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Foremost Virus Hunter Finds Biomarkers, Few Viruses in Big Chronic Fatigue Syndrome Study

Dr.Ian Lipkin collaborated with Dr. Peterson, Dr. Klimas, Dr. Bateman and others

A Surprise Presentation

We will publish data very soon on biomarkers of cytokines. Our evidence now suggests there is ongoing stimulus to the immune system. Dr. Ian Lipkin

You don’t usually get study results in talks like the one put on by  the CDC yesterday but this time Dr. Ian Lipkin spilled the beans on the results from the big pathogen studies sponsored by the Chronic Fatigue Initiative (n=200) and Dr. Montoya (400).  (From notes taken on the talk)

Virus Study Results Revealed

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The Simmaron Foundation provided a rare resource: sixty cerebral spinal fluid samples

Viruses have always been the elephant in the room in ME/CFS; everybody has wondered about them but until the Chronic Fatigue Initiative came along, few major studies had been done.  This landmark  study, using the one of the top virus hunters in the world and epidemiologist  Mady Hornig, and containing hundreds of patients from ME/CFS specialists (Dr. Peterson, Klimas, Montoya, Levine, etc.) from across the country, sets a benchmark for pathogen research in ME/CFS.

A special feature of the study involved Simmaron Research’s spinal fluid samples. Called a ‘unique resource’ earlier by Dr. Mady Hornig, these samples allowed the researchers to get as close to the brain – long thought to be a key area in chronic fatigue syndrome – as they could.  And the spinal fluid results were spectacular.

The Studies

virus cartoon

This study funded by the CFI, using top labs, and involving hundreds of people with ME/CFS, is a benchmark in ME/CFS research.

The studies looked at both pathogen presence and  the immune response in hundreds of people with chronic fatigue syndrome.

Pathogens

  • First Phase – Screens for 18 specific pathogens already implicated in ME/CFS (herpesviruses, HTLV, enteroviruses, West Nile Virus, etc.) were done on blood from Montoya’s patients and the CFI’s group (Dr’s Peterson, Klimas, Bateman, Levine, etc.).  Dr. Lipkin was looking for the virus, not a indication it was present, but the virus itself. Any finding of a virus in the blood would indicate it was active.  The same screen was done on Dr. Peterson’s sixty spinal fluid samples.
  • Second Phase – The second phase involved sequencing all the DNA/RNA in the blood to identify  known and unknown viruses. Dr. Lipkin’s lab has been able to identify hundreds of novel viruses using this technique.
  • Third Phase – Any finds in the second phase are confirmed/denied by more accurate testing.

Immune Response

A ‘multiplexed immunoassay’ looked at 50 proteins associated with immune activation/inflammation and oxidative stress.

Active Viruses Strike Out

Four of the 285 ME/CFS blood  samples tested positive for HHV-6B.  One of the sixty spinal fluid samples tested positive for a virus (HHV-6B).  None of the other viruses commonly associated with ME/CFS (Epstein Barr-Virus, enteroviruses, the cytomegalovirus, etc.) commonly associated with ME/CFS showed up in the first pathogen screen.

The high throughput screening designed to look for any viruses including novel viruses drew a blank as well. Dr. Lipkin was confident in his results stating his lab had found over 500 new viruses using this technique.

Infections

Lipkin’s search for 18 viruses and for novel viruses in hundreds of people with chronic fatigue syndrome largely turned up empty

The  news – that fewer than 2% of patients  with infectious onset – tested positive for viruses in the blood was stunning but not without precedent.  Dr. Unger reported earlier that  the first stage of the CDC’s BSRI pathogen study  drew a blank.  A spinal fluid study also turned up no viruses, and PCR analyses done by the Dubbo group were unable to find evidence of a virus in their post-infectious cohort.

With two large sample sets turning up negative in the lab of one of  most acclaimed virus hunters on the planet, it’s probably safe to say that the hunt for an virus in the blood of people with ME/CFS is over.

(Lipkin did report 85% of pooled samples possibly showed evidence of a retrovirus but believes they will not be related to CFS. He also dismissed earlier rumors that a novel infectious agent had been found.)

Infectious Agent Still Proposed

That doesn’t mean an infectious agent is not involved. In  fact, Dr. Lipkin stated he didn’t doubt that an infectious agent was involved.  He didn’t say where and he didn’t say it was still present.  His allusion to the importance of finding evidence of a past infection (“researching the shadows”) suggested  he could  be leaning to the ‘hit and run’ hypothesis where a pathogen sweeps in, does its damage, and then gets removed by the immune system.

The Dubbo studies’ finding that high cytokine levels early in the infection were strongly associated with getting ME/CFS later on suggested an overactive immune system may have a blown a few fuses somewhere.

On the other hand, Dr. Lipkin specifically alluded to an ‘agent’ driving the immune activation he found in both the blood and spinal fluid of ME/CFS patients (but not the healthy controls).

Localized Infections Still Appear to Be a Possibility

Dr. Lipkin didn’t discuss this possibility. The blood is the most convenient place to search for an virus and active viruses usually do travel through the blood but central nervous system or localized infections may not show up in the blood or the spinal fluid.

Some evidence of localized infections in the gastrointestinal tract has been found in ME/CFS. A De Merileir team found evidence of HHV-6, EBV and parvovirus B-19 in 15-40% of gut biopsies. Eighty-two percent of stomach biopsies tested positive for a protein associated with enteroviruses in Dr. Chia’s 2008 study. Dr. Chia reports enteroviruses are found much more readily in the stomach than the blood (but he is able to find it in the blood). No enterviruses were found in the present study.

Vanelzakker proposes that a localized vagal nerve infection is causing the symptoms in ME/CFS.  It’s not clear what these results mean for Dr. Lerner’s theory that an aborted EBV infection is spilling viral  proteins into the blood that are sparking an immune result.

The Three Year Breakpoint 

Data suggests there may be substantial differences in biomarkers in people with less than 3 years of disease and those with more than 3 years of disease. Dr. Lipkin

subsets

Two recent research findings suggest the immune systems of people with recent onset and longer duration ME.CFS are significantly different.

Echoing similar recent findings from the Broderick/ Klimas team at NSU, Dr. Lipkin stated the immune system in ‘newbies’  (patients with recent onset), and patients with a longer case of  ME/CFS was different.  Dr. Lipkin’s ability to independently differentiate ‘newer’ from ‘older’ patients using  cytokine results is pivotal, and points to the central and progressive role the immune may play in this disorder.

With Broderick suggesting that two distinct illnesses emerge over time, and Lipkin proposing treatment options should reflect illness duration, it was clear these changes were significant indeed.

Natelson, on very different track, is finding changes over time as well with more POTS in his adolescents and a different kind of orthostatic intolerance in older patients.  Studies are underway to understand why this might be so.

An Early Allergic Response

Allergy is not usually mentioned in association with ME/CFS but eosinophils and other markers suggested to Dr. Lipkin that  the allergic response was enhanced in ME/CFS early on. The cast of immune characters Lipkin’s biomarker search fleshed out was refreshingly familiar with IL-17, IL-2, IL-8 and TNF-a leading the list.

IL-17

Levels of Il-17 were raised in recent onset ME/CFS patients. Lipkin suggested immunomoculators able to bring IL-17 levels down might be a treatment option at some point.

No mention, interestingly, was made of autoimmunity, but Lipkin, pointing at the high IL-17 levels in the newbies,  embraced the idea (only after further validation) of using immunomodulators in some ME/CFS patients  to turn down the fire in the immune system.  Immunomodulators exist now, he said, that can bring that IL-17 cytokine  down.  (He stressed, however, that there is not enough research to start using them on patients.)

The spinal fluid, interestingly enough, showed a very different pattern. It showed a consistent profile of immunological dysregulation in CFS, regardless of duration of illness. Dr. Lipkin identified increased IL-10 and IL-13 levels suggesting enhanced Th2 activation and increased IL-1B, IL-5 and IL-17 suggesting Th1 (proinflammatory) activation. Dr. Lipkin was obviously intrigued by the differences in cytokine findings between spinal fluid and blood.

A Focus on the Gut

I think the gut microbiome is going to be where the action is (in chronic fatigue syndrome). Dr. Ian Lipkin

Lipkin’s prime focus at this point is the gut and fecal matter. He  believes the gut microbiome is going to play a, perhaps the key role in ME/CFS.

The Hornig/Lipkin team has had considerable experience with the gut microbiome. They’ve been successful  finding gut abnormalities in autism, a disorder that shares some intriguing commonalities with ME/CFS, including low natural killer cell functioning.  Noting that the gut can modulate immune functioning, not just in the gut, but across the body he asserted the gut is going to be ‘where the action is’ in ME/CFS.

gut picture

Lipkin believes ‘the action’ in ME/CFS is going to take place in the gut microbiome (flora)

Unfortunately, the fecal samples originally collected didn’t provide enough material for analysis so they’re restarting that part of the study.

Even more unfortunately, characterizing the bacteria in fecal matter is extremely expensive and with Lipkin, with just 10% of the money needed to do the job, evidenced considerable frustration at having his hands tied  by lack of money.

Stating that he was not pointing fingers, he then proceeded to point  them everywhere:  at federal politics of funding, at NIH budget cuts, and at the paucity of research funding in our field. As at his last public talk, he urged patients to get active and enlist their congressman in  their cause.  Oddly enough, he also said Dr. Fauci, long considered a kind of ME/CFS nemesis by patients, was supportive of more work in this area.

Reiterating his belief that chronic fatigue syndrome has pathophysiological roots, Lipkin noted his history with it. Dr. Lipkin’s 1999 ME/CFS  study did not find the virus he was researching but it did find a great deal of immune (polyclonal B-cell) activation, a pattern that was recently repeated when he didn’t find XMRV but was impressed by the evidence of immune activation he did find.

Next Up

Lipkin, in close collaboration with his ME/CFS experts, Dr. Peterson, Dr. Montoya. Dr. Klimas, Dr. Komaroff, etc. is following these results with deep sequencing of samples, completion of fecal matter analysis and larger studies to confirm and deepen the understanding of cytokines as biomarkers. Protein analysis was not mentioned but it was part of the original project. Tracking down evidence of past infection was also on the agenda.

Conclusion

The Chronic Fatigue Initiative’s pathogen study set a benchmark for rigor and size in the ME/CFS research field, not the least because of Dr. Lipkin’s leadership. Surprisingly few viruses were found in the blood of ME/CFS patients, yet Lipkin asserted that an infectious agent was likely driving the immune activation he found in the blood and spinal samples.  Cytokine analyses of the blood suggested a different pattern of immune dysregulation was present in  newer onset patients (<3 years) and patients with a longer duration of illness.

Dr. Lipkin believes the “primary cause is likely to be an infectious agent” and the gut microbiome is where ‘the action’ will be in ME/CFS.

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48 Comments

  • Chanda

    September 11, 2013 at 7:22 pm - Reply

    Wow great article!!! I listened to the phone conference and was very impressed with Dr. Lipkin. So are they still going to try and look at the gut and fecal matter?? Or are they out of money?

    • Cort Johnson

      September 11, 2013 at 7:32 pm - Reply

      Thanks Chanda and thanks to Courtney for her help with the blog…

      The fecal matter was always intended to be part of the study but Lipkin says he’s only got about 10% of the money he needs to study it. If you think about it 400 plus samples is alot of sh….fecal matter :). I don’t know what he wants to do; if he wants to go beyond the original study projections, but its clear he needs more money…

  • floydguy

    September 11, 2013 at 7:39 pm - Reply

    Lipkin also mentioned what I thougt was high FGF. I’ve never heard this mentioned before. Can you elaborate? Sounds related to the IL-17 and maybe TGF Beta that has been mentioned in the past.

    • Cort Johnson

      September 11, 2013 at 7:49 pm - Reply

      I don’t know…The sound was not great in my little cell phone. Could it have been TNF-a? Or maybe it’s TGF B – that might make sense. There is an FGF called fibroblast growth factor (FGF) but it doesn’t really seem to fit. http://en.wikipedia.org/wiki/Fibroblast_growth_factor

      • floydguy

        September 11, 2013 at 7:59 pm - Reply

        Cort,

        Around the time he was talking about the spinal fluid he said the only difference between classic cfs patients those who go on to develop other diseases (such as lymphoma) was increased FGF beta (I think that’s what he said). If anyone heard this differently I’d appreciate hearing what they thought he said.

        Thanks.

        • Cort Johnson

          September 12, 2013 at 12:53 am - Reply

          That part got garbled for me. I missed the entire differences in lymphoma patients part.

  • Eric

    September 11, 2013 at 8:06 pm - Reply

    There’s one other finding he mentioned, even though I don’t know how important it is. He said they found anellovirus (I think that’s what he said) in 3/4 of the sample pools or so. I’ve never heard this virus mentioned before.

  • Guido den Broeder

    September 11, 2013 at 8:09 pm - Reply

    Finally some systematic research is getting done. The outcomes so far are as expected, that is our disease model of ME still lives. :)

  • Dr. Gregory G Cutler

    September 11, 2013 at 8:22 pm - Reply

    Again, we need to organize a national write in campaign to our representatives to get support for Dr. Lipkins Fecal Study! Make them get money to this Internationally recognized figure to help our cause!

    Greg

    • Cort Johnson

      September 12, 2013 at 12:52 am - Reply

      I agree!

      • Dr. Gregory G Cutler

        September 12, 2013 at 2:32 pm - Reply

        How can we go about organizing such a write in campaign?

  • Otis

    September 11, 2013 at 9:24 pm - Reply

    I’ve listened to a recording, specifically the part speaking about retroviruses, and Dr. Lipkin clearly says that they were found in Dr. Montoya’s samples and apparently only his samples. “I’m going to be very clear in telling you although I’m reporting this at present in Professor Montoya’s samples neither he nor we have concluded that there’s a relationship [of the retroviral sequences] to disease”

    • Stephanie

      September 12, 2013 at 5:39 pm - Reply

      Can you tell us where this recording can be found?

  • Skepticon

    September 11, 2013 at 9:39 pm - Reply

    Thanks for the article. A couple points – you said “With two large sample sets turning up negative in the lab of one of most acclaimed virus hunters on the planet, it’s probably safe to say that the hunt for an active infectious agent in the blood of people with ME/CFS is over.” It sounds like he looking for viral DNA/RNA, then that doesn’t rule out any other kind of pathogen in the blood. Also, it’s always a mistake to declare a search like this over based on one study that is thought of as definitive. Technologies are not perfect, neither are single studies, and the results of this study would still have be confirmed in a different cohort. I’d say it adds to the evidence against a virus circulating in the blood is responsible for ME/CFS, but like you said the local infection issue is a big one.

    Also – “Eighty-two percent of stomach biopsies tested positive for a protein associated with parvovirus B-19 in Dr. Chia’s 2008 study.” – don’t you mean “enterovirus” there? Chia describes VP-1 as “Enteroviral capsid protein 1″ in that study.

    • Cort Johnson

      September 12, 2013 at 12:32 am - Reply

      You’re right I should have said virus and enterovirus. Thanks for the heads up. Technologies will certainly improve in the future but I would be surprised if we see any studies devoted to looking for viruses in the blood in ME/CFS for quite a while.

      It took a new non-profit with a substantial budget to produce this one. Now that Lipkin, of all people, hasn’t found viruses using two powerful techniques I’d be shocked if anyone in the ME/CFS field will be devoting precious resources to this hunt when so many other possible avenues are present.

      • Rob

        May 28, 2014 at 7:41 pm - Reply

        I am not surprised Dr. Lipkin didn’t find any viruses in blood samples. Is he planning to continue search for viruses in tiissue samples (gut, muscle, nervous tissue). I am sure you wouldn’t find Herpes Zoster virus in blood samples of patients who have Shingles. Does that mean Shingles is not triggered by reactivation of Herpes Zoster virus in nervous tissue.

        I am not a virologist, but my understanding is that it is very difficult to test for latent viruses in tissue samples.

        I hope his research continues and perhaps we will have a better understanding of physiology of CFS/ME in the future. Is it viral persistence, immune dysfunction or perhaps both?

  • FancyMyBlood

    September 11, 2013 at 10:06 pm - Reply

    Thanks for the excellent summary Cort!

    I’m intrigued by Lipkin’s microbiome research proposal. To my knowledge there was nothing in his talk that implies the microbiome is involved (maybe the cytokine findings fit that theory though?), so I’m kinda missing his explanation to pursue this avenue.

    On a related note, have you heard anything about Unger’s and Miller’s basal ganglia research? There hasn’t been anything published yet and I believe this is THE single most important research going on at the moment. I’d be kinda dissapointed if this doesn’t get published or followed up.

    • Cort Johnson

      September 12, 2013 at 12:51 am - Reply

      I got the microbiome quote from the meeting; the sound was not so good so it was easy to miss things. In fact it cut out completely at one point.

      You’re right – the Miller basal ganglia paper has NOT been published. He’s a fascinating researcher. Here’s one he did on basal ganglia and cytokines! Right up our alley.

      http://www.ncbi.nlm.nih.gov/pubmed/23000204

      Front Neuroendocrinol. 2012 Aug;33(3):315-27. doi: 10.1016/j.yfrne.2012.09.003. Epub 2012 Sep 21.
      Cytokine effects on the basal ganglia and dopamine function: the subcortical source of inflammatory malaise.
      Felger JC, Miller AH.
      Source
      Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA.
      Abstract
      Data suggest that cytokines released during the inflammatory response target subcortical structures including the basal ganglia as well as dopamine function to acutely induce behavioral changes that support fighting infection and wound healing. However, chronic inflammation and exposure to inflammatory cytokines appears to lead to persisting alterations in the basal ganglia and dopamine function reflected by anhedonia, fatigue, and psychomotor slowing. Moreover, reduced neural responses to hedonic reward, decreased dopamine metabolites in the cerebrospinal fluid and increased presynaptic dopamine uptake and decreased turnover have been described. This multiplicity of changes in the basal ganglia and dopamine function suggest fundamental effects of inflammatory cytokines on dopamine synthesis, packaging, release and/or reuptake, which may sabotage and circumvent the efficacy of current treatment approaches. Thus, examination of the mechanisms by which cytokines alter the basal ganglia and dopamine function will yield novel insights into the treatment of cytokine-induced behavioral changes and inflammatory malai

  • Rhonda beech

    September 11, 2013 at 10:18 pm - Reply

    my problem is I got sick post viral sudden onset and was sick for 2 years.
    then well for 5 years and got sick again post virally.. different type of virus and am still sick 13 years later.
    I wish they had done some immune testing when I was actually sick.
    I had very high esr. opposite to what others say. I also had 3% nk cells . other cells were affected and out of kilter.
    t cells . b cells t suppressor cells. extremely high ANA
    now it seems all these are normal. I have done gene testing nothing showed up.
    So I would think it has more to do with immune lack of response. over responding. or faulty immune system.
    I am not sure . I am not a doctor

  • Esther Siebert

    September 11, 2013 at 10:46 pm - Reply

    My personal experience getting a dramatic improvement of my CFS symptoms from the long-term use of Xifaxan 550mg 2-3X/day for more than two years now leads me to believe Dr. Lipkin is right about the action being in the gut microbiome. Other ME/CFS doctors have been experimenting with Xifaxan but from my information use it only for the short term, maybe anywhere from 10 days to three months before discontinuing it–even when the patient gets great improvement on it and relapses after going off of it. I was given 3 short courses, getting dramatically better within several days on it and getting worse each time I went off of it. It is used on a long-term basis for hepatic encephalopathy (I think it is called) which I discovered doing my own research. So I asked my gastroenterologist to have it on a maintenance basis. Somehow, a fluke apparently, my insurance is paying for two pills a day which I have to supplement by taking 3 pills a day from time. Now I take 2 pills one day and 3 pills the next. I have IBS and SIBO which when untreated allows the overgrowth of bacteria to send toxins to my brain causing a lot of my CFS symptoms. I’m hoping that the work done by Dr. Mark Pimental at UCLA/Harbor General which definitively through stomach tissue samples shows the link between IBS and SIBO will ultimately result in the FDA approving the use of Xifaxan for IBS and SIBO. I am a lay person and I don’t know how to get the word out on this to researchers and CFS doctors effectively. But I am encouraged to see Dr. Lipkin is on the right track. I will consider a fecal transplant to see if by changing my gut microbiome I can go off of Xifaxan,which causes me no side effects. If anyone can help me communicate my success to scientists, I’d appreciate it so much. Discovering the Xifaxan works for me was a fluke as was getting it covered by insurance; I’d like to see this help others as well. My illness began with a documented EBV infection and I’ve been ill for 27 years. Xifaxan is incredibly expensive, out of pocket 3 pills of 550 mg is almost $2200.00 a month. I’d be happy to discuss my experience and be tested to see if this could help others. It breaks my heart when I talk to patients who do well on the Xifaxan, only to have the doctor take it away. If you have SIBO, the problem can be ongoing and needs to be treated continually to prevent the reoccurrence of bacterial overgrowth. Why it reoccurs in us when maybe in others a short course treatment solves the problem, I suspect, has to do with our incompetent immune systems. Cort, I’d appreciate any suggestions you have.

    • Cort Johnson

      September 12, 2013 at 12:44 am - Reply

      What a story Esther. Congratulations on getting better. The gut is getting more and more interesting!

  • R.A.Perill

    September 11, 2013 at 11:49 pm - Reply

    It’s all in the gut, the last frontier!
    I just returned from a few days in the hospital, due to acute renal failure, brought on by a “cleanse” of the gut that released so much toxin that my prostate swelled so to the point, it cut of my urine flow, which backed up to my kidneys!
    This can be lethal. RP

    • Cort Johnson

      September 12, 2013 at 12:41 am - Reply

      That’s a heck of alot of toxins…You’ve got a loaded gut there!

      • R.A.Perill

        September 12, 2013 at 4:04 pm - Reply

        Yes Cort, a heck of a lot of toxins. Primarily “ACETALDEHYDE”, one of the waste products produced by CANDIDA in the gut that transfers to other parts of the body (prostate) for example and is also responsible for the degradation of the liver over time. An overgrowth of Candida is usually due ta an altered or damaged immune system, which is common in our community. Perhaps, Acetaldehyde is one of the primary toxins we deal with? RP

  • Gayl Hamilton

    September 11, 2013 at 11:49 pm - Reply

    I may have not run a fancy study, but my N=1 study of myself says autoimmunity following viral insult should be looked at more closely. My case in particular regarding influenza vaccines. Highlighted by significant relapse 7 years later after “real” influenza infection. Anecdotal evidence from patients with similar symptoms following a variety of vaccine insults. The findings of overactive Th2 arm of immunity by the various IL factors supportive of that IMO…Viruses such as influenza, Hep B, rubella are known to cause autoimmune disease…the particular manifestation would be somewhat individualized given an individual patient’s genetic make up…maybe CFS/ME, maybe RA, maybe lupus, maybe undifferentiated connective tissue disease…and have they looked at mitochondrial DNA issues as well? Ahhhhh…it’s a good start at any rate…

  • Kerry Johnson

    September 12, 2013 at 1:05 am - Reply

    Hello. I don’t understand much of this, but I’m wondering how Dr. Lipkin’s research corresponds with a recently reported study by the University of South Florida, which looked for “messenger RNA” as a sign of viral activity, and found it.
    http://scienceblog.com/64945/chronic-fatigue-syndrome-patients-may-benefit-from-anti-herpesvirus-drug-treatment/

  • jJulia Hugo Rachel

    September 12, 2013 at 2:09 am - Reply

    We are lucky to have Dr. Lipkin working on this issue. I believe in his “hit and run theory”- leading to a cascade effect and decline of the immune system. I also believe that we will not find the virus in the blood or spinal fluid. We need tissue samples. We need to invent more sensitive testing methodologies for the blood (or biofilm?). Science is not there yet.
    Also, action may be in the gut, but when I see CFS patients, I see a brain disease or neurological impairment.

  • Guido den Broeder

    September 12, 2013 at 9:48 am - Reply

    It’s not all in the gut. The respiratory tract is just as important in ME. I hope that breath analysis will be included in Lipkin’s research.

    • R.A.Perill

      September 12, 2013 at 9:59 am - Reply

      I was referring to the origin. It goes to any weak point from there. The immune system resided primarily in the gut and when a pathogen takes residence in the gut, it degrades the immune system as well. From there, anything can happen, depending on genetic components. RP

      • Guido den Broeder

        September 12, 2013 at 6:13 pm - Reply

        Latent EBV is present in the respiratory tract.

        ME does not go to ‘any weak point’., but the inflammation will go to the muscles and the stomach, en eventually the heart and the kidneys will fail.

    • Gail

      September 12, 2013 at 7:12 pm - Reply

      I noticed that I feel my worst when my breathing gets labored, along with having gut difficulties and brain fog. One thing that makes sense to me is the student (VanElkazzar?) who hypothesized that the vagus nerve was infected. It made sense to me because it connects the gut, lungs, heart, brain and other organs. I hope they did into this area of research.

  • Valerie

    September 12, 2013 at 2:12 pm - Reply

    I remember hearing about looking for bacteria and fungi in Dr. Lipkin’s talk later on. That seeking these is not complete. Does anyone remember this part? Also there was another virus mentioned Anello? and ?. I had not heard of it either.
    Thank you for the summary. Will the recording be available to the public or just the summary they put on the CDC website which they mentioned?

  • Jeanie Pochatko

    September 12, 2013 at 3:52 pm - Reply

    Cort, trying to follow all of these discussions, and they are all interesting. So many researchers have said that this is probably a neurological disease. If it is found to be something going on in the gut, does tha rule out it having anything to do with the brain?

    • Cort Johnson

      September 12, 2013 at 5:26 pm - Reply

      My understanding is not at all. In fact gut researchers very much believe gut issues can affect the central nervous system…

      • Jeanie Pochatko

        September 13, 2013 at 4:21 pm - Reply

        Thank you for your reply, Cort. You have an ability to understand all of these very technical aritcles and then deliver them in a way that is pretty understandable to someone like myself who is scientfically challenged, to say the least!

    • anne

      September 12, 2013 at 11:40 pm - Reply

      There is a lot of research to show that the gut can affect the brain, which i think is what’s happening here. http://www.medicalnewstoday.com/articles/261173.php is a recent study that showed that just a simple OTC probiotic affected brain function.

  • Thomas van Gerven

    September 13, 2013 at 12:47 am - Reply

    silly question time

    I remember when I first got the CFS ,reading all about Mycoplasmas,and how they take over by HIDING inside the blood cells
    there was nice pics even using Dark Field Chromotography (?) to highlight the Mycoplasmas inside the blood cells

    it also went on to say how the mycoplasma basiccly “fed” off the HDL good cholesterol ,basically stripping it out,and a good reason why 30 perc or so of CFS Fibro had ensuing heart attacks

    im just wondering if this “camouflaging” effect ,once the mycoplasmas/virus took over to extent that CFS/FM etc develop,could throw out most tests being done
    ie nothing to detect in the bloodstream,because its all “hiding” inside the actual blood

  • Frank Twisk

    September 13, 2013 at 3:04 pm - Reply

    Thanks Cort.

    Great report.

    Just a small remark:

    Il-5 is indicative for Th2, IL-17 for Th17 (not for Th1)

    The spinal fluid samples seem to implicate inflammation (and encephalomyelitis!) and Th2/Th17 immune activation.

    • Cort Johnson

      September 13, 2013 at 3:15 pm - Reply

      Thanks Frank..

  • Terrilyn Partrodge

    September 20, 2013 at 2:47 am - Reply

    Amazing!! I am so excited for my Husband. Where do I sign him up? We are going on 4 years of him being so sick. They have done biopsies, colonoscopies, lower GI’s and upper GI’s and Nothing! I can’t wait to take this article to his GI doctor next week at the VA. I just wish the doctors at the VA would read this stuff too.

  • Sue

    September 22, 2013 at 3:54 am - Reply

    Great article. I am intrigued by the Xifaxan story. I myself went on a lower dose of Xifaxan for documented SIBO. I was on it for 2 weeks and it did not help while I was on it. However, about 10 days after I stopped it, I had several days or near-recovery….after decades of severe illness! Sadly, my second attempt at a higher dose made me ill and not better.

    Dr. DeMeirleir is all over this …he has already amassed evidence of HERV activity in the gut. It is a pity that researchers do not collaborate more with eachother.

  • Ron

    September 24, 2013 at 4:42 pm - Reply

    The gut will offer answers for Dr. Lipkin and at least a sub set of MECFS patients.

    To treat my intestinal dysbiosis my doctor initially prescribed antibiotic Xifaxan 200 for 21 days, followed by probiotic VSL#3, March 2010. No marked change occurred. I went through several iterations of that protocol over the years again without marked change. More recently in December, 2012, I was prescribed Xifaxan 550 for 28 days followed by VSL#3 twice a day indefinitely. Something happened with this last treatment. Gradually I began to feel as though I could actually accomplish something and more important had the energy to do it. I had gradually declined since the 1980s with ME/ CFS. When I began the VSL#3 after the antibiotic my energy fell down several levels. Despite not having the energy I had while taking the antibiotic I was able to do some basic exercises which added to my confidence. However, In May my energy declined, the exercises stopped, my ME/CFS symptoms returned and I was back in the trenches.

    Beginning September 20, 2013, I began the treatment again with Xifaxan 550, however this time it is for 21 days, because my Intestinal Permeability exam indicated my gut was in better shape. I guess we’ll see. However, I think I most likely will need to use the antibiotic on a maintenance basis as indicated by earlier comments by Ester Siebert and it won’t be too soon, I have been pursuing treatment for over 25 years and I know there are many others out there with similar stories.

    • Sue

      October 15, 2013 at 6:31 pm - Reply

      I also had an interesting incident with Xifaxan. I took the drug at a low dose for 2 weeks, after testing positive for SIBO via breath test. Nothing happened while I was on it; I may have felt worse but I cannot remember. However, 10 days after I stopped the drug, I had 3 days of near-recovery. I am a severe, long-term (>20 yrs) CFS patient. My doctor and I tried this experiment again with a higher dose, but this time, I just got sicker and never felt better. I spoke to a renowned CFS specialist about this, who did not seem surprised, and commented that dosing is very important.

      • Cort Johnson

        October 15, 2013 at 8:16 pm - Reply

        Wow – that certainly suggests the gut is a big (albeit very complex) player doesn’t it…

        • Sue

          October 15, 2013 at 8:44 pm - Reply

          oops i posted my story twice. damn fog. sorry about that

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