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Michael VanElzakker Ph.d Talks – About the Vagus Nerve Infection Hypothesis and Chronic Fatigue Syndrome (ME/CFS)

 An Interview with Michael VanElzakker Ph.d

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Van Elzakker’s hypothesis could explain several of the mysteries associated with chronic fatigue syndrome

Michael VanElzakker’s Vagus Nerve Infection Hypothesis (VNIH) for Chronic Fatigue Syndrome may be the most intriguing hypothesis to come along in the last twenty years.  If it’s correct it could explain several mysteries including how a virus might trigger the disease and then seemingly disappear, why the Lipkin study failed to find an active infection, why cytokine studies have trouble finding evidence of the ‘never-ending cold’, why when antivirals work they often take so long to do so.

It’s raised a lot of interest. Now Michael VanElzakker ‘sits down’ and answers some questions about it.

Background

What is your background? When did you get interested in this subject and start  developing this hypothesis? 

I am a neuroscientist. I mostly focus on posttraumatic stress disorder (PTSD), which I consider to be very different from CFS and a separate arm of my research interests (although there are many interesting overlaps between the views of CFS and PTSD within our culture).

sick person

A sick friend prompted his interest in this disorder

However,  I got my bachelor’s and master’s at the University of Colorado – Boulder, at a time when the Psychology & Neuroscience department there was very focused on psychoneuroimmunology-related phenomena. Some of the many research programs there related to neuropathic pain, cytokines, and the vagus nerve. All it took was for someone who was thinking about CFS to be exposed to these different literatures and to start fitting them together.

I started thinking about CFS because I have a sick friend. She got sick back when CFS was viewed even more skeptically than it is today – I remember one MD referring to it as “yuppie flu.” I knew that my friend was not malingering – why would she be? She had to put her life on hold. It was pretty devastating.

The focus on the vagus nerve is simply because that organ is responsible for symptoms during “normal illness” that strongly overlap with CFS symptoms.

Testing the Theory

Apparently imaging techniques are not able yet to find localized infections in the vagus nerve. How far are they from being able to that? Is there interest in developing those kinds of techniques?

You reported that  PET scans have shown ‘promise’ in identifying activation of the microglia – a prominent part of your theory. (The VNIT proposes chronic microglial activation causes the vagus nerve to send signals to the brain that result in flu-like symptoms.)  It seems that we could settle the VNIH theory right now if PET scans showed clusters of infected areas around the vagus nerve. How effective are PET scans at doing something like this now?

I’ll answer these two questions together. As far as the effectiveness of PET scans finding local vagus infection: We don’t know. That’s part of what my group is trying to work on. There are a lot of technical problems that will require pilot testing.

PET Scan

Most PET scans are done of the brain. VE would like to do one further down in the vagus nerve area

One of the big problems is that PET scans cost thousands of dollars per hour. It’s difficult to convince funding agencies to give us money to pilot test a method so that we can even begin to ask questions about a hypothesis that may or may not be accurate. But I’ve got some really good people on my team and we’re working on it.

There’s interest because of this hypothesis, but most imaging of the vagus nerve thus far has been at the level of the brain, trying to understand the mechanism of vagus nerve stimulation for epilepsy or depression. We’re trying to image it farther down.

If someone made an animal model of the hypothesis, that would help raise interest. I laid out a protocol in the paper for creating an animal model; I hope somebody with a rat lab takes the idea and runs with it. I’m not jealously guarding these ideas, I put them in the paper in the hopes that other groups would work on them too.

You suggested that future CFS research  use radiolabeled antibodies to localize clusters of specific virus types. This is done to find tumors. Is it possible to radiolabel antibodies so that they pick up clusters of infection in the body?

Yes, it is. But there are several problems to this with regards to the VNIH of CFS. One is that antibodies are specific, but CFS could be caused by a number of different pathogens. So, we could flood someone’s body with radiolabeled antibodies against HHV-6, but maybe in that specific case, their symptoms are caused by HHV-4 (Epstein–Barr).

Another problem is that some of the pathogens that might be most likely to cause CFS are found in the vast majority of humans. So, radiolableled antibodies against HHV-1 would find a signal in most people, but only cause CFS if the viruses are in a vagus (para)ganglion. And the vagus nerve is so highly branched, that could be all over the trunk. Another problem is that antibodies cannot always get inside ganglia, which are immunoprivileged. But despite all of that, I still think it’s a research program that is worth pursuing.

Treatment

Herpesviruses apparently love to set up house in the sensory ganglia, but you suggest that antiviral drugs might have trouble getting to them and destroying them there. Why is that?

drugs

Antivirals may take much longer to work in ME/CFS because they have difficulty accessing the vagus nerve where the viruses are present

Similarly to how the central nervous system has a blood-brain barrier (BBB), peripheral nervous system ganglia are immunoprivileged. According to the hypothesis, the frequent failure of drug therapy and also one’s own immune system to eliminate infections within vagal ganglia and paraganglia is just like how some drug doses and antibodies do not penetrate the BBB.

You noted that behavioral/stress management therapies such as CBT are moderately effective in about 30% of people with chronic fatigue syndrome, and that CBT resulted in lower viral loads and improved immune functioning in HIV. Why would this be?

Stress causes a cytokine response. So, if someone who doesn’t like public speaking is giving a presentation, their immune system is generating a cytokine response. If such a person even thinks about giving a presentation, they are likely to generate a cytokine response.

People with CFS have an authentic reason to be concerned about any activity that requires physical exertion, and it’s called post-exertional malaise: worsened symptoms after exertion.

According to the vagus nerve infection hypothesis (VNIH), there is a physiological reason behind post-exertional malaise: Exercise provokes muscle tissue to produce the proinflammatory cytokine IL-6, which would then exacerbate the ongoing  local cytokine response within vagus nerve ganglia or paraganglia. That’s the hypothesized mechanism behind post-exertional malaise.

The CBT practitioners in the infamous PACE study were focused on avoidance/fear of activity because they began with the assumption that CFS is psychological. They think the fear of activity itself is the cause of CFS; I’d say that fear of activity is justified, but like all fear, it can become dysfunctional. For the vast majority of their patients, CBT did not help. The three out of ten that found some slight improvement may have used CBT to figure out exactly what level of activity they should be worried about. So, the moderate improvements they reported in a minority of patients were probably related to stress reduction.

In patients with HIV, reducing something like stress that taxes the immune system is bound to help a little bit.

I understand that this is a really charged topic among CFS advocates, and there is a lot of misinformation out there. Just to be clear, cognitive-behavioral therapy (CBT) does not get at the root cause of CFS. CBT offers coping strategies and is not a cure. But I can’t think of a single medical condition that isn’t exacerbated by stress. CFS is no different. Having a chronic illness is stressful and it makes one’s life complicated and there’s a grieving process. CBT is for those parts of the illness. It’s intended to help people solve problems and to challenge dysfunctional patterns. If you’re seeing a CBT practitioner who views CFS as a psychologically-based illness and is approaching your CBT that way, fire them. Find someone else.

While CBT can help people with serious and chronic medical problems, it should be used as an adjunct and not a primary treatment. It would be crazy, for example, for a doctor to prescribe CBT instead of chemotherapy for cancer. But chemotherapy is a known, empirically tested treatment for cancer. CFS doesn’t have such a thing yet.

stress

Behavioral practices like CBT that reduce stress can be helpful in immune mediated diseases such as HIV and ME/CFS, but are adjunct, not primary therapies

Without a cure, the next best thing is to focus on quality of life. I am very much focused on finding an explanation for CFS, which would then lead to a cure. I have hypothesized that CFS is a neurological illness triggered by a foreign pathogen infecting the vagus nerve. But the fact is that stress has profound impact on immune system function. CBT for CFS patients can reduce stress, which is one mechanism of action to improve symptoms.

I should also say – CBT sometimes gets conflated with graded exercise therapy as well. Some studies have combined these two techniques but they are not the same thing. In the paper I gave an example of a treatment regimen that included graded exercise therapy.

Again, to be clear, if the VNIH is correct and some combination of glial inhibitor, antivirals and vagus nerve stimulation can be used to quell symptoms, then and only then does it make sense to begin graded exercise therapy. At that point, the root cause of CFS symptoms has been dealt with, and the next priority is to deal with muscle deconditioning which is not an insignificant factor in ongoing symptoms.

I absolutely do not condone forcing still-sick patients to exercise if it’s making their symptoms worse. This should be obvious.

Others

The heart rate variability evidence suggests the parasympathetic nervous system (vagus nerve) is under-activated in ME/CFS while the sympathetic nervous system is over-activated.  The SNS activation, in fact, may be due to the PNS’s inability to rein it in.  The increased heart rate at rest, for instance, could be due to be due to the inability of the vagus nerve to slow it down. In your theory, though,  the vagus nerve appears to be activated by the localized infection.  I’m a bit confused.

ANS

Is an infection contributing to the autonomic nervous system problems in ME/CFS?

This has to do with the fact that the vagus nerve is a mixed cranial nerve, meaning it has both sensory (afferent, or towards the brain) and motor (efferent, or away from the brain) divisions. Its parasympathetic influence over the body results from efferent activity; its function in detecting peripheral infection and triggering sickness behavior results from afferent activity.

However, terms like over-active and under-active are a bit too simplified – what matters is that the nerve is able to respond and signal appropriately, to be able to create a functional signal-to-noise ratio.

Researchers have been looking for cytokines in ME/CFS for decades. Sometimes they find them, sometimes they don’t. When they do find them sometimes research groups find similar cytokines and sometimes they don’t. The one constant is that they keep looking. You mentioned that lung infections are also not associated with increased cytokine levels in the blood.  Are there many other infections like this?

Well, to be more accurate, it’s not necessarily that lung infections won’t show a cytokine response in the blood. It’s more that we cannot be certain to find a cytokine response from a local infection – that is, any local infection. If a lung infection were severe enough, you might find cytokines in the blood. Cytokine studies are quite prone to false negatives, and it’s a mistake to infer from a negative cytokine blood test that there is no cytokine response happening anywhere in the body.

In studies that look for cytokines in blood, there are 3 relevant questions:

  1. Is there any cytokine response in the first place?
  2. Did that cytokine response diffuse into peripheral blood?
  3. Did the method of detection work?
IL-1B

VE notes the difficulties present in finding a cytokine response in an infectious disease

The question we’re interested in is #1, however it’s a big assumption that the answers to #2 and #3 are “yes” when we infer from a negative blood test that there is no cytokine response.

Those of us who think that CFS is not psychologically-based tend to think there’s an immune dysfunction of some sort. People have been looking for cytokines because they are an obvious potential link between the immune system and CFS symptoms, but a lot of studies have ignored how cytokines work.

If a research group is unfamiliar with the cytokine literature they may have also made some easy mistakes in the cytokine assay – the actual lab methods for looking for these proteins.

For example, cytokines are relatively labile, meaning unstable. If someone who didn’t know any better stored their blood samples in a refrigerator instead of a -80° freezer, you can bet they did not find cytokines. If blood samples went through freeze-thaw cycles, the cytokines will also start to denature (break down). There are definitely a lot of really good researchers who have looked into cytokines, but the literature can get muddied pretty easily by bad studies. And because the symptoms are systemic, most people have been thinking in systemic terms (i.e., not thinking about a localized infection causing CFS).

In general, I’m skeptical of any attempts to find a “cytokine profile” for CFS or any other infectious disease. That doesn’t mean it can’t be done, but it’s difficult. Cytokine responses are very complex, they interact with each other and they change in daily and hourly rhythms. You could study one individual and not find a “cytokine profile” unless you took several samples a day for many days.

Response to the Hypothesis and the Future

This is a really intriguing theory. Kristin Loomis of the HHV-6 Foundation was excited by it.  Have you gotten much response from it? 

I’ve actually been really pleasantly surprised by the response. I’ve had the idea for quite a long time, and spent a lot of time and effort trying to set up a collaboration with a rat lab, to create an animal model. To make a very long and frustrating story short, nothing worked out.

people networking

The response to VE’s hypothesis has been very positive; he is working on putting a study together to test his hypothesis

I’ve been telling anybody who would listed about the hypothesis. It’s not like doors were getting slammed in my face, but most people simply didn’t have a background in the different literatures that the hypothesis ties together.

It wasn’t until recently that I discovered this unique journal, Medical Hypotheses, so I made some time to write up the idea. It gave me a forum to really give people the background they needed to understand the idea, and allows people to check the citations themselves. Based on past experience, I thought I’d have to keep cold-calling researchers to push the hypothesis. But it really took off right away.

I put it up online for free, and it’s been downloaded over 1000 times there; I don’t know how many people have downloaded it from the publisher through a university or hospital subscription. I’ve heard from researchers from 5 continents. Somebody translated the paper into Dutch and put it up online.

The week the paper came out, Anthony Komaroff contacted me, we’ve been in contact since. He finds the hypothesis to be “provocative and plausible” and shares my hope that functional imaging can help to shed some light on it. I’ve been in contact with a lot of other well-known CFS researchers, and I think the idea is at least changing the way that some people think about the problem.

VanElzakker

Van Elzakker will be at the IACFSME conference with a poster presentation of his hypothesis

I also know that the paper is already being taught at some universities and medical schools, so hopefully it will at least get young scientists to start thinking about CFS. I hope people start to think about new CFS findings through the lens of this hypothesis because in my experience, it explains a lot of phenomenology.

Even if the hypothesis doesn’t turn out to be accurate, or is only partially accurate, I hope that it gets us closer to effective treatments that are actually attacking the root causes of CFS symptoms and not just helping people cope with them.

Some reports suggest you’re engaged in a pilot study. Can you comment on that?

On the record, I’d just say that I’ve put together a really great team to pursue the VNIH and that Dr. Komaroff is part of it. There are a lot of technical issues but we’re hoping to use functional imaging to gain enough preliminary data that we can pursue it further.

 

 

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32 Comments

  • Jeanie

    February 14, 2014 at 5:56 pm - Reply

    What an encouraging article! Thank you, Dr. Van Elzakker, for taking CFS on! We all sure do need you and researchers like yourself. What a light in the dark you are. And I am so glad Dr. Komaroff if going to be a part of this research. He has been with us forgotten sick people for so long. He is one of my heroes in this, and you are now one, too.

    • Cort Johnson

      February 15, 2014 at 4:54 pm - Reply

      I’ve had some concerns about Dr. Komaroff, from time to time, but he jumped on this very quickly! He’s also talking on new advances in ME/CFS at the IACFS/ME conference. I imagine this theory will be a central focus of that talk.

  • Kathy

    February 14, 2014 at 6:50 pm - Reply

    I’ve had this awful illness for more than 30 years and for many years now I’ve stayed away from trying anything ‘new’ in treatment because I came to believe that it was useless until someone had a real understanding of just what is going on in ME/CFS. Then I read Dr. VanElzakker’s theory and shouted EUREKA! it was a moment of clarity and certainty and I have absolutely no doubt that this theory will play a major part in the understanding and hopefully treatment in the hopefully not too distant future.

    Thank you, Dr. VanElzakker, please keep up the great work!.

    • Cort Johnson

      February 15, 2014 at 5:03 pm - Reply

      I think you’re not alone, Kathy…Of course, you never know until the fat lady sings, but hopefully VE will get the study together and it will work. To me it has more going for it than any other theory that I’ve seen. :)

      • Jeanie

        February 16, 2014 at 3:20 pm - Reply

        Just “hearing” you say that , Cort, give me so much happiness and hope.

  • Virginia

    February 15, 2014 at 3:12 am - Reply

    My son developed Vagus nerve issues after a severe case of appendicitis. The fatigue is awful.

    • Cort Johnson

      February 15, 2014 at 4:55 pm - Reply

      No kidding. Did the doctors state why they think that happened. Are they able to do anything for him?

      • Virginia

        February 18, 2014 at 5:35 pm - Reply

        The response to Cort and VE re my son. Yes, they are able to treat his symptoms to make him feel better. If you would like a more full report of his treatments please e-mail me and I will send you a few pages worth of his current treatments and medicine list. He has been going through treatment for 4 years now. . Three months ago I took him to an Internist/Integrative Medical doctor that also found he had an underlying infection of Babesia Duncani-tick borne infection. Now he is undergoing 8 months of antibiotics for that as well. Never give up is my motto. My theme song is” Your an Overcomer”. Being a nurse helps but sometimes I feel like I am trying to understand a whole new language.

        • Witherwings

          February 19, 2014 at 1:09 pm - Reply

          That’s very interesting, Virginia. I’m curious to know his treatment plan, but I don’t think I’m able to contact you about it. Interestingly enough, I also had a positive test on a tick-borne infection, namely lyme disease and rickettsia. But me and my docs are still doubting to try AB because of my severe GI-issues and because we are still not entirely sure how big a role these possible infections play in my case (the test I’ve done (an LTT) also isn’t recognised by every doctor and my antibodies don’t come out positive). My doctor also spoke about the coxsackie virus because of my symptoms and if this would be an issue, the treatment plan would be a lot different. I wish you and your son the very best!

    • Kathy

      February 15, 2014 at 5:02 pm - Reply

      I had ‘chronic appendicitis’ at age 17, it took months of sickness before a doctor correctly diagnosed it just as it was becoming acute and I had surgery to remove it. That at age 17 and severe mono at age 14 that put me in the hospital for a week in isolation are a combination that I believe led to my developing CFS later.

      • Cort Johnson

        February 15, 2014 at 5:06 pm - Reply

        I know of several people who developed ME/CFS after gastrointestinal infections. and, of course, Dr. Chia thinks they play a huge role. I think any serious infection might do, though. In VE’s theory, as I understand, a gut infection could lead to viruses establishing in the ganglia associated with the gut.

        Pridgen believes the same thing in FM; in about a month we should have the results of his first trial – and he’s checking gut tissues for bugs. It’ll be interesting!

        • Witherwings

          February 18, 2014 at 2:28 pm - Reply

          Very interesting to see these cases of appendicitis over here. I also have developed a serious condition after I had an appendicitis (with peritonitis and sepsis as a result – I was REALLY ill) as a teenager – for a few years now I’m bedridden because of this – doctors still haven’t any clue what has exactly happened back then that has made me this ill. Sure, I got diagnosed with CFS/ME, but what does that actually mean? I’m very eager to find out what is exactly wrong with me and I find this study very promising! I also have dysautonomia (POTS) and serious stomach issues so this whole hypothesis really makes sense to me. Thank you very much for publishing this and I’m looking forward to the results of their research.

  • Kirsten

    February 15, 2014 at 4:54 am - Reply

    Thankyou so much to Michael and Cort for this interview. The hypothesis has intrigued me from the first time I read about it and I’ve become a bit obsessed with trying to understand it ever since (and frustrated that my brain doesn’t seem to have the knowledge or function to compute the complexities).

    In reading some of the forum comments about this I was quite saddened and embarrassed by the way in which Michael’s work was being received by many in the ME/CFS community. While I very much understand (and I am so glad to read that Michael does too) how loaded some words and concepts are for us given the history, I also despair when it seems people can’t look a bit deeper and actually make sure there really is some sinister intent before jumping to conclusions.

    All to say that I very much appreciate both this interview and the time and effort Michael has put both into the hypothesis and into communicating with the community in various ways since it was released. I wish him only the best as he follows this lead and hope that it might turn out to be the game-changer we so desperately need.

    • Cort Johnson

      February 15, 2014 at 5:00 pm - Reply

      Thanks Kristin, I’m kind of flabbergasted to hear that. I imagine it has to do with the comments on CBT. Focusing on those and ignoring the rest, reminds me of the princess and the pea story or someone dying of thirst in the desert complaining there’s no ice in the drink you’re rescuer’s gave you. If VE is right the theory opens up huge vistas for chronic fatigue syndrome.

      I’m sorry they’re missing the huge promise in this theory.

  • Kirsten

    February 15, 2014 at 4:57 am - Reply

    PS – I started seeing an oesteopath after I began looking into the vagus nerve theory. I have tried osteopathy before to no avail (with the same practitioner, which keeps the variables at a minimum here!). So far I’ve had two appointments, specifically working on vagus nerve impingments, and have felt some subtle but certain changes. I’m going to be very interested to see what happens as we progress with the treatment.

  • Lilly

    February 15, 2014 at 2:53 pm - Reply

    Where is he located now and does he need patients to test?

    • Cort Johnson

      February 15, 2014 at 5:01 pm - Reply

      I hope to learn more about the parameters of the study which is hopefully getting underway at the IACFS/ME conference.

      • Carol Larsen

        February 22, 2014 at 9:38 pm - Reply

        PS If participants are needed for this study, please let me know.

  • Ann

    February 16, 2014 at 1:52 am - Reply

    This is exciting research. I’m also interested in when the FDA approves Ibudilast. That drug sounds promising too.

  • est_sunshine

    February 16, 2014 at 4:12 am - Reply

    Dr. Van Elzakker’s hypothesis resonates with me, I have POTS, Dysautonomia, CFS, IBS. Histamine issues. I had gut infections as a child and never really recovered. I notice my vegas nerve is very sensitive and can give me electric shock like jolts after eating. If certainly feels like it could be infected. I have unbalanced gut flora according to a bioscreen test, with high Streptococcus and almost no E-Coli. It all makes for an interesting jigsaw puzzle! Good luck with the next stage of the research.

  • PALLINE

    February 16, 2014 at 4:55 am - Reply

    This would fit well with the hypothesis that a subset of CFS is actually Post Polio Syndrome, because it seems that polio survivors have damage in the area of the brain that control the vagus nerve according to Dr Richard Bruno’s writings. I am of the right age and have many symptoms of both, some of which were finally elucidated by the vagus nerve theory.

    • Carol Larsen

      February 22, 2014 at 9:48 pm - Reply

      Yes! I’ve been interested in the Post-Polio Syndrome connection. I was conceived when my Dad had polio. The symptoms are similar

  • Bev Bentley

    February 16, 2014 at 5:21 am - Reply

    Thank you for this research. People with MS have CCSVI and have treatment to open blocked veins. The vagus nerve is often involved. Would you comment on this please. My son has such terrible lower back pain and all over his body at times due to his MS. Thank you.

  • Bl Br

    February 17, 2014 at 10:13 pm - Reply

    Cort Johnson, I am extremely interested in conversing with fellow researchers with this disease who also make great efforts to read all of the latest studies on it. May I have a link to your website and any other groups you are in such as Facebook, Meetup.com, etc.?

    • Cort Johnson

      February 18, 2014 at 4:54 am - Reply

      Hi Bl Br I post here on Simmaron Rising and on my own website at cortjohnson.org – hope to see you over there.

  • Caron Ryalls

    February 19, 2014 at 1:04 am - Reply

    Some patients with ME or CFS became ill after a vaccination, My daughter was diagnosed with ME/CFS and later POTS after her HPV vaccination at the age of 13, three years ago. How does this theory account for ME/CFS after vaccination, as Many vaccines (including HPV vaccine) do not contain live viruses. How then would the Vagus nerve become infected?

  • JCB

    February 20, 2014 at 4:31 am - Reply

    This is very encouraging! I’ve had this condition for well over 30 years, and this is the first concept comprehensive enough to capture most presentations. I also just recently found that I have Lyme, a very old case. Neurological Lyme is microbes within the CNS. I assume it is just as likely that microbes enter the vagus. Would love to hear his thoughts on that sometime. Thanks for the good news!

  • Carol Larsen

    February 22, 2014 at 9:34 pm - Reply

    Thank you so much, Cort, on your very helpful interview & views on MS?CFS! I’ve had this illness for 22 years beginning with a Mono infection. Other medical issues have come about since then. It is exciting to read this study and realize that it is carrying on. I’d love to be kept informed about all of this, though it might take reading it a few times-over (with brain fog & non-medical background). Thank you for the interview & Michael’s research! GOOD LUCK!

  • Joan Zeiber

    February 28, 2014 at 9:03 pm - Reply

    Pretty interesting stuff. I have been ill for nearly 30 years with CFIDS/Fibro and 7 years ago had a benign meningioma removed. I am pretty curious as to whether CFIDS/Fibro played a role in the development of this brain tumor. Perhaps this research will shed some new light on the never-ending battle.

  • reven

    March 5, 2014 at 10:02 pm - Reply

    a study in the Netherlands
    The vagus nerve as a regulator of immune tolerance in the intestinal mucosa
    http://www.zonmw.nl/nl/projecten/project-detail/the-vagus-nerve-as-a-regulator-of-immune-tolerance-in-the-intestinal-mucosa/samenvatting/

    • Cort Johnson

      March 10, 2014 at 8:53 pm - Reply

      Cool – thanks Reven

  • Stefie

    March 25, 2014 at 3:58 am - Reply

    Thanks Cort for this article! Not sure how this all fits together but I will be interested in following this. I have severe gastroparesis and damage to the vagus nerve is sited as one of the reasons for this.

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