Leonard Jason and Ben Katz have been doggedly trying to catch post-infectious ME/CFS in the act for over a decade. They weren’t the first – we can credit the still groundbreaking Dubbo studies in the mid-2000s for that – but they’ve been persistent, and their persistence is paying off as they extend their efforts into long COVID. Not that it’s been easy. If memory serves, they had their samples long before the NIH was willing to give them the money to actually test them. (The NIH could have learned from that approach with long COVID.)
Similar, but much more comprehensive, studies are doing for the SARS-CoV-2 coronavirus and long COVID what Jason/Katz have done for infectious mononucleosis/glandular fever and ME/CFS: they’re getting samples from people as they become infected and then are attempting to learn what happens as some people come down with ME/CFS.
Jason and Katz, though, have a twist that most long-COVID studies lack: they’ve gathered samples from before the college students became infected. Potentially, that means they could identify risk factors that were present when healthy, what changed during the initial infection, and finally what changed as they got full-blown ME/CFS months later.
Since they added a long-COVID cohort to his studies, they now have the opportunity to do the same with long COVID – and then compare the two post-infectious illnesses. It’s a fantastic project that’s been weighed down by the usual bugaboo – funding. They lack the funding to do the really comprehensive analyses being done in long COVID. Their studies, though, provide the first opportunity I know of to compare the differences and similarities between Epstein-Barr virus-induced ME/CFS and a SARS-CoV-2 (coronavirus)-induced ME/CFS in real time.
It’s a precious opportunity, indeed, and one that could be of immense importance to this field – if they get the funding to really dig in and figure out what happened.
Dr. Koroshetz has talked about the great opportunity the coronavirus provides for researchers to focus on one pathogen and one post-infectious event. The Dubbo studies and the Jason-Katz studies have shown that that opportunity always existed. All the NIH had to do was pick an infection like infectious mononucleosis (IM), or Lyme Disease, or the flu, and provide the funding to follow them. (The Dubbo studies were funded by the CDC’s ME/CFS program). That could, and should, have been done preparatory to the pandemic that kept Anthony Fauci up at night, worrying.
The study, “Predictors for Developing Severe Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome Following Infectious Mononucleosis“, followed 4,501 college students, of which 238, or about 5%, developed infectious mononucleosis. They were then followed up at six months to determine when they met the criteria for ME/CFS or had recovered. The study focused on about 50 students who met the criteria for chronic fatigue syndrome after six months and about 60 students who had recovered. About 10% of the students who came down with infectious mononucleosis met the criteria for chronic fatigue syndrome at six months.
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Those who met the Fukuda criteria (n=30) were labeled as having ME/CFS, while those who met the Canadian Consensus criteria (n=18) were denoted as having severe ME/CFS.
The study used questionnaires and cytokine results across the three time points; before infectious mononucleosis, during infectious mononucleosis, and six months later.
The findings, at least to my mind, were remarkable. The symptoms that distinguished people who would later come down with severe ME/CFS (those people who met the Canadian Consensus Criteria) from those who recovered or met the Fukuda Criteria for ME/CFS involved the gut.
The gut problems preceded the exposure to the Epstein-Barr virus; that is, the people who later developed a more severe form of ME/CFS – the kind that most of the people reading this blog probably have – experienced more gut symptoms and lower levels of IL-13 and/or IL-5 when they were healthy.
Gut issues were also strongly predictive of who came down with more severe ME/CFS. People with irritable bowel symptoms (bloating, pain etc.) when healthy, severe gastrointestinal symptoms when they came down with mononucleosis, and low levels of IL-13 and/or IL-5 at baseline had nearly an 80% chance of developing severe ME/CFS six months following IM.”
A pre-infectious immune hole appears to have shown up in the gut.
That was interesting to me personally, as minor gut problems were about the only sign that I could think of that something was maybe a little off prior to becoming ill. Plus, I was exposed to Giardia a couple of years before becoming ill. Perhaps my infectious insult – which I appeared to have fully recovered from – occurred years earlier. That and a concussion are the only two factors that I can discern that differentiate me from my twin – who never came down with ME/CFS. (Check out our gut trigger poll below.)
Who would’ve thought, though, that gut problems might stick out more than fatigue or sleep or exertion problems? Jason and Katz might have, actually. We don’t often link gut problems to autonomic nervous system dysfunction, but the autonomic nervous system controls gut motility, and problems with the gut motility can affect the gut flora, and alterations in the gut flora can affect the integrity of the gut lining, and leaky gut lining can result in inflammation that travels all the way up into the central nervous system. Speaking of leaky vessels, evidence of leaky vessels – in the gut, blood, and brain – have shown up in ME/CFS.
This is the second of the Jason/Katz IM cohort studies to highlight autonomic nervous system problems. Plus, the low cytokine readings (IL-13, IL-6) suggest that some sort of immune protective factor (the hole?) may have been missing. They bring to mind Nancy Klimas’s finding of sparse cytokine networks in ME/CFS, which suggested that quite a few holes may be present, and that ME/CFS patients’ immune systems are not as resilient as they should be.
- The Jason-Katz ME/CFS project’s unique asset – samples and questionnaires taken before college students came down with infectious mononucleosis/glandular fever – came up with a startling finding: the college students who later came down with more severe ME/CFS – had gut problems and low levels of cytokines before coming infected with the infectious mononucleosis/glandular fever that ultimately triggered their ME/CFS.
- The finding were remarkably predictive and indicated that patients with symptoms of an irritable bowel at baseline, and severe gastrointestinal symptoms when they contracted mononucleosis, as well as low levels of IL-13 and/or IL-5 at baseline had nearly an 80% chance of developing severe ME/CFS six months following IM.”
- The study was small and its findings need to be validated but it suggested that an immune hole in the gut could have laid the way for the development of ME/CFS after the infection.
- Over time we are learning more and more about how viruses can affect the immune system. For instance, studies suggest that gut microbiome plays a key role in fighting off the flu. Stomach problems similar to those in ME/CFS have been found in long COVID and it appears that the virus may reach the gut as well.
- Animal studies suggest that antivirals may, in fact, provide an effective way to treat the kind of gut issues found in GWI, ME/CFS, and long COVID. With long COVID spurring interest into better antivirals and the gut we can expect to see more and better ways to modulate the gut microbiome – and perhaps close the immune hole that opened a door to these diseases.
Still, these cytokines are clearly connected to the gut – apparently, in ways we don’t understand. Derya Unutmaz has found that regulatory T-cells he calls “guardians of the gut” that regulate gut functioning are not working well in ME/CFS. Untumaz, though, also found that the gut microbiome largely returned to normal after about ten years in ME/CFS.
The authors noted that if they were validated, these risk factors could significantly alter the therapeutic strategies in IM and other triggers of ME/CFS in adults and adolescents. They will certainly need validation as the study was small.
Jason reported that they are continuing to follow and assess their mono/ME/CFS patients.
Viral Gut Connection
While no studies reach as far back as Jason’s, gut problems are cropping up very early in long COVID. Su found that aberrations in T-cells targeting the SARS-CoV-2-virus and/or the cytomegalovirus were associated with what they called “gastrointestinal PASC”. That finding suggested that the coronavirus may be reaching into the gut.
Animal models indicate that the gut flora may, at times, play an important role in fending off pathogens. Antibiotics, for instance, have been shown to increase one’s vulnerability to the flu virus. In the case of the flu, the microbiome appears to activate an inflammasome that plays a crucial role in defending against it. If that’s so, it’s possible that something that went awry in the gut – maybe something that produced only a few symptoms – played a role in opening the door to an unusually devastating and long-lasting post-infectious event illness.
Indeed, we’ve seen that the viral component of the gut is a critical gut microbiome regulator. A Gulf War Illness animal study found that changes in the virome were associated with increased IL-6 levels – and microglial activation in the brains of the mice. Then they used a broad-spectrum antiviral called Ribavirin to reverse the changes in the gut virome, reduce the animals’ leaky gut and their gut inflammation, and even their neuroinflammation.
The authors, one of whom was Nancy Klimas, suggested that antivirals like Ribavirin, by themselves or in combinations with “complementary and alternative compounds and probiotics”, could “form the basis of a novel treatment strategy for GWI (Gulf War Illness). Given the very similar gut findings in ME/CFS/FM and GWI, that treatment strategy should apply to ME/CFS/FM as well.
The coronavirus pandemic is sparking new interest in developing better antivirals. Along the way, we should learn more about how viruses impact the gut and how manipulating gut virus may help to return the gut flora to health. If the Jason/Katz study findings hold up – that could enable us to fix the original immune hole that helped to started all this off in the first place.
Gut Trigger Poll
Please take the Gut Trigger Poll and tell us about your experiences with your gut.
Gut Trigger Poll
Lenny Jason’s Long-COVID Study is Open (People with ME/CFS and long COVID are invited)
If you or someone you know has been infected with COVID-19, you are invited to participate in a research study that seeks to identify the long-term effects of COVID-19 to help the international community better understand and address this illness and similar ones.
You must be 18 years old or older and able to read and write in English to participate. Participating requires completing an online questionnaire that takes about 30 minutes. People who had ME/CFS before coming down with long COVID are invited to participate.
You can access the questionnaire here: https://redcap.is.depaul.edu/surveys/?s=8RM33AP373
More Reasons Long-COVID Research Can Benefit From ME/CFS
It’s silly, it’s beyond silly, really, not to integrate a field – even a small field – that has been working out the same problems found in long COVID for over 30 years. The decision to remove even the mention of ME/CFS research from the RECOVER website is shortsighted, indeed.
As the U.S. Moves Forward on Long COVID, and the NIH Flails About on ME/CFS, the ME/CFS-Long COVID Webinar is Upon Us
As we continue a series on how long-COVID research can benefit from ME/CFS, consider this:
- Accurate Symptom Assessments – The long-COVID studies are using symptom questionnaires that are outdated, inaccurate, and misleading. Recognizing that the standard symptom questionnaires didn’t work in ME/CFS, Leonard Jason created the DePaul Symptom Questionnaire, which uses both frequency and severity of a symptom to assess significance. Until Jason created this questionnaire, there was no way to differentiate the most important symptoms – those which occurred frequently and were severe, such as fatigue and post-exertional malaise, from lesser symptoms.
- Accurate Definitions – With Jason often leading the way, ME/CFS researchers, doctors, and advocates not only battled inaccurate definitions foisted on this field by federal institutions (Holmes, Oxford, Fukuda, Empirical) – some of which emphasized psychological interpretations of this disease – but came up with their own definitions (Canadian Consensus Criteria, International Consensus Criteria), which over time have won out. These definitions introduced the key symptom – post-exertional malaise – to the medical field.
- First Post-Infectious Cohort Studies – The same type of effort that now permeates long-COVID research – which is attempting to trace a post-infectious illness like long COVID from its infectious onset to its realization – were birthed in the ME/CFS field over 15 years ago. Those studies indicated that every infectious event – whether triggered by a bacteria or a virus – resulted in 5-10% of those afflicted coming down with a long-lasting ME/CFS-like (long-COVID-like) illness.
The Jason/Katz study offers something unique – a chance to assess people symptomatically and biologically prior to coming down with infectious mononucleosis and ultimately chronic fatigue syndrome (ME/CFS). The study found that gut symptoms were increased and two cytokines associated with the gut were decreased in people who later came down with the more severe form of ME/CFS (as denoted by their ability to fulfill the Canadian Consensus Criteria). Furthermore, gut symptoms and reduced cytokine levels were remarkably predictive of who would come down with the more severe form of ME/CFS.
The study was small and needs to be validated but it suggests that some sort of immune hole pertaining to the gut may have left some people vulnerable to coming down with ME/CFS after an infection. The authors also noted a possible autonomic nervous system connection to the gut.
Other studies have found that viruses can affect the gut microbiome and the ability to respond to infections. In fact, a Gulf War animal study found that an antiviral was able to improve the animals’ microbiome, reduce both gut and neuroinflammation and improve gut lining integrity. Given the increased interest in developing better antivirals and the findings of gut problems in long COVID we should see more opportunities open up to manipulate the gut and perhaps close an immune hole in both long COVID and ME/CFS.
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What is exactly meant by ‘hole’ in the gut? Thanks!
There do appear to be “leaks” in the gut or holes through which bacteria from the gut is escaping into the bloodstream – particularly during or after exercise, but I was referring to some sort of compromised immune system in the gut which was resulting in gut issues and perhaps immune issues overall. Derya Unutmaz is looking into this.
I always felt that there was a “hole” somewhere inside me where all my energy was leaking out. However, about a year after I started ( after 13 years of ME/CFS) taking 2 capsules of cistus 3x a day (works antibacterial/–viral/fungal) I felt that the hole was slowly closing. Today, three years later, I am still limited because I have little energy, but what little I have is reliably available! – Which was not the case before. I have not experienced any severe collapses/bedriddenness since then and my stomach/intestinal problems have also completely disappeared.
Translated with http://www.DeepL.com/Translator (free version)
Can we measure these bacteria in the blood?
Yes, and its was done in ME/CFS following an exercise challenge in 2015. The study “hypothesized that post-exertion worsening of ME/CFS symptoms could be due to increased bacterial translocation from the intestine into the systemic circulation.” and found “high levels of bacterial sequences maintained at 72 hours post-exercise in ME/CFS patients versus clearance in the controls.”
They also found that exercise produced changes in the gut microbiome.
Something of interest maybe gliadin (a peptide that is one of the building blocks of gluten).
It was Dr Fasano’s team that discovered the protein zonulin that regulates intestinal permeability.
They discovered this protein while researching how cholera makes people so sick. Now apparently gluten has the same affect on people by increasing zonulin and increasing the leakiness of the gut.
Fasano’s theory is that the body regulates zonulin as it needs to for normal ‘housekeeping’ purposes but if zonulin levels are permanently elevated via the consumption of gluten then undigested gluten, large proteins & other foreign substances are gaining access to the body that shouldn’t.
That triggers inflammation which if chronic from the constant exposure to gluten is being linked to a number of inflammatory & automimmune diseases not just celiac disease.
The interest is in determining if people with non-celiac gluten sensitivity are highly sensitive to gluten & zonulin upregulation. These people may not have celiac disease (a specific autoimmune response) but they may be reacting to gliadins in other ways
Fasano explains it here at 19:30 – well worth watching how the gliadin protein is so antagonistic to our immune systems.
I would suggest to anyone with CFS to try quitting gluten entirely (ensure that cross contamination is avoided entirely) for a few weeks and see if that corresponds with an improvement in condition.
If gluten is eliminated from the diet than zonulin levels should decrease and the gut integrity should restore and that should reduce inflammation.
Truly amazing finding.
For anyone interested, the gut/ANS link seems to me to work in BOTH directions. IBS symptoms (e.g. food sensitivity, bloating, climate change inducing flatulence) largely disappear within 24-48 hours after a faecal matter transplant. I recently had left and right C4 and C6 sympathetic nerve chain blocks done, taking the lead from the recent stellate ganglion block article:
Similarly, a significant reduction in those IBS symptoms occurred in the same time frame as the FMT after the nerve block. Other improvements after the nerve block (for me at least) appear to be better sleep, less allergic rhinitis/sinusitis and less nocturia. Perhaps the improved sleep is linked to the reduced gut/nocturia symptoms. For what it is, the pain doctor is also recommending vagus nerve stimulation.
Can you get FMT in the US? My son just went through a lengthy SIBO treatment and when it was finished his test came out worse than when he started.
I don’t know if this is related, I had a biopsy done on my terminal ileum, the findings, erosion in the terminal ileum. what’s sad is my HMO doctor never explained this finding to me, the how, what or cause.
CFS/ME hit after 4 months of severe infection with clostridium difficile, contracted in hospital. According to Borody that year many people died from C diff, and it was one of the most virulent of strains. Question is: how does the gut get repaired. CFS patients take tons of probiotics, and other GI supplements, but nothing repairs this ‘hole.’
Its funny (ha ha) that we don’t often think of gut infections when we think of ME/CFS – we think of more EBV, coronavirus or something else. Have you tried fecal transplants? I think they were first used for C. dificle. You’re probably lucky you made it. Nasty, nasty bug even in its less virulent forms.
Could be EBV infection of the gut endothelial cells and immune response causing inflammation and holes in blood vessels causing gut problems. EBV reactivation is behind M/E CFS and long Covid.
In year 7 (age 12) my daughter had food poisoning. She seemed to recover fine.
Later at school camp for year 7 she got a throat infection that has at least two rounds of antibiotics to get it under control.
She was also identified as coeliac so we changed her diet at the end of that same year. (Naturally she was suffering gastrointestinal bloating and discomfort due to the gluten!!! )
Hep A/B shot in prep for travel early in the new year. Seemingly inflamed thyroid soon after the shot. Opted to go to year 8 introductory camp to meet the new kids (instead of to the doctor) caught a virus at camp……13 years later….. semi functional.
After several weeks of low body temp after getting the virus, spending 20 hours in bed a day… she dragged herself to school just to see her friends. Fatefully, the authorities were there on that day (of all days) and despite her very piqued appearance and wearing a pullover on a warm day they administer the first of the 3 scheduled HPV vaccines. Approval for this had been signed three months earlier!!!
So, take your pick…which one or ones precipitated the ME/CFS??
These sequential insults to her system have wrought damage that we have tried in so many fashions to remedy. She is on a plateau… which we cannot seem to shift!! Soooo frustrating for her.
This is why i truely feel for the researchers.
there can be so many factors involved in precipitating these events.
So presumably they didn’t find anything significant for those who don’t (like me) meet the Canadian consensus for more severe CFS/ME?
No they didn’t. I don’t know how close they got – I don’t believe they provided those statistics. Statistics are pretty black/white – if you don’t meet a certain threshold the result is not presumed to be “significant”. It’s possible they came close but didn’t quite reach it.
Chimes with me. I had gastroenteritis -> EBV infection* -> ME/CFS symptom onset within the space of 1-2 years.
(*raised EBV VCA IgG/normal VCA IgM antibody titers almost 2 decades later)
I was given the antibiotic cotrimoxazole (aka Septrin, Bactrim) for the gastroenteritis. The antibiotic has itself been linked with ME/CFS:
As have enteroviruses:
Every single doctor I’ve met over the past 14 years, I’ve always told about the only thing pre-existing my ME/CFS: gut issues. I’ve always been sensitive to certain foods (mainly bloating and diarrhea whenever I ate at my aunts house) and had a ruptured appendix only 1 year before I came down with ME/CFS. This was a bad rupture, it had gone unnoticed for too long and could have killed me. This information has always been dismissed by doctors as being completely unrelated. Now I wonder…
The problem is that gut issues are always present in every disease with immune deregulation (e.g.MS). Correlation and causation are different terms…. Similarly, just bc HHV6 and EBV is also reactivated almost always does not mean that these are viral diseases. Once the immune system collapses it has a fundamental impact on any major metabolic processes. IgA decreases, different species appear in the digestive system, there is a switch from TH1 to TH2 immune profile etc.
Right. All it means right now is that we have to take the gut into account and do our best to ensure that it’s in as good of shape as possible. Time will hopefully tell how this all works out.
What if DN A issue in gut passed down from mothers side?
Certainly possible. My mother used to have IBS-like symptoms.
I run the National Birth Defect registry that has comprehensive data on 6344 cases. We collect information on both structural (ex. cleft palate, spina bifida) and functional (autism, endocrine, immune) disorders. Included in our data collection is a category for Chronic Fatigue Syndrome.
We currently have 511 cases and 399 of these are in the children of male Vietnam veterans. That is nearly 18%. These veterans were exposed to Agent Orange, a combination of two herbicides and dioxin, perhaps the most potent toxin known. Dioxin is stored in body fat and targets the thyroid and immune system.
Scientists should be looking much further back into the histories of people who develop ME/CFS or Long Covid. The determining factors may have been there at birth just waiting for an appropriate trigger.
Betty, I’m curious what your registry has to say about the roots of autism.
Really, who knows what all these untested chemicals in our environment may be doing to us. It’s a huge experiment we have going on. I can’t imagine that at least some of ME/CFS/FM for some people is not caused or at least contributed to by reactions to these chemicals.
How do u fix the leaky gut to recover
Diet, pre and probiotics, fermented foods can all help.
I think CFS is caused by inflammation as a result of persistent antigen presence, now what actually is causing that could vary on an individual basis, it could be a virus, something passing from the stomach, or mold toxin or other bacterial toxin. Its probably not Metabolic Trap, HPA axis dysfunction, mitochondrial problem, small nerve fiber neuropathy, CDR, mitochrondrial fragmentation + ( insert 100 other theories ). It appears to be simply a problem where oxygen can’t get to the cells due to action of the immune system including so called microclot, when that happens you cant do much before you start to hit limiting factors and negative after effect.
Very possible. I believe several groups are looking for an antigen – which apparently is not an easy thing to find. The oxygen explanation makes perfect sense to me.
For the past 14 years, I have wracked my brain (and medical records) for clues preceding ME/CFS. I had my gall bladder removed, been diagnosed with GERD and prescribed Prilosec (now Omeprazole). I only learned years later that this med is only supposed to be used for 2-3 weeks at a time. I’m still on it 20 plus years later. I’ve tried getting off it and can’t. Sooo…wondering if the medication is a trigger/contributor.
Additionally, I had a complete hysterectomy prior to becoming ill. Some recent research is finding differences with female hormones. I really wonder if hysterectomies (partial or total) or menopause are taken into consideration when screening subjects.
I’ve had sinus issues my entire life. I had a horrible infection of some kind in October after having a polysomnogram. I had a slight sinus infection and asked if I should delay the test, but was told no. Now, I regret that. I became ill with ME/CFS in December. My sinuses have really been bad the past couple of years. I’ve had lifelong Candida issues as well. All of these things seem to come up in research at one time or another.
Before coming down with ME/CFS, I referred to myself as a ‘virus magnet’. I had chicken pox, roseola, rheumatic fever, and German measles as a kid, with various infections along the way. It did not help that I was an elementary teacher for 26 years prior to becoming ill. Classrooms, especially elementary ones, are basically petri dishes. This was prior to the Pandemic, so they weren’t cleaned as thoroughly as they (probably) are now.
I think my body must have experienced the Perfect Storm of triggers.
Hi Gail, In 2009 we did a report on 137 ASD cases in our registry. Two interesting findings emerged. The most commonly taken medication during pregnancy was acetaminophen and 60% of our ASD cases also had a structural birth defect.
Since our report was presented at a national autism conference in Chicago, there have been 16 studies that have found an association between neurodevelopmental disabilities and maternal exposure to acetaminophen. In one study sponsored by the NIH, acetaminophen was measured in cord blood and the babies were followed through a number of years. The highest rates of acetaminophen in cord blood were associated with increases in Autistic Spectrum Disorders.
Oh my God, acetaminophen is so common and so many people use it. No wonder autism rates have increased.
Betty, have you heard about the high rates of brain cancer associated with people who attended Colonia High School in New Jersey? Do you know of birth defects in that area (Colonia, NJ)?
El estrés podría estar detrás de ese “agujero”.
El estrés hace que los niveles de cortisol suban y este es responsable del debilitamiento de la barrera intestinal.
De esta forma las bacterias intestinales se van a colar en el torrente sanguíneo provocando una reacción antígeno-anticuerpo, liberándose citocinas inflamatorias.
Un estrés prolongado hace que el eje Hipotálamo-Hipofisis-Suprarrenal este Continuamente activado.
En cuanto a los microorganismos que pasan al torrente sanguíneo, tal vez virus pues el aparato digestivo es reservorio de virus del herpes como el Epstein Barr
I believe that our guts and the gut microbiota have a much larger role to play in diseases than we ever thought.
Do you know of any studies linking “non secretor” status , due to the FUT2 polymorphism? I am a non secretor as is my mother do a double whammy for me.
I would be interested to know what percentage of us are non-secretors.
Moi aussi je suis FUT 2 non sécréteur
I wonder how celiac disease fits in. I got really sick with it 15 years before ME, but it all cleared up with a gluten free diet. I was having a little trouble but not too bad when I got ME.
Basically leaky gut theory
I’ve been focusing on my gut health for years now because it seemed clear to me that it was an issue. I took caprylic acid and Citricidal (grapefruit seed extract) to try and clear unhelpful gut bacteria. I tried to cut down on sugar. I then added in various probiotics over the years, psyllium husks and green leafy vegetables.
My brain definitely took a hit when I had the nasty flu, with a high temperature, five years ago. I think that activated the microglia and since then various foods really seem to irritate them. I call it irritable brain syndrome. Over the years, I’ve managed to figure out quite a lot of things. Sugar, processed foods and anything that sets off my IBS, also sets off my brain. Thankfully I can improve it and I’m getting better at managing it. I eat a small amount of mackerel every day for the omega 3’s and try and eat an anti inflammatory diet. I think the vagus nerve maybe involved in signalling the irritation in my gut to my brain. I’m continually trying to balance everything as I’m so intolerant to so much food and my brain seems to run out of glucose fairly quickly.
I am male and 71 in May 2022. I have never had any gut problems as far as I am aware in the whole of my life pre-COVID. I caught COVID-19 in March 2020 and was ill for about 5 weeks with all the listed symptoms except(!) significant respiritory ones. I started to develop Long COVID (now it has a name!) in May 2020 and still have it – headaches, joint aches, brain-fog, paraesthesia (pins and needles in arms, hands and one foot), extreme fatigue at times. All normla vital signs are absoltely OK. For the past 18 months I have also now had gut and digestion issues leading to difficult and messy bowel movements. GP doesn’t know why. I primarily eat a vegetarian diet (I have done for many years) but I have also tried periods of more traditional meals and also exclusion diets – nothing has helped so far. So I do not fit the pattern described here. I think micro-clots are more likely to be causing most of my issues, but I don’t know about my gut ones.
Non-secretor! I had never heard of that. Another thing that clearly needs to be followed up in ME/CFS. Thanks for the link.
Hi, Gail. I just saw your message. I am aware of the cancer cluster of 100 cases potential linked to a school in New Jersey. We have not heard from any parents about birth defects at this time.
I don’t understand all of this informative article, but my gut feeling (pun intended) tells me it’s spot on!
I was healthy and very energetic and now I’ve been sick for more than half of my life (34 years old). In Switzerland there is hardly any help for ME/CFS patients at all. Some years ago, at University Hospital of Zurich, I was told they are “no fans” of this diagnosis and my symptoms must be psychological. However, it’s documented that I had a severe infection with borrelia burgdorferi bacteria and also mononucleosis (apparently I had it twice). But whatever triggered ME/CFS in my body, I’m convinced the gut plays a key role as I keep having issues with it on a daily basis (bloating, fatigue after eating, sometimes diarrhea for no reason, etc).
I really hope this study gets the funding it needs.
Thank you so much for this blog!
At the time of my first major ME crash, when my health and my life turned upside down, I also started exhibiting what I saw to be IBS. It was pretty severe, and lasted around three years. It cleared up for the most part after those three years (while my ?ME remained), and the only thing that I can associate to the improvement was an extreme resting regimen. I’ve since worked my way through various probiotics and fermented foods. I also just eat more healthily overall. I haven’t eaten a pizza, for example, for 10 years, and I try to avoid sweeteners, which are notorious for allowing growth of detrimental bacteria in your gut. I’ve learned a lot about the various probiotic supplements as I’ve gone along, and I would say that it’s really difficult for a layperson to get things right. Some ‘good’ probiotic supplements are actually not that good for ME sufferers, as you can risk overgrowth of certain types of bacteria, as well as having lots of dead bacterial waste in your gut. For anyone with gut issues, I would strongly advise getting a reputable stool test (many can be done at home), and getting a proper analysis of results so that you can better target your diet. There was recently a very fascinating documentary on YouTube produced by .Singapore’s CNA channel that shows the diagnosis someone got following taking one of these tests. Look after your gut, everyone!
I have a lot of food sensitivities now and various new symptoms that I can’t explain but extreme stomach gas was one of the first new ones I noticed, most of my new issues look a lot like CIRS but i’ve discovered recently that some were caused by certain foods, I had severe cognitive impairment that stopped when I stopped eating a cereal that had oats and barley in it ( gluten source ). When I started taking activated charcoal my fatigue and general poor functioning especially neurological stuff and ability to do various activities rapidly cleared up, however I still experienced a sort of crash after doing to much physically ( forces on my leg muscles making them ache / regrow ), I then experienced a new reaction to chicken, which was previously fine, my digestion also seems quite slow lately even before taking the binder. I suspect in the past few years I have developed bacterial dysbiosis and leaky gut and a combination of these is causing many new symptoms and also multiple chemical sensitivity and food sensitivity. I also considered mold as a possible cause of all of this but I need to investigate both.