test tube; look at gene expression of these lncRNA and metabolic profile
    * Put small quantities of healthy members genes in thousands of very small test tubes
    * Throw in each small test tube some “bad stuff” that is suspected of causing/triggering/maintaining ME
    * Find the small test tubes that have gene expressions and or metabolics resembling that of ill twin
    * Use combined results of gene expression and metabolics to see if there are “locking pairs” like for example peroxide causes problematic gene expression; metabolics reveals that tube of healthy twins cells + peroxide produces more proteinX; look if ill twin also has more proteinX in metabolics; look if adding more proteinX in tube of healthy twin cells does generate more peroxide creating a locking pair (self maintenance of disease even after removal of initial trigger) .

    Give it enough resources and this could be one nice lab tool for researching our disease if it were only the expression, not mutations. That is one of the few research results that can get me carefully excited so far ;-).

  • Sarah R.

    November 23, 2018 at 7:44 pm - Reply

    Thanks, Cort. This is a very promising study, and I’m glad to know about it. You’re the best! I don’t always comment, but I read every word you publish. I’m sure I’m not alone in couting on you to keep us informed. Many, many thanks for your ongoing hard work.

    • Cort Johnson

      November 24, 2018 at 5:42 am - Reply

      Thanks Sarah,

      Keeping up with the scientific literature keeps me engaged and hopeful. I’m so glad that I’m able to do this and very glad you find it helpful 🙂

  • Forebearance

    November 23, 2018 at 9:17 pm - Reply

    Wow! This is really cool!
    I can imagine a time when a patient would give a saliva sample and be diagnosed with ME/CFS. That would be so great!

    • Cort Johnson

      November 24, 2018 at 5:48 am - Reply

      That’s the great hope isn’t it? I think with all the molecular stuff going on it’s going to happen at some point.

  • Nancy B.

    November 23, 2018 at 9:22 pm - Reply

    This is indeed an interesting finding. I skimmed the research article and wondered if they had also done correlations between other illnesses which expressed with chronic long term fatigue–like MS, Fibromyalgia, Ehlers-Danlos, Gulf War Syndrome, etc. Fatigue is a common symptom of many conditions so is there a way to sort CFS/ME from the others–or did they just do a comparison of CFS/ME patients and ‘normals’?

    Still, using a whole exome sequencing to diagnose CFS/ME would be rather expensive–at the moment–but prices are falling. In fact, just lately, two sequencing companies have offered WES for the sale price of $199 (Veritas and Dante, I believe) but the depth is only 30X. Guess you get what you pay for…

    I find it interesting that in France, oxygen therapy is used for many disorders involving fatigue, including EDS. I wonder if they are on to something that is overlooked by American doctors.

    Gotta love that ‘junk’ (DNA)!

    • Cort Johnson

      November 24, 2018 at 5:48 am - Reply

      I think this is pretty cutting edge stuff. I don’t know about EDS and GWS but I’m pretty sure lncDNA has not been assessed in FM. It’s perhaps no surprise that lncRNA’s have been assessed quite a few times in multiple sclerosis. Here are two 2018 studies.

      Mol Ther Nucleic Acids. 2018 Sep 7;12:393-404. doi: 10.1016/j.omtn.2018.05.022. Epub 2018 Jul 11. LncRNAs expression profile in peripheral blood mononuclear cells from multiple sclerosis patients. Fenoglio C, Oldoni E, Serpente M, De Riz MA, Arcaro M, D’Anca M, Pietroboni AM, Calvi A, Lecchi E, Goris A, Mallants K, Dubois B, Comi C, Cantello R, Scarpini E, Galimberti D. J Neuroimmunol. 2018 Nov 15;324:129-135. doi: 10.1016/j.jneuroim.2018.08.008. Epub 2018 Aug 27.

      Immunology. 2018 Apr;153(4):479-487. doi: 10.1111/imm.12850. Epub 2017 Nov 16. HOTAIR but not ANRIL long non-coding RNA contributes to the pathogenesis of multiple sclerosis. Pahlevan Kakhki M1, Nikravesh A2, Shirvani Farsani Z3, Sahraian MA4, Behmanesh M1.

  • Nancy B.

    November 23, 2018 at 10:55 pm - Reply

    Sorry but I have to correct my last post, I meant to say WGS–whole genome sequencing NOT WES, whole exome sequencing (which my fingers, with a mind of their own, inadvertently typed).

  • Catherine F.

    November 24, 2018 at 4:12 am - Reply

    The idea of malfunctioning DNA makes sense to me. I’ve often wondered about the interaction of my gene-mutation abnormalities: MTHFR (problems with B vitamin absorbtion) CYP450 (problems with most pain and anti depressent meds) and chronic epstein barr and fibromyalgia. Discovering more about these genetic influences has helped me better treat and cope but further scientific study may show how they may all be part of some interactive chain.

  • Conny

    November 24, 2018 at 9:31 am - Reply

    Thank you Cort for another hopeful article. It is my hope that all these amazing researchers will come together at a special summit and start to put the pieces of the puzzle together. This particular study once again reminds me of what I have read about mammals in hibernation, also a hypometabolic state:

    “this study provides the first evidence for differential expression of lncRNAs in torpid ground squirrels, adding lncRNAs as another group of transcripts modulated in this mammalian species during hibernation.”

    [Up-regulation of Long Non-coding RNA TUG1 in Hibernating Thirteen-lined Ground Squirrels
    Jacques J. Frigault, Daneck Lang-Ouellette, and Pier Morin, Jr.]

    It seems that LncRNAs are involved in entry and exit of a hypometabolic state. So what has impacted these LncRNAs and caused them to change? Perhaps the cell danger response?

    We know that the cell danger response impacts serotonin levels and we know that serotonin plays a role in instigation hibernation in mammals. We have a theory that high serotonin levels in humans could play a role in chronic diseases. I just wish that someone or a group of people would take responsiblity for looking at everything we know so far to start building a global picture.

    • Cort Johnson

      November 24, 2018 at 3:14 pm - Reply

      Wow. LncRNA’s, hibernation and the hypometabolic state. I hope that Dr. Scheibenbogen is reading this! In fact, I just sent her an email. Wouldn’t it be wonderful if all of this merged together.

      Both Cortene and the Metabolic Hypothesis are high level attempts to explain ME/CFS. Cortene, in particular, looked at every angle from triggering events to gender to study results before they submitted their drug to trial in ME/CFS. Robert Phair used modeling and then test results to assess his Metabolic Hypothesis. Both predict high serotonin levels in the brains of ME/CFS….

      Thanks!

    • dejurgen

      November 24, 2018 at 11:01 pm - Reply

      Nice and original find :-). Thanks!

  • Margaret

    November 24, 2018 at 4:29 pm - Reply

    Just a hunch, but it sounds to me that these results suggest a fundamental role for anti-oxidants and keeping infections at bay, as an avenue of treatment (or management). (Since the researchers were able to worsen the expression of the genes via oxidative stress and exposure to viruses). But the question then remains: are the genes or other aspects of those suffering with CFS/ME somehow more vulnerable to these exposures? Might there be a deeper, more preventative form of treatment?

  • Del

    November 25, 2018 at 5:58 pm - Reply

    Is there a way, I or anyone with CFS/ME can be screened to see if we have more lncRNA in our DNA or what their talking about here?

    • Cort Johnson

      November 25, 2018 at 9:42 pm - Reply

      My guess is that these tests are only available to researchers at this point.

  • Lynne

    November 26, 2018 at 6:30 pm - Reply

    I too am overwhelmed – by almost every article. Concentrating is really a challenge, but then connecting the dots and tying things in together is impossible. Then I read comments and its so far beyond my thinking capacity. There are so many new discoveries in different realms, it is encouraging. Hopefully something in the pipeline will trickle down to relief. I recently had the CPAP test by Dr. Systrom; of course I went into this expecting informative results as it wasn’t most pleasant and also expensive. For me, it was not, unfortunately, useful. One day’s invoice 40k. My share was $1400.

    • Nancy

      November 29, 2018 at 9:31 pm - Reply

      I always look for a section at the bottom of “any” article entitled “Conclusion” or something of that nature. I tend to learn more by those than anything else. When I was younger (40s) I could do so much better than now (79). So I and many others I’m sure can relate to you. But I thank Cort for ensuring we get to see all this so that if we by chance can decipher meaning, we’re able to thanks to him.

      • Lynne

        December 2, 2018 at 7:23 pm - Reply

        Thanks much for the tip. And for sure, many readers are astute even with the small details.

  • Francis Martin

    November 28, 2018 at 8:14 pm - Reply

    Hi Cort,
    great article; thank you.

    I’ve just been notified of this paper by Amit K Saha, Ron Davis and others “Erythrocyte Deformability As a Potential Biomarker for Chronic Fatigue Syndrome” [http://www.bloodjournal.org/content/132/Suppl_1/4874?sso-checked=true].

    Bits from Amit/Ron’s paper and this (Scheibenbogen’s) paper look similar. Oxidative stress problems with microvascular dysfunction (small blood vessels).

    The link to LPS (bacterial translocation i.e. into bloodstream) in this (Scheibenbogen’s) paper, and also found by Maureen Hanson, and Unutmaz’s MAIT cell findings, all seem interesting.

    What is the cause of this immune activation; leaky gut?

    Also, can you reverse leaky gut?

    • Conny

      November 29, 2018 at 8:45 am - Reply

      Hi Francis,

      It would seem that leaky gut is indeed present, but that it is just another symptom of the hypometabolic state. Weakening of the gut barrier has also been observed in hibernating mammals. Look at this information:

      “Hibernation leads to substantial atrophy of the small intestinal mucosa in ground squirrels, and as reported in this study, cecal mass is also reduced. Hibernation also alters expression of several apoptosis-related proteins in the intestine, and it increases gut permeability.”
      [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3543654/]

      “ME/CFS is therefore […] not directly the result of leaky gut (cell walls in the body and gut are intentionally less boundaried during states of dauer / freeze / hibernation).”
      [https://chronicillnesstraumastudies.com/mecfs-freeze/]

      You can improve leaky gut by cutting out gluten, and in some cases also lowering intake of lectins and phytates but that would depend on your own personal sensitivities. Many foods have an impact on gut barrier function and it’s not always what you would think! Here’s a good overview:

      Nutritional Keys for Intestinal Barrier Modulation
      [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4670985/]

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