Chronic fatigue syndrome from vagus nerve infection: psychoneuroimmunological hypothesis

[Richie]

Tito
Looks like I was wrong about use of term "illness behaviour".
I read of one case where an antiviral successfully supressed ME symptoms without reducing cytokine levels. May be related to what you say.

 

[Tito]

I read of one case where an antiviral successfully supressed ME symptoms without reducing cytokine levels. May be related to what you say.

Interesting! Do you remember where you read that? Was it with Ampligen?

 

[Richie]

It was a s far as I remember on another forum.
I wonder if cytokines work as amplifying factors to intensify or spread illness communications, which would explain pre cytokine in blood changes from e.g. e coli, while recognising the role cytokines play in symptom expression.
If the original cause of the raised cytokines is gone, maybe there is no "message" to amplify even if cytokines persist.

 

[A.B.]

It seems to suggest cytokines are not a prerequisite to a 'sickness behaviour' like fever.

Fever disappears after a week in human volunteers injected with sickness behavior inducing cytokines, while the other symptoms remain.

That is, absence of fever does not indicate that there is no cytokine related sickness behavior.

 

[Tito]

But none of that is not the hypothesis of VanElzakker. Rather, his hypothesis is that infection of the vagus causes the vagus dysfunction, when then leads to ME/CFS.

Hip, Dr Chia has done extensive research on enteroviruses infecting the nerves surrounding the stomach and intestines, traveling up the vagus nerve and infecting the brainstem. He is a highly regarded researcher in the field of ME/CFS.
Once more, I am not saying that this area of research is worthless, I am just saying it is not new. Dr Chia did not simply make hypotheses, he also conducted research to show HOW biologically this process was taking place. He participated to many international conferences and I am sure you will find research papers and video recordings of these findings.

 

[Hip]

Hip, Dr Chia has done extensive research on enteroviruses infecting the nerves surrounding the stomach and intestines, traveling up the vagus nerve and infecting the brainstem. He is a highly regarded researcher in the field of ME/CFS.
Once more, I am not saying that this area of research is worthless, I am just saying it is not new. Dr Chia did not simply make hypotheses, he also conducted research to show HOW biologically this process was taking place. He participated to many international conferences and I am sure you will find research papers and video recordings of these findings.

I have to admit, that I had also considered the idea of vagus nerve infection myself some time ago, as a possible explanation for the autonomic symptom of ME/CFS, and I am sure other people must have pondered upon this idea of an infected vagus nerve.

Though it is one thing to ponder an idea to yourself, and another to spend months of your time fully researching the idea, writing it up, and publishing a paper on the subject. We don't have institutional access to the full paper, we don't know exactly what is written in it.


I guess, though, my concern is really about how the ME/CFS community come across to researchers who dedicate their time to ME/CFS. Researchers do read the ME/CFS forums sometimes. Although the anger felt by the ME/CFS community towards those psychiatrists and psychologists who effectively trivialized ME/CFS by claiming it was a psychosomatic illness was justified, I would hate to see the ME/CFS community come across as an angry mob that just attacks or criticizes anything that looks psychological. We need to be a rational and discriminating. I know your remarks were just off the cuff, so I am not really referring to you here; I just think we need to show gratitude to those that are helping us and dedicating their time researching the physical causes of ME/CFS.

There are now, thank goodness, real signs of a watershed in ME/CFS research, with biomedical ME/CFS research finally returning to the fore, after decades of ME/CFS being left in the psychosomatic wilderness. So we need to lavish praise on those research the physical causes of ME/CFS, but keep pouring scorn and anger on those who still persists with the psychosomatic model.

 

[Enid]

Philosophy aside for a moment one of my Docs said "myelin sheath damage" - and one of the many possible viruses/infection probable.

 

[Hip]

Philosophy aside for a moment one of my Docs said "myelin sheath damage" - and one of the many possible viruses/infection probable.

Can you explain in more detail. Are you talking about the vagus nerve, or a diagnosis you have received from your doctor?

 

[Enid]

Nerves in general Hip - vagus or otherwise. This was one of my specialist Doc's conclusion but no more investigation or treatment offered (MS/Polio ruled out). But this is usual in the UK NHS. The point he was making was CNS damage.

 

[John H Wolfe]

enterovirus infection can actually get into the vagus nerve, where this nerve links to the stomach, and then the virus can travel along the entire length of the vagus nerve until it reaches the point where this nerve enters the brain

If 20% of the population test positive for enteroviruses present in 80% of those with 'CFS' assayed, according to Dr. De Meirleir, then it seems there is a missing link

Dr. Rowe, would likely argue that nerve restriction and associated (sensitising) mechanical tension may provide such a link (e.g. the potential for enhanced/prolonged disease associated with such infection of peripheral nerves)

It seems likely that there may be a role for both such sources of (interacting) pro-inflammatory neuronal irritation/inflammation: mechanical and microbial, as per this portion of my 'disease cascade' (the principals may be extended to other such agents, in other regions of the peripheral nervous system):

• ≈ Chronic Systemic Inflammation e.g. thanks to inflammatory cytokines
• (+) ~ Idiosyncratic epigenetic autoimmune reactivity e.g. to 5-HT, HERVs
• (+) ~ Local inflammation in the DRG e.g. linked to viruses e.g. EBV
• (+) ~ NH-NSarising from concomitant behavioural/postural effects
  • ≈ Escalation of the neurogenic sensitisation loop

 

[natasa778]

Back on topic, I recall reading years ago that severing the vagus nerve can sometimes induce remission in type ONE diabetes, though I think that was only in animal models. Nerves do effect peripheral systems, and the vagus nerve is critical for autonomic function.

I am right in thinking that even if/when not directly infected, vn could be made dysfunctional (and lead to dysautonomia etc) through its interaction with other body systems that could be harbouring chronic infection/s. Such as the gut.

 

[Hip]

Nerves in general Hip - vagus or otherwise. This was one of my specialist Doc's conclusion but no more investigation or treatment offered (MS/Polio ruled out). But this is usual in the UK NHS. The point he was making was CNS damage.

Perhaps you have one of these demyelinating conditions.

 

[alex3619]

I am right in thinking that even if/when not directly infected, vn could be made dysfunctional (and lead to dysautonomia etc) through its interaction with other body systems that could be harbouring chronic infection/s. Such as the gut.

I think so, but I am not fully sure. It could also be under autoimmune attack, or inflammatory processes.

 

[natasa778]

... evidence has mounted from studies in rodents that the gut microbiome can influence neural development, brain chemistry and a wide range of behavioral phenomena, including emotional behavior, pain perception and how the stress system responds.

... How could gut bacteria influence the brain and behavior so profoundly? One way, some studies indicate, is by co-opting the immune system itself, using immune cells and the chemicals they synthesize to send messages to the brain. But as Lyte's 1998 study showed, some bacteria can induce behavioral changes even without triggering an immune response, suggesting that other channels of gut-brain communication must be at work. In other studies, Bienenstock and others have found that at least in some cases, bacteria communicate with the brain via the vagus nerve: When the vagus nerve is severed, effects of gut bacteria on brain biochemistry, stress response and behavior evaporate. Those findings not only shed light on how bacteria may influence the brain, but also fit with other work in humans that suggests that vagal stimulation can be used as a last resort for treating depression. "This opens up the idea that once we learn how the bacteria talk to the vagus, we may be able to simulate that with novel molecules – drugs without the bacteria," Bienenstock says....

http://www.apa.org/monitor/2012/09/gut-feeling.aspx

 

[Firestormm]

New research on Chron's establishes enterovirus link - paper speculates on nerve storage and transmission. Thread discussion here. Appears relevant to this discussion as others have said. Small study, authors hope to conduct larger ones with controls. See thread for details

 

[RobinDurham]

Hi everyone. I'm a friend of Mike VanElzakker, and also a patient of 18(!) years. He learned about Me/CFS through his friendship with me, and for years has been thinking about what the cause could be based on his knowledge of neuroscience. Even though he studies full time (in a different field) and works, he used his spare time for over a year to work on this paper and get it published.

I just wanted to address a few things brought up in the thread. Mike is a neuroscientist, not a clinical psychologist. He's a PhD candidate who studies PTSD, thus his lab falls under the department of psychology. From what I understand his work is largely looking at and analyzing brain scans.

I think the people on the thread did a great job of explaining sickness behavior and psychoneuroimmunology, terms that were off-putting to me as a patient at first. But, yeah, sickness behavior is just a research term to describe what people and animals do when they get in infection - they feel crappy and get aches and chills, maybe a fever, they lie down and rest. (I tried to link to wikipedia in that sentence but I'm not sure if it did it right!) It's involuntary.
When you get sick, the immune system tells the vagus nerve which tells the brain, so in this case it's psycho (brain) neuro (vagus nerve) immunology (response to infection.)

So, with this paper Mike is doing what people do in science - proposing an theory. The cause of this disease has remained elusive for so long and it's beyond frustrating that after thirty years that it is still a diagnosis of exclusion, that we still don't have a diagnostic toolkit at the primary care level. Mike understands that, he's a passionate and empathetic person who wants patients to have diagnostics and treatment options. I'm so glad that he has pitched in his theory and I hope more young scientists become interested in the field too.

 

[A.B.]

I've got to nitpick a little here. "psyche" doesn't refer to the brain, but to the soul or mind. The brain is a physical entity, whereas the mind and soul are metaphysical.

So the point that there is no reason to add the "psycho" prefix remains.

I still see the "psycho" prefix as attempt to portrait psychological theories as relevant when they are not.

 

[lansbergen]

I've got to nitpick a little here. "psyche" doesn't refer to the brain, but to the soul or mind. The brain is a physical entity, whereas the mind and soul are metaphysical.

So the point that there is no reason to add the "psycho" prefix remains.

I still see the "psycho" prefix as attempt to portrait psychological theories as relevant when they are not.

I agree.

I guess he had to include it because of the situation being in a psych department.

 

[MeSci]

I've got to nitpick a little here. "psyche" doesn't refer to the brain, but to the soul or mind. The brain is a physical entity, whereas the mind and soul are metaphysical.

So the point that there is no reason to add the "psycho" prefix remains.

I still see the "psycho" prefix as attempt to portrait psychological theories as relevant when they are not.

I agree broadly. Here is a definition of psychology:

http://oxforddictionaries.com/definition/english/psychology

The danger to us, and others with physical/neurological conditions for which the discourse has long been dominated by an erroneous school of psychological thought, of including the 'psycho-' prefix, and the word 'behaviour' to describe physiological responses, is that such usage can easily be picked up and (ab)used by those who seek to perpetuate the incorrect theories and treatment, to our severe detriment.

 

[Firestormm]

I don't give a ****. Sorry. All this about terms appears superfluous to hypothesis.