A Gulf War Illness study finds a connection between dysregulated gut flora, leaky gut and neuroinflammation – and a new way to potentially resolve it.
It’s nice when the government has your back. After years of neglect, the federal government finally appears, at least regarding medical research, to have Gulf War Illness (GWI) veterans’ backs.
The study showed the toxic chemicals can alter the gut flora, produce leaky gut and induce neuroinflammation. (image of oil field fire during Gulf War from Wikimedia Commons)
The feds are not just interested in understanding GWI – their goal is to develop new treatments. That focus has lead to the development of animal models which have allowed researchers to do extensive testing. (When exposed to the chemicals and stressors, the mouse model of GWI experiences cognitive problems, learning difficulties, fatigue and GI issues.) By paving the way for treatment trials, the GWI animal models are making a significant difference – as they did in this case.
Toxic Chemicals And Your Gut Flora
No one during the first Gulf War almost thirty years ago would have dreamed that the gut, of all places, might hold the key to the health issues veterans face. The latest studies suggest that the gut does play a role, however, and may even play a crucial role in their illness.
If the gut is impacting people with GWI, it would be shocking if it’s not impacting people with chronic fatigue syndrome (ME/CFS) as well.
Altered gut microbiome in a mouse model of Gulf War Illness causes neuroinflammation and intestinal injury via leaky gut and TLR4 activation. Firas Alhasson,#1 Suvarthi Das,#1,¤ Ratanesh Seth,#1 Diptadip Dattaroy,1 Varun Chandrashekaran,1 Caitlin N. Ryan,2 Luisa S. Chan,2 Traci Testerman,3 James Burch,4 Lorne J. Hofseth,5 Ronnie Horner,6 Mitzi Nagarkatti,3 Prakash Nagarkatti,3 Stephen M. Lasley,7 and Saurabh Chatterjee1,*PLoS One. 2017; 12(3): e0172914.Published online 2017 Mar 22. doi: 10.1371/journal.pone.0172914
Saurabh Chatterjee, an environment health science researcher at the University of South Carolina, has been methodically describing the strange flora that’s lurking in GWI patients’ guts. In 2017, Chatterjee and his team showed that exposing GWI mice to chemicals and stress altered their gut microflora and caused the junctures of their gut lining to loosen – producing a “leaky” gut. As their gut bacteria spilled into their blood stream, it triggered a condition called “systemic endotoxemia”. The same leaky gut problem has been found in chronic fatigue syndrome (ME/CFS) and fibromyalgia.
The bacterial phylum Firmicutes that was found enriched in the exposed mice has been associated with obesity, metabolic syndrome, chronic fatigue and inflammatory bowel disease – and was found increased in ME/CFS in one study.
The Gut – Brain Mystery
The mouse problems didn’t stop at their guts, though. Specific gut bacteria (Coproccoccus, Turicibacter) were also associated with neuroinflammation in the GWI mice brains.
How changes in one’s gut bacteria result in inflammation in the brain is, of course, a big question. For one thing, there’s this blood-brain barrier (BBB) that’s been specifically erected to stop bad actors from getting into our brain.
Some researchers have hypothesized that high levels of pro-inflammatory cytokines are wreaking havoc on the formerly tight junctions of the BBB but this group had a different twist on that idea.
They hypothesized that toxins produced by the bad bacteria (endotoxins) were binding to receptors in the brain and small intestines causing the cells there to produce localized explosions in pro-inflammatory cytokines. (VanElzakker proposed that a similar localized immune response was present in ME/CFS eight years ago.)
These localized concentrations of cytokines wouldn’t necessarily show up in a blood test but could causing be oxidative stress, inflammation, etc. around the BBB – disrupting its junctions. Or, as VanElzakker also suggested, they could be producing signals that get transmitted to the brain and trigger an inflammatory response there.
Given that idea, it was intriguing, indeed, to see the same bacterial receptor (TLR-4) get triggered in both the gut and in the olfactory lobe of the brains of the mice despite the fact it was clear that the bacteria themselves had not made their way to the brain. It suggested that a signal from the gut was making its way to the brain – and likely producing inflammation there.
The findings suggested to the authors that antibacterials like minocycline and probiotics might be helpful not just in returning the gut to health, but also in reducing the neuroinflammation present in Gulf war Illness and similar disorders.
Demonstrating that toxic chemicals had likely whacked the gut bacteria of GWI patients, messed up the tight junctions in both their guts and their blood-brain-barriers, and caused inflammation in their brains, was pretty darn good, but it was all just a setup, though, to the big finding Chatterlee produced in his most recent study.
The Viruses in Us
Gut DNA Virome Diversity and Its Association with Host Bacteria Regulate Inflammatory Phenotype and Neuronal Immunotoxicity in Experimental Gulf War Illness. Ratanesh K. Seth,1 Rabia Maqsood,2 Ayan Mondal,1 Dipro Bose,1 Diana Kimono,1 LaRinda A. Holland,2 Patricia Janulewicz Lloyd,3 Nancy Klimas,4 Ronnie D. Horner,5 Kimberly Sullivan,3 Efrem S. Lim,2,* and Saurabh Chatterjee1,6,* Viruses. 2019 Oct; 11(10): 968. Published online 2019 Oct 21. doi: 10.3390/v11100968
Chatterlee’s next goal was to learn why the guts of his mice and people with GWI had stayed stuck in a suboptimal state. Why had healthful regulatory mechanisms not returned their guts to their former state?
Toxic exposures significantly increased gut viral populations.
The Gist
- A South Carolina researcher showed that toxic chemical exposures dysregulate the gut bacterial flora in a Gulf War Illness mouse model.
- The altered gut flora was associated with leaky gut, reduced blood-brain barrier integrity, endotoxemia and neuroinflammation.
- A second study examined bacteriophages – viruses which have infected gut bacteria – which are believed to be key regulators of the gut flora.
- The study found that toxic chemicals increased gut viral levels and were associated with signs of neuroinflammation.
- A Ribavirin antiviral trial returned the gut flora to normal, stopped the leaky gut, and reduced the neuroinflammation.
- The authors suggested that antivirals, perhaps in combination with other treatments, present a new possibility for rebalancing the gut flora in GWI and other diseases to normal, and combating neuroinflammation.
- A gut virome study funded by Solve ME is underway in ME/CFS.
Chatterlee’s was the first study to assess the virome in GWI illness. It surely won’t be the last.
Chatterlee found that the bacteriophages (virus infected bacteria) in the GWI mice seemed to thrive on the chemicals that so badly affected the Gulf War soldiers.
Once again, changes in the gut seemed to be associated with changes in the brain. Changes in the virome were associated with increased IL-6 levels and microglial activation in the brains of the mice.
That finding opened the door to a potential new gut treatment.
Fixing the Gut (and Neuroinflammation?)
The gut viruses may have been happy with the toxic exposure they got in the first part of the study, but they didn’t like what Chatterlee did next. Not only did Chatterlee’s use of a broad spectrum antiviral called Ribavirin reverse the changes in the gut virome, it also reduced their leaky gut, reduced their gut inflammation and even reduced the neuroinflammation found. In one fell swoop, Chatterlee introduced a new possibility for returning the guts of GWI and other diseases such as ME/CFS to health – an antiviral.
Ribavirin is mostly used to treat hepatitis C and viral hemorrhagic fevers. It’s the only effective treatment for a variety of viral hemorrhagic fevers, including Lassa fever, Crimean-Congo hemorrhagic fever, Venezuelan hemorrhagic fever, and Hantavirus infection).
An antiviral called Ribavirin restored the gut flora, stopped the leaky gut and reduced neuroinflammation.
Going to the nuclear option – antibiotics which essentially sterilized the gut – produced the same result (but would require rebuilding the gut flora.)
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”, might “form the basis of a novel treatment strategy for GWI and similar disorders.”
While this was a mouse study, it opened the door to experimentation with FDA-approved antivirals like Ribavirin, perhaps in combination with other treatments, to reset the gut flora and possibly even reduce neuroinflammation in the brain.
Given the federal emphasis on finding effective treatments for its now very long suffering veterans, you can bet that a gut treatment trial featuring Ribavirin is in the works for GWI.
Chatterlee’s study underscores the fact that one ignores the gut – and that means both the bacteria and the viruses found in it – when talking about neuroinflammation at one’s own peril.
Chronic Fatigue Syndrome (ME/CFS)
Chronic fatigue syndrome (ME/CFS) is not Gulf War Illness. Some people with toxic exposure-linked illness may be similar to GWI patients but the illness is usually triggered in other ways.
Because both diseases are symptomatically almost identical, and gut dysbiosis is present in both, it stands to reason that, like GWI, returning the gut flora – including its virome – to homeostasis using antivirals, antibacterial or alternative approaches (prebiotics, probiotics, fecal transplantation) could be helpful.
Treatment Takeaway – While no studies have assessed the effectiveness of antivirals in resolving the gut flora and its effect on symptoms in GWI or ME/CFS, the mouse finding suggests antivirals could conceivably be helpful . If the viruses in our gut are, indeed, major regulators of the gut flora, antivirals could even play a critical role. Much more study, of course is needed.
In 2017, Solve ME funded a gut virome study, and a fecal transplant study is underway in Norway. We should also be hearing much more about the gut from Derya Unutmaz soon.
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Thanks for including The Gist Cort!
So extremely helpful!
Appreciate all you do 🙂
Thanks for reminding me to do it:) Did you see the little abstract at the top – that was a great idea. We’re also going to regularly include a Treatment Takeaway section
I am a 69 yo retired RN with CFS for about 9 years. I believe there is a viral element to this disease so I have been taking L Lysine 1000 mg and Oxymatrine daily which really seems to help. If necessary I take them twice a day. Just an FYI. I manage my disease fairly well and only occasionally have big crashes after too much stress and activity.
A member of the viral subset 🙂 Thanks for passing that on.
Hi cort,
I am to ill to find the facael transplant in norway you wrote. can you help me please?
you wrote;
Norwa2017, Solve ME funded a gut virome study and a fecal transplant study is underway
also with the gut virome study. looked at the link for solve me but head must be to bad, could not find it. looked for the norway study.
Also to ill to understand is Nancy klimas for cfs now wotking on thist? the antivaral you wrote about? are there going to be clinical trials for cfs? or only for gw i or on mousmodels for gwi?
I thought that she wanted to do another combo medication trial to reset homeostasis in cfs. has she now changed her mind? do you know? she askes donations for it.
donation will come as always but now to ill tocall bank. this week I hope, end of week, a bit better.
Of course. Here’s a link to it – https://clinicaltrials.gov/ct2/show/NCT03691987 – and I put one in the blog. The 80 person study apparently began in Feb of this year and the primary completion date, whatever the heck that means, is Feb 2020. (Total completion date is 2023 :().
I think its a great opportunity: Contact numbers –
Linn K Skjevling, MD +47 97673939 linn.christin.kallbekken.skjevling@unn.no
and Peter H Johnsen, PhD +47 77015278 peter.holger.johnsen@unn.no
Dr Klimas was a co-author of the this study, but not one of the two main authors. She participated in some way – perhaps by contributing patients – but I don’t know specifically. It’s probably one of the many GWI studies that she is in some way participating in.
So far as I know Dr. Klimas is continuing on her path. She’s using treatments that her neuro-immune models suggest will work. She hasn’t incorporated the gut, so far as I know, into her models (that would take a lot of work (lol) so she’s more focused on immune and hormonal treatments.
In any case, she’s clearly fully aware of it. I don’t know if anyone at her Center is trying out antivirals for the gut, though.
What great news and article!
So looking forward to outcome on the findings..bet it will be just the ticket ?? Thanks Cort for keeping us in the loop!
Lomatium is a great help. Just make sure liver is in good detox shape to avoid dreaded rash. I’m doing good with it. Making a difference.
Issie
@ Issie
Thanks going to check it out!
Your a sweetheart..
I’m experiencing reduction of symptoms improved baseline from slow steady steps toward gut health. Dr Mark Donohoe has been treating MCS, ME, FM & CFS patients for decades. Happily, I found him & commenced probiotic treatment & dietary modifications 2 years ago. The addition of antivirals targeting the gut is very interesting.
Several years ago Dr. David Bell put me on an experimental program of daily doxycycline. While an antibiotic and not an anti-viral, it nonetheless might have helped reset my gut flora, as per this article. It did nothing, unfortunately.
I am wondering if this connects with multiple chemical sensitivities, exposure to certain chemicals triggering the sickness. My daughter found that taking bravo probiotic from Europe has helped her MCS a lot.
Nice article Cort even if, as you know, I am a deep cynic of a chronic virus perpetuating CFS!
I think you mean 30 years since the first gulf war? The moment I read 40 years I felt ancient 🙂
Right – Jeez Louise – 1990 was about 30 years ago – not 40!
After 6 months on an herbal/ supplement anti-viral protocol my CFS went away. I also added more thiamine, riboflavin and essential amino acids at the same time so can’t guarantee anything but I know a virus is at least part of my problem.
I have read that Europe is the best resource for all supplements as they dont add all the things that are added to things in the States. These additives apparently cause a “diluted” effect on what you’re supplementing with.
Did you and your daughter just choose Europe for her supplements by chance, or did you know about those studies?
I’m very interested in this for myself and my daughter who was recently diagnosed with fms and ME/CFS.
both of us have quite a lot of problems with Irrital bowel.
Hi Maschelle,
I live in Ireland and generally take Viridian supplements from the UK. I just get them in my local health food shop. Apparently they don’t have a lot of fillers. I’m very sensitive to all sorts of things and I can take them.
I have recently discovered a filler in supplements, microcrystalized cellulose, was causing MCAS issues with me. It can be saw dust from 2 different trees. One being pine that I’m really allergic to. Also a vegetarian capsule is cellulose too. So could be a potential issue.
You can get product from BulkSupplements off Amazon. I have a friend who has lab tested several of their things for purity and says they are good. You just will need either a scale to weigh or micro spoons to get proper dosage. I use the spoons.
Cort, Do you think my wife’s Dr. could prescribe Riboflavin for her to try and see if that will help her CFS/Fibro??
It depends on the doctor but in general I think the chances would not be good. Ribavirin is FDA approved but many doctors want human studies to try out new drugs.
Did you mean Ribavirin (antiviral) or Riboflavin (vitamin B2) ?
Cort,
This is a fascinating article. Not sure if it was mentioned in the article, but; the vagus nerve also interfaces with the digestive tract. If you think along the ? brain, gut, immune system axis, a lot of stuff is happening to the parasympathetic. What is driving the dysbiosis, dysfunction, and disturbances? Could it be the body’s response to a toxic exposure such as a chemical or a ?? ?
I also noticed a question in response to your article regarding how to get a doctor to prescribe ribavirin. As someone who has been able to get antiviral off label prescriptions written by doctors, I think a mutually effective communication platform between patient and doctor is absolutely essential and paramount. The doctor must have complete faith in the patient and be willing to comply with such a request out of sincere respect for the patient himself. The scientific literature a patient might bring with him to the doctor will quite often be met with skepticism when it comes to traditional medical practitioners. Basically, most doctors who are compassionate toward the patient and who respect the patient tend to think along the lines of, “well, it won’t help you but it also won’t hurt you and if it makes you feel a little better psychologically then….”
I sure do hope Dr. Skip Pridgen is successful in getting his new antiviral Fibro drug approved soon because if a drug is not FDA approved to treat a specific condition, then this only prolongs the amount of time it will take to get the majority of doctors ? to start thinking outside the ? and try a plethora of treatments.
The NIH drives the present skepticism of science. So does the CDC. They minimize the work of virologists and others who don’t prescribe to traditional thinking. Look at what’s happening to Dr. Prusty right now. I’m sorry to kind of go off on a tangent but, in a way, what I’m trying to convey is relevant and I hope someone out there is listening. ? ? ?
Oh boy, is Prusty getting some flack?
Flat earth thinking.
Haven’t some of the medical profession become very ‘precious’?
Some of these doctors/psychiatrists seem to have gone rogue. Is there no one in charge of them?
I was diagnosed a few years back by an immunologist by eliminating all 10 other possible diseases for my symptoms. As per most people with ME/CFS, all doctors and specialist I went too said something similar “there is nothing we can do for you try a dietitian sometimes that helps”. So I tried to tackle each major symptom (sleep, pain, brain, fatigue) and ignored the minor symptoms, with mixed results, mostly with small incremental improvements. For example, for sleep I used sleep hygiene, daily pacing, cbd oil, a magnesium complex powder, low caffeine, which got me massive improvements but did not fully resolve.
The last thing I tried, and I’m still working through it, is my gut. I saw a naturopath, in Sydney Australia, who specialises in gut problems. We did a breath test for SIBO and got a positive result (although I have heard there’s debate on false positives). He subscribed me natural herbal antibiotics and gradually I saw improvements, over several months. I moved from the beginning of severe end (I could get out of bed but spent 2-3 days a week mostly on the floor) to now early stages of mild (can get out of the house most days, go for gentle walks for 15min- 45min a few times a week, plus get to my classes 3 times a week. These natural antibiotics have been resolving a lot of my issues. Most days I don’t have pain, my brain is far less foggy, my PEM has improved dramatically although I am really tired all the time (what most non-ME/CFS people call exhausted!) and sleeping has dramatically improved. Also rarely do I have restless leg syndrome these days.
I’ve heard Dr Datis Kharrrazian say if you have a leaky gut you have a leaky brain. Could ME/CFS (or at least for a percentage of us) start in the gut, cause leaky gut (through SIBO, inflammatory foods, dysbiosis, parasites etc), then in turn cause the immune system to overact from the bacteria, food particles and toxic molecules from bacteria entering the blood stream, the liver becomes toxic, the brain blood barrier becomes leaky, the lungs become leaky (apparently that’s a thing) which then each has a continuous knock on affect to other different system within the body? Treating my gut has been the only thing that has given me such major improvements.
Thanks for passing that on Angelique and congrats on your success thus far and here’s hoping it continues and gets better.
Your comments reminds me that Dr. Chheda regularly finds SIBO in ME/CFS and it’s one of the first thing she treats. She does believe that SIBO and leaky gut can produce all sorts of problems including autoimmune ones. Read more about that here:
https://www.healthrising.org/blog/2019/08/26/bela-chedda-chronic-fatigue-syndrome-center-complex-diseases/
Certainly, this latest research suggests that it can either impact the BBB or through a signaling process, bypass and add to or produce inflammation in the brain.
For those interested in an herbal approach to SIBO – check out this blog – https://www.healthrising.org/blog/2014/06/25/cheaper-safer-better-herbal-approach-small-intestinal-bacterial-overgrowth/
Angelique- Since you have done all the rest, look into using Thiamine and Riboflavin and see if it won’t bust your fatigue. It worked for me! https://www.healthrising.org/blog/2013/07/05/is-simple-relief-from-fibromyalgia-mecfs-found-early-reports-spark-interest/
This whole area fits with my current belief of what’s going on with me.
Last month, November 14, Solve ME/CFS Initiative (SMCI) invited Amy Proal PhD to speak on their SMCI webinar series.
I couldn’t even begin to sum up the vast range of information she covered in her talk but I believe it’s very much related to the area being discussed in this piece.
The webinar can be found on the Solve ME/CFS Initiative website in the For Patients/Caregivers section and then Resources for people with ME and caregivers.
You then need to scroll down to a small paragraph with SMCI Webinar series written in orange lettering.
Then scroll down to the View past Webinars on Demand.
Amy Proal’s webinar was broadcast on November 14 2019 and is entitled ME/CFS in the era of the Human Microbiome…
The slides from the webinar can also be downloaded.
I would recommend a look at it, if you are able…
I missed that. Thanks for the tip!
Thanks for the great blog Cort!
This viral – gut bacteria idea seems to resonate with me.
After I got mono / EBV at the age of 20 my health started to deteriorate but only in a delayed way. I got over mono but did not take the time for a prolonged rest but rather tried to make up for the lost time and doubling efforts to try and pass university exams. I did succeed at that goal. Along the road I learned to “better” push trough exhaustion and had a few years of a sort of adrenaline driven “high” where I lived fuller then ever rather then rest and get over this likely harsh on my body period.
But after a few years I started to have increasing pain levels all over my body. Over a few years pain reached totally excessive levels but I was hardheaded enough and driven by massive adrenaline levels to push through. I tried to not let pain stop me in my track. My body reacted with ever increasing pain levels.
Then I suddenly started to switch from a person who could eat almost anything without gaining a single bit of weight to someone gaining weight very easily, something that was near impossible during all of my young age. That links with these bacteria being associated with weight gain. In its wake, I was on a slow but ever lasting cycle of declining health where I had to dig ever deeper in my reserves to get even the most basic things done. Trying to stay as functional as possible and having no idea what was going on, I kept on depleting my body this way till it halted me in my tracks when I was unable to do the most basic and minimal tasks effectively halting me in my self destructive track.
When switching to a person that gained very easily weight, I lost the sensitive gut I had since birth and that is prominently displayed along my mothers family. I was happy with it and thought I had “grown out of it”. Reality later appeared that where I used to have single episodes of bad gut reactions in my youth, I now had them so often they just blended as one continual disease state and I lost the connection between what I ate and having a strong averse reaction to it.
Less then two years ago I learned that my gut was a or the dominant part in my disease. I learned I am highly intolerant to half of what I used to eat and intolerant to about 90+% of what I used to eat. Before that I thought I was lucky to have no food intolerances at all. I just reacted to so much I wasn’t the least bit aware of it.
Improving my gut health has been an important part of my slow and ongoing health improvement. Using digestive enzymes in the form of fresh papaya and using psyllium without pre- or probiotics in stomach acid resistant capsules (to avoid MCAS against psyllium in the stomach) have been two good tools since then.
Those in fact mainly reduce (the enzymes, by allowing better absorption in the small bowel) bacterial content in the large gut and provide binding surface (Psyllium, indigestible fiber with very large surface area due to it being dust sized) for bacteria so that they less interfere with the gut wall and find a quicker path out of the body.
Another vital part of course is reducing intake of food I am intolerant too a lot. That basically sums up to avoiding the entire FODMAP series and fructose the most. It appears I have a fructose malabsorption. This provides plenty of resources for gut bacteria to grow at an explosive rate due to fructose not being absorbed by the small bowel but ending up in the bacteria rich large bowel. Some grains like wheat and worse liquid wheat (beer) are a no no too. These weaken the gut wall.
It seems I have to avoid all food helping to form a large amount of gut bacteria. I also react very poorly to any and all prebiotics (digestible fiber) and probiotics both increasing the amount of gut bacteria no matter if those bacteria are good or bad. It seems that my gut is leaky enough to have any increase in gut bacteria impacting the amount of bacteria invading my blood supply.
certainly infection by EBV virus of gut epithelial cells can play a role, but EBV is a human virus ,not a bacteriophage.
It has been postulated earlier that infection of Escherichia coli with T-bacteriopages pays a role in FM:when infected E-coli cells come into logaritmical growth phase they lyse (= burst open)and set free the bacteriophages it contains.
It are the remaining fragments of bacterial cell wall that penetrate through the gut wall and enter the bloodstream were they induce an inflammatory reaction.
afterwards a new growth cycle of E. coli begins, they lyse again etcet. Hence the often cyclic character of symptoms.
I cannot find back the reference but I remember it was from a Dutch MD who treated his patients with probiotics without E.coli. His brother published and article with electron microscope pictures showing E.coli cells from FM patients filled with T-phages.
It struck me at that time because a long, long time ago (1972) a wrote my PhD thesis on the electron microscopy of E.Coli infected with bacteriophage MS2…
Apparently FM did not prevent me becoming quite old…
Thanks ChrisB for the high quality biological information!
So back to the drawing board. From https://en.wikipedia.org/wiki/Bacteriophage I got:
“Phages of Inoviridae have been shown to complicate biofilms involved in pneumonia and cystic fibrosis and to shelter the bacteria from drugs meant to eradicate disease, thus promoting persistent infection.”
Issie can tell plenty of biofilms and how they can colonize veins and organs. With a disrupted gut wall they could hide both “in” and “out” the body or let me say out of reach and less out of reach of the immune system.
If there was a combination of a bacteria that can both live in the gut and in the veins (in or out of biofilms in both cases) and a single bacteriophage or virus that can infect bacteria that can make biofilms more resistant to cleaning up by either drugs or the immune system, that may be a very nasty combination being as hard or worse to eradicate then the formerly proposed EBV – gut bacteria combo.
If you or anybody else has some thoughts on it, please bring them on!
Also of interest: best prescription drug for me is Isoprinosine also known as Imunovir. It’s a combined anti viral and immune modulating drug.
I wouldn’t be me if I didn’t search for a plausible candidate nasty combo. So here is a quick option:
From https://en.wikipedia.org/wiki/Bacteriophage I got:
“Phages of Inoviridae have been shown to complicate biofilms involved in pneumonia and cystic fibrosis and to shelter the bacteria from drugs meant to eradicate disease, thus promoting persistent infection.”
From https://en.wikipedia.org/wiki/Inovirus I’ve got:
“Inovirus is a genus of viruses, in the family Inoviridae. Gram-positive and gram-negative bacteria (specifically Enterobacteriaceae, Pseudomonadaceae, Spirillaceae, Xanthomonadaceae, Clostridium and Propionibacterium) serve as natural hosts.”
And Clostrodium is often named by ME/FM patients.
And Propionibacterium can cause more nastiness then just creating ugly pimples https://www.ncbi.nlm.nih.gov/pubmed/22114965:
Title: “Propionibacterium acnes: infection beyond the skin.”
With content “Propionibacterium acnes is a Gram-positive bacterium that forms part of the normal flora of the skin, oral cavity, large intestine, the conjunctiva and the external ear canal.”
To make things worse: ALL humans are infected to some degree with this “benign” bacteria that sometimes isn’t (from above paper: “P. acnes may play a role in other conditions, including inflammation of the prostate leading to cancer, SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, sarcoidosis and sciatica.”).
So medical (blood) test must be made such that they *ignore* the presence of this bacteria at least to some extend.
Also, Propionibacterium is considered a commensual bacteria meaning that it doesn’t harm much but commensual bacteria are also supposed to help and train the innate immune system. That is the part of the immune system that acts early and leaves very few to no specific antigens against what it does react to. So again this would make detection more difficult.
=> So Propionibacterium could be a valid candidate to both live in the gut and inside the human body AND be prone to a virus colonizing it and form *VERY* hard to destruct biofilms in human blood vessels and even organs. And infection of gut and blood vessels by it likely would be quite difficult to detect as the bacteria is soooo common and a specific test for it might be riddled with false positives.
Please shoot any thoughts!
Thinking on this further I made me a new hypothesis:
What *IF* EBV was able to infect a part of the bacteria species in the gut? The blog clearly states that bacteria can be infected by virusses. And in Legionnaires Disease it is believed that part of the potent disease does stem from the viruses infecting the bacteria rather then from the bacteria itself infecting the human victims. If this is correct then there are viruses that can infect both bacteria and humans and can causes serious illness in humans. Now EBV is one of the most successful human viruses ever, with 90+% of human adults infected worldwide. So it may have learned this trick too.
Let us suppose it can infect a part of the gut bacteria species. EBV is a virus that has an active phase and later on turns to a latent phase. When a human is infected the human has the virus for several weeks in the active and fast multiplicating phase. Then it turns to the latent phase. Such is needed because if the virus kept multiplicating at that rate it would just kill us.
So in order to be successful the virus needs to stop spreading itself further IN the infected organism when it infected a certain percentage of cells of its host. But *IF* it also could infect certain types of gut bacteria it could infect billions of host rather then just one. Think of it. EBV gone latent in the human host but spreading as a wildfire among millions to billions of gut bacteria. Permanent EBV activation in the human body but outside the bloodstream when the gut barrier is intact. A permanent battlefield in the gut lining if the gut lining is broken.
Infected bacteria could infect part of the (B type) immune cells that try and track and destroy the bacteria invading the leaky gut lining and blood stream. Infected immune cells on their turn could destroy one and infect two invading gut bacteria, leaving the option to have a double infection path:
* Gut bacteria infecting each other and part of the B-cells that can avoid the immune system and travel throughout the body.
* B-cells that can infect the bowel and gut bacteria anew even after it has been cleansed time and again with antibiotics (doesn’t affect the infected B cells a lot), fasting, bowel cleansing procedures…
Having either EBV or a leaky gut but not both would in that hypothesis be a totally different thing then having a sizeable EBV infection when also having a leaky gut or the other way around.
This could help explain why near all humans are infected with EBV but few have ME,FM,MS… Both being present at the same time would be a strong initiating factor (for this sizeable subgroup).
This could also help explain why in so many EBV patients there is no clear EBV reactivation. Most would be either “outside” the body (the gut *bacteria*) or confined to a limited area of the body: the inflamed gut with poor blood flow due to the inflammatory effect of the disease and the strongly reduced blood flow in bowel.
EBV also happens to be mainly active in immune cells… …and epithelial cells such as the gut lining. EBV infected cells are good at increasing local oxidative stress. According to the blog that helps to make the gut leakier and allow gut bacteria to infect it better.
EBV also tends to reactivate when the body is weakened and especially when it endures a strong infection. Immune cells in the bowel (with poor blood flow) might “experience” such situation of strongly increased infection and a small (small enough to not be detected as reactivating?) but sufficient part of them might be reactivated to infect the gut lining and gut bacteria.
The older people get, the worse the impact of getting mono (EBV) usually is. In this hypothesis this could be due to kids growing at a fast rate so that the bowel repairs much faster and that the percentage of EBV infected bowel cell is constantly decreased by cell division and growth. The older an adult gets, the lower the amount of growth hormone he has.
It could also hint at why the initially succesful Rituximab study later failed. Killing all B-cells with this chemical could interrupt the cycle but may only be enough in certain subgroups of patients.
Could this interaction be close to the “ultimate” vicious circle many of us experience? Some other pathogens may have learned the same trick.
It is unfortunately a very small study, but https://www.wellnessresources.com/news/epstein-barr-virus-ulcers-inflammatory-bowel-disease-and-other-gut-disorder:
“A number of studies over the last 20 years have explored the link of EBV and inflammatory bowel disease (IBD). In one very small study, 63 percent of patients with Crohn’s disease and 60 percent of ulcerative colitis patients had active EBV infection within the gut tissue. Another study found those with active ulcerative colitis, Epstein Barr Virus had accumulated within and under the lining of the gut and within lymphocytes.”
Note “had active EBV infection within the gut tissue.” and “Epstein Barr Virus had accumulated within and under the lining of the gut and within lymphocytes.”
That is what they are thinking with post Lyme disease. They can’t detect it with test, but there is still symptoms. And with retrovirus, it is thought to invade the cells and can become a part of them. So if it’s a part of self, then self won’t recognize it and destroy self. And if it does, then it may destroy things in a wrong way, setting up autoimmune response in a negative way. So it causes all sorts of issues with a vicious never ending circle. That’s where Lomatium comes in. They have found a long course daily treatment can eliminate these type virus. The doc whose husband used it for 18 months, that told me of it, got rid of his Post Lyme issues. It very well could take care of many different types of virus. It has helped my gut tremendously and I am seeing much improvement.
de Jurgen ,
please read “bacteriophages as human pathogens” George Tetz and Victor Tetz
microorganisms 2018 June;6(2)54
lysis of bacteriophage infected cells >>>HUGE amounts of bacterial cell wall fragments>>>increase intestinal permeability>>>>phagemia (presence of pages in blood and CFS cerebrospinal fluid>>>autoimmune cascade and altered inflammatory response
also:
lysis of bacteriophage infected cells>>>release of cell-free bacterial DNA in blood stream >>>altered immune response
note: bacteriophages are the most abundant members of the gut microbiome ; the number of intestinal bacteria x 10
So I suppose when you perform a faecal transplant you mainly transplant bacteriophages
a few excerpts from the article;
In another way of indirect interaction, phages can affect human hosts through the induction of increased intestinal permeability. We were the first to show that bacteriophages could induce leaky gut and an impaired intestinal barrier with an elevated lactulose/mannitol ratio, due to a cascade of microbiota alterations finally resulting reduced Lactobacillus spp. and Feacalibacterium spp., which are important regulators of the intestinal barrier [19,20]. The phage-induced intestinal permeability was accompanied with an increase in plasma endotoxin concentrations and elevation of inflammation-related cytokines, reflecting chronic inflammation. The fact that phages have been previously overlooked as a cause of increased intestinal permeability is notable as leaky gut is a well-known trigger of various poly-etiological diseases associated with chronic inflammation and underlies the development of various multifaceted diseases, such as AD, PD, amyotrophic lateral sclerosis, chronic fatigue syndrome, diabetes, autism, and certain cancers [74,75]. Moreover, phage-induced altered gut barrier results in phagemia and the circulation of phages in the CSF contribute to phage interplay with human cells and proteins that normally are not exposed to phages.
I’m not dejurgen, but I read this. Really seems to fit in with my experience. Also fits in with the video Tracey Anne tuned me in to.
Interestingly, for years I’ve known there are pathogens and organisms that are not being detected. I was a patient of Dr. Fry and we found a fungus not only in my blood but a thyroid biopsy. And it can cause tumors. It has been found in brain tumors too. So we know it can cross the blood brain barrier. It forms biofilms and avoids detection from the immune system. How many more things don’t we know about? But, the one thing we know that can keep this down and has been shown to eliminate it from the blood is enzymes. Now whether or not this works on proteins of these organisms……I can’t say. But seems it’s possible, to me. And if there is faulty protein folding….there again, maybe this helps. Along with antivirals and rotating between 3 different combinations of enzymes…..I’m seeing improvement.
I must also mention, in my early 20s, I had a horrible lack of medical care with a ruptured appendix and didn’t get operated on until 2 years later. But due to that, and massive antibiotics and no insurance- I got life threatening colitis. I had to actually do two complete rounds of chemo to kill off all the bacteria in my body. That included the good bacteria. So coming back from that and getting my gut ecology in better shape has been a huge endeavor. But, I do feel Lomatium and these enzymes have helped more than anything else I tried.
Since I do feel virus has been a role since a young age and all other things compounded……this has been a good approach for me.
https://www.ncbi.nlm.nih.gov/m/pubmed/17584121/?i=3&from=/15377262/related
I did find an article suggesting enzymes to help with protein folding. Though couldn’t get to full article.
@chrisB: Thanks for pointing to such an important and new topic! And thanks for the clear overview in your comment! I’ve thought about it and will write at the end of this blog.
@Tracey Anne: The video is on my list. Just dragging my feet as videos and especially long and difficult videos are very demanding to my brain. So it likely will be seen in many small parts. But thanks for pointing at it!
? Yes Dejurgen go carefully – my brain sort of ended up a bit stewed, as I watched it ‘live’ and didn’t want to switch it off!
You can download Amy Proal’s slides, from her talk and then have a look at your own pace.
I find the articles/talks that are more relevant to me more difficult to process, strangely enough. I think that’s because there’s so much more information to sort through, I get a bit bogged down mentally…
Hi Dejurgen and Issie,
I think you two, in particular, would find the Amy Proal PhD Solve ME Initiative webinar, (I mentioned above) very interesting. It’s not exclusively about the Microbiome – Amy talks about bacterial, fungal and viral pathogens etc
I can’t do her justice and can’t afford to use up my mental energy listening to it again this morning, to be able to describe it to you! So please could you watch/listen to it? ?
@Tracey Anne, that’s the best video I’ve seen in awhile. Is completely in line with my way of thinking and the direction I have taken. Addressing virus with Lomatium and multiple enzymes that I rotate has been a huge step forward with me. The enzymes may address the biofilms from pathogens and the pathogens themselves. Also another thing I’m doing with tweaking histamine receptors. It ups T cell function and may in fact cause the autoimmune system to kick into gear more effectively. Then, as the presentation mention VDR receptors as possibly playing into this (and mine being genetically faulty), addressing that may help.
Since I feel a vaccine at around age 8 is what set off my (and my sister) rollercoaster, this has been a life long ride. But I finally feel I’m getting somewhere with what I’m doing. Didn’t help to add on Lyme and mold and having faulty genetics – including mitrochondria issues. And a fungus found in both blood and organs (and can cause tumors) that had not before been known to be in humans. (Work being done by Dr. Stephen Fry in that regard. He also has a lab that is detecting things previously unable to detect.) But that video addressed the mitrochondria and how it could also be compromised by virus and pathogens.
I’ll be adding to the blogs that dejurgen and I have ongoing about this in the forum here. Still a work in progress. But definitely……PROGRESS. Yayyyyyy!!!!!
Thanks for tuning me in to the video. Very glad to have heard it and the progress being made in this direction.
Oh great, so glad you got something from it Issie – I didn’t have a hope of articulating all of that! ?
I found her snowball example made sense to me, that someone could start with something, like Epstein Barr and then gather more symptoms over the years.
I am so delighted to have made progress – sometimes it feels a bit hit and miss – but at times I can actually feel completely normal ?
Yes, I heard her video and she is Spot On! It is must to listen to as she brings alot to the table that I had no clue about such as teeth..Check it out as she is teaming up with sorry cant remember his name..but he is the Vargus Nerve Dr. Van something..excuse me ..sorry Dr. but giving you and her props..??
Lora, do you think he might be Dr Michael VanElzakker?
@TraceyAnne
Yes, exactly that is him…
Thanks brainfog …
FYI: Illness and age weakens the blood-brain barrier (BBB)
This might explain why we can not consume things as before.
https://secureservercdn.net/198.71.233.129/f5o.aea.myftpupload.com/wp-content/uploads/2019/11/DRACO3.pdf
DRACO,
Great breakthrough for mankind and great potential for FM/CFS sufferers!
https://riderinstitute.org/discovery/
I was just thinking the rogue bacteriophages maybe learned the “fungus ant” trick.
ChrisB talked of “lysis of bacteriophage infected cells” above and linked it to fragmented bacterial shells and the needed immune response to it.
The paper states “In recent experiments, after oral administration of different bacteriophages in mammaliananimal models, we detected the phages in the blood, as well as increased intestinal permeability,regardless of whether bacterial hosts existed in the gut microbiota”.
That clearly points to the ability of bacteriophages to increase gut permeability. But I keep thinking that also the opposite, something like for example over-exhaustion increasing gut permeability can improve the chances for rogue bacteriophages to settle in.
As such, an increased presence of bacteriophages at a time where another factor increases gut permeability could create a far stronger assault to the body and may create a crippling run-away effect (like switching from healthy to chronically very ill after an ME-type hit and run infection with for example the flu).
So I think that a badly damaged gut interface has both a strong causing and perpetuating effect increasing the power of these rogue bacteriophages a lot. I mean, take these bacteria with their bacteriophages and over time in a remotely healthy person given diet changes, fasting, drugs, action of the immune system, supplementing with probiotics (not all strains are equally vulnerable to a single strain of rogue bacteriophages)… it should fade out. If not, why are so many healthy people not affected as in their guts being dominated by these rogue bacteriophages?
The gut mircobiome, if healthy, is largely regulating itself it seems. So it should be capable to self regulates those baddies. But it fails for ever with us.
It seems the perpetuation of this condition depends upon the gut barrier be broken and or there to be a strong immune reaction. And here comes in “lysis of bacteriophage infected cells”.
A large subgroup of virusses spreads through lysis or in plain words by first multiplying and accumulating in a cell and then letting that cell “pop and burst” so to release and spread its thousands or more viral particles. When that happens in the body, the immune system tries and cleans them up. But what if it happens right at the edge where the immune system largely splits between being very active and leaving it up to the gut microbiome to self regulate.
So lets get back to the “fungus ant” trick. There is a certain fungus that grows in the brain of (certain species of) ants. When the fungus “reaches adulthood” it is able to “force” the ant to climb up to a high and open position like going to the end of a branch. The fungus then kills the ant there and the fungus grows out of the head of the ant. The fungus then forms sort of spore rich branches growing vertically up and those are in an ideal situation to be spread further by the wind to new victim ants.
So this fungus doesn’t need individual ants to live and survive. It needs them to die at the opportune moment. It actually needs to kill it’s host to survive and needs to get them to the right location before killing them.
Now back to our gut bacteria and bacteriophages. How to spread quicker as a gut bacteriophage then other competing bacteriophages? If you are of the “spread through lysis type” then get the bacteria you live in to kill itself once you reach maximum viron content in the bacteria you live in.
But how to speed up the process? Note that in competitive species like bacteria and viruses a small difference in spreading speed easily can make a huge difference in dominating or failing to do so.
Killing it is one thing but if it goes in lysis too late then other bacteria and bacteriophages “ate their lunch” before them. So speed up the process and reprogram the bacteria you live in to commit suicide by “driving straight into the frontline of the battlefield”. Or in other words: let the bacteria seek out classic immune indicators like increased ROS, HClO, antigens, cytokines, whatever. Just let the bacteria track, follow and crash into the immune system like a heat seeking rocket tries to track, follow and crash into a plain by following its key signal, the heat of its engines exhaust.
So: once the bacteriophages filled the bacteria to the max with virons, reprogram it to crash into the immune hot spot and let the immune system do its work and destruct the “hull” of their ride. In our gut: just drive it in and through the cracks of our leaky gut and let it crash and stick there. Even better, if possible override the bacterial defense system to so it even gets killed quicker.
So why doesn’t the immune system just disables the virons? Well, it likely does try and remove all those that try and get into the blood stream. Or those that linger too long around the crash zone. But even if 90% of them is disabled that way, the remaining 10% can escape to the gut where they are largely out of reach of the immune system and can infect new young virgin bacteria and do the same trick all over again. That’s just millimeters away, a bit like criminal border gangs use border hopping to steal in villages near the border and get back over the border again where they are safe of pursuit from cops from the country they committed the crime in. Police officers have to stop at the border. The criminals don’t care if they can pass.
Even if their virons are destroyed ten times more then that of competing bacteriophages, if they can manage to lyse and spread two or three times faster then their competition they may outnumber their competition over several generations. Or in other words each time you go from fasting to having new food in the large bowel.
That trick of crashing the infected bacteria in the damaged gut wall would also challenge the immune system to carpet bomb that zone and to increase the number and size of cracks and leaks in the gut where their next generations can crash into again and again. That would perpetuate and lock in the following:
rogue bacteriophages infecting bacteria – infected bacteria crashing and self destructing at young age in the damaged gut wall – provocation of the immune system to carpet bomb the gut wall – maintenance and increase of damage in the gut wall as side effect of the immune effort – rogue bacteriophages dominating at the site where they multiply very quickly and can dump more then enough of their viron load in the less rigorously protected gut to continue the vicious circle.
It could even explain why our blood volumes are so low. How to best decrease the amounts of virons escaping back to the gut? Physically there is near no better trick then to create an under pressure. That way blood and liquid tends to flow inwards in the body rather then outwards. Most often, the body tries to prevent infection of wounds by creating an outflow of blood so that bacteria and viruses get washed away. But here the opposite could work far better: draw those viruses in the bloodstream so that they can be destroyed by our immune system. Force them to “swim against the current” if they want to “escape” to the gut, the “free zone” where they almost can multiply at will.
This hypothesis of rogue bacteriophagues crashing into the gut wall to get their host bacteria’s shell quicker dissolved so that they can release their viron load and multiply quicker then their competition may link to a few ME ideas / observations:
In case lower blood pressure indeed helps protect the gut against these rogues (at the cost of a high influx of inflammatory stuff):
* Many mainly FM people are quite sensitive to weather pressure changes. At low pressure they get worse. Under this hypothesis, small weather pressure changes would make this hypothetical “under pressure protection mechanism” quite a bit less powerful as the lower air pressure with equal blood pressure would reduce the small pressure difference between the two to a large degree.
* Hyperbaric oxygen therapy has shown promise in small scale ME trials. Next to easier providing oxygen, the therapy obviously provides more pressure empowering this hypothetical “under pressure protection mechanism” strongly while being in the high pressure environment.
* Circulation exercises have helped me quite a bit. They allow for better blood flow to many parts of the body. Or they allow for lower blood pressure while maintaining the same amount of blood flow. Lower blood pressure with equal air pressure strengthens this supposed mechanism too.
* High blood pressure is know to correlate well with many inflammatory diseases and many of these diseases correlate will with poor gut wall quality.
* Conditions of prolonged high oxidative stress cause RBC to become less flexible and reduce blood flow for the same blood pressure or in other words require higher blood pressure for the same blood flow. High oxidative stress also helps degrading gut wall quality and depleting the bodies anti-oxidant defenses against it. By the effect of degrading gut wall quality, high oxidative stress like in long lasting overexertion or a short-ish strong body wide immune assault like having a bad flu could increase chances of getting ME/FM… a lot. The ability of EBV to colonize epithelial cells (gut wall) and to let these cells produce more ROS could explain why adult mono people are more vulnerable too.
Looking at using antivirals, reducing the number of virons in the gut shifts chances for better multiplication to slower dividing cells that have most of their virons alive away from those dividing a lot quicker but losing the bulk of their virons in the blood stream.
Looking at digestive enzymes, if they show still enough activity in the large bowl:
* They may further reduce the number of virons, see above.
* They may help speed up breaking open the bacterial shell of old and deceased “friendly” bacteria – bacteriophage combinations in the gut, decreasing the difference in multiplication speed again favoring the multiplication of friendly bacteria – bacteriophage combinations versus the rogue ones.
The good news? If the above would be in effect, it shows that the gut content can be altered quite quickly even without fecal transplants. Weather pressure changes act quickly and using papaya gave me remarkable results within a single week topping out at two weeks. Better understanding the underlying process and how to steer it may yield worth full results.
I know in my case, using Lomatium as my antiviral and rotating between 3 different combinations of enzymes……I’m much further ahead than I’ve been in years.
Even seeing lipomas be dissolved that have been there for 30 years. Hoping that if these enzymes affect the fungus found in my blood and organs (that can form tumors)…..they too may dissolve those tumors in my body too. (I have many on my thyroid, kidney and a brain tumor. So I really want this to work.)
This combination addresses biofilm and proteins and also a way to kill virus and other pathogens. I’m finding my gut to be in better shape than it’s been in for many decades now.
de Jurgen
just a small comment: I don’t think bacteriophages compete that much with other bacteriophages. But they are committed in a constant struggle with their hosts, the bacteria: they mutate constantly -bacteriopages and bacteria so that they can invade/ escape.
Note that there is also lysogenic growth whereby bacteriophages escape in smaller numbers through the -intact-bacterial cell wall.
@Issie
Can I ask what 3 enymes u are using?
PS. Were u ever on Prohealth blogs? I was and seen a Issie there that was always commented as well as I did..
I may have commented once or twice there. I’m mostly here and on DINET site. Have random comments here and there.
The main enzyme for biofilm and the fungus is Serrapeptase.
Also use Vascuzyme by Empirical labs and Repair by Enzymedica.
I rotate these three daily and take 2 to 3 times a day away from food.
I forgot two of the most important ones.
I use this one with lutolin in the morning as it gives energy.
Mirica® Palmitoylethanolamide… https://www.amazon.com/dp/B078VW2CQ1?ref=ppx_pop_mob_ap_share
And this one without lutolin at bed. Both help pain and build up to work more over time. I’m off all my POTS, MCAS and pain meds. For 3 months now.
Ergomax – Palmitoylethanolamide -… https://www.amazon.com/dp/B071HVC8PW?ref=ppx_pop_mob_ap_share
Yes, it’s viral. My 22-years with ME/CFS is slowly and steadily healing thanks to the books and free recordings from Anthony William, Medical Medium. He’s been teaching for decades that it’s viruses—mostly from the now over 60 strains of Epstein Barr; which are undetectable via medical tests and live deep in our organs and brain.
He was the first to tell the world the cause of ME/CFS and many, many more diseases.
The treatment? Life-changing foods and herbs and minerals and supplements (which he doesn’t sell, btw). And also by eliminating the foods that feed the viruses. Yes, viruses eat food; they then release neurotoxins that make us sick.
I have been so busy with work and the holidays that I missed this post and an opportunity to, once again, mention the remarkable recovery in symptoms my daughter has had each time she has taken Tamiflu. Although Tamiflu is an antiviral, it appears to inhibit certain pathogenic bacteria.
https://veterinarypartner.vin.com/default.aspx?pid=19239&id=4952180
My daughter is not the only CFS patient to report remission of symptoms with Tamiflu.
This was posted on a CFS thread.
” The doctor who diagnosed the influenza immediately put me on Tamiflu, which I took for ten days. I honestly felt better on Tamiflu than I have in years. By day three of the Tamiflu course, after being bedridden and sick with very high fever and some of the worst body pain I’ve ever experienced, I was full of energy and strength. I did things that haven’t been possible for me for years, like take down and pack up the Christmas tree and lift the entire thing and haul it out to the street alone. I traveled across the country alone with my daughter and felt fine the next day, even energetic the same day I got home, unpacking and doing more chores. I even wanted to exercise. This level of physical exertion would normally have me, at best, resting for a few days to recover. More than likely they would result in a full week of pain and exhaustion before finally returning to “normal bad”. I was wondering how Tamiflu might fight in your model? Or, if you think that its effects aren’t microbiome related, that I may see more health gains by pursuing and possibly even rotating antivirals.”
We have heard of another case that has had the same response.
A French company has bought the rights from Roche to put Tamiflu on the over-the-counter market. We are not sure how long that will take. In the interim, Tamiflu was originally made from “star anise” an aryuvedic plant that has been used for thousands of years. Star anise has a licorice taste and makes a tasty tea or you can grind it and put it in capsules. (You should always take it and/or Tamiflu with food.) It has antiviral and antibacterial properties, but has not as worked as quickly as Tamiflu did for my daughter.
Unfortunately, it is difficult to get doctors to prescribe Tamiflu off label to see if a longer trial would eliminate CFS symptoms permanently.
CFS and GWI both symptomatically virtually identical? That is utter nonsense. Please edit this – there is little similarity except in how patients are treated by many doctors.
Both are diagnosed based on symptoms rather than a biomedical test, so obviously they are not sympathetically identically.
GWI is not classed as a neurological disease, unlike ME and CFS.
The article here is reaching so far behind what has been established, and what may be the case – including theories that have previously been considered but found not particularly relevant.
Given the cause of GWI is not fully known, any mouse model is highly suspect. There will never be a mouse model for Chronic Fatigue Syndrome since it does not occur in mice, a few references to animal models exist but they are solely based on chronically fatigued rats who were tortured by being repeat forced to swim until exhaustion (or drown).
There is no confirmed link between leaky gut or digestive symptoms and the cause of CFS – a minority have severe digestive symptoms but those may be the result of neuroinflammation or other issues rather than a contributor. Mitochondrial and blood plasma testing from the Severely Ill Big Data study does not appear linked to this.
Anti-virals *including this one* have proved ineffective. Chia’s trial of rivavirin showed patients who did improve relapsed and it wasn’t taken further. And only those with a viral trigger to their illness took part.
Ribavirin and Interferon-α for the Treatment of Patients with Chronic Fatigue Syndrome Associated with Persistent Coxsackievirus B Infection: A Preliminary Observation. https://pdfs.semanticscholar.org/efa7/e33bd109ec4e17e1f71f7b07ee5e37c7f04a.pdf
I will stick with Nancy Klimas – GWI and ME/CFS researcher and doctor – on the symptom issue.
The consensus regarding GWI is that a combination of vaccines, toxins and stress proved overwhelming.
It’s not necessary for a disease to exist in mice for mice to be used as models. Researchers for instance often manipulate mice genetically to create mouse models.
Check out Lipkin’s work for a strong indication of gut subset. Given the many advances being made in gut engineering it would be foolhardy to abandon the gut manipulation as possible treatment avenue. See the recent fecal transplant study published in the UK.
Chia’s conclusion to that study was “These results suggest that chronic CBV infection causing symptoms of CFS may be amenable to antiviral therapy. The change of neutralizing antibody titer to CBV may be a good marker of therapeutic response”.
Any antiviral therapy directed at the gut would also presumably be boosted by other gut treatments such as fecal transplants, probiotics, prebiotics…