Van Elzakker's Vagus Nerve Hypothesis for Chronic Fatigue Syndrome (ME/CFS)

Van Elzakker's Vagus Nerve Hypothesis for Chronic Fatigue Syndrome (ME/CFS)

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Cort submitted a new resource:

Van Elzakker's Vagus Nerve Hypothesis for Chronic Fatigue Syndrome (ME/CFS) - Does a vagus nerve infection cause ME/CFS?

A neuroscientist, Michael Van Elzakker, has proposed that a infection in or around the vagus nerve is causing it to tell the brain to produce the flu-like symptoms found in chronic fatigue syndrome (ME/CFS). His hypothesis is currently being tested.

Read more about this resource...
 

Tammy7

Well-Known Member
Hey Cort...........Anthony William talks about how a neurotoxin from the EBV can cause inflammation of the vagus nerve.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Hey Cort...........Anthony William talks about how a neurotoxin from the EBV can cause inflammation of the vagus nerve.
This is the guy who wrote the book? Someone just emailed me about him - I'm looking forward to reading it :)
 

Tammy7

Well-Known Member
This is the guy who wrote the book? Someone just emailed me about him - I'm looking forward to reading it :)
Yes...........the guy who wrote the book. I think you will find also the EBV/Lyme connection pretty interesting.
 

Remy

Administrator
If anyone knows the answers to these questions...(or how to ask the people involved!), I'd be very grateful. I'd be very interested in any insight from @Diana Driscoll as well. The vagus nerve is clearly a critical component and I look forward to understanding these theories better.

This is the comment I posted in response to the interview with Dr Van Elzakker on TLHC but unfortunately never got any replies.

I've really enjoyed these two interviews with Dr Van Elzakker and Dr Diana Driscoll, both focusing on the vagus nerve and it's role in illness.
I'm hoping someone can help me figure out if/how these theories fit together though...as I understand it, Dr Driscoll is saying that low acetylcholine release from the presynaptic neurons of the vagus nerve are responsible for the symptoms experienced.
Dr Van Elzakker seems to indicate it is more of an over active vagus nerve caused by an infection, or a lingering sickness response that was initially provoked by an infection or trauma of some sort.
So is it an overactive or underactive vagus nerve? Should we be trying to stimulate it if it's already over-stimulated? Or is part of it overstimulated and part understimulated? Or have I got this all completely wrong?? :)
Also, I'm interested both in the study Dr VanE referred to regarding the viruses and appropriate antivirals...do you have a link to the work?
 

weyland

Well-Known Member
Remy said:
I'm hoping someone can help me figure out if/how these theories fit together though...as I understand it, Dr Driscoll is saying that low acetylcholine release from the presynaptic neurons of the vagus nerve are responsible for the symptoms experienced.
Dr Van Elzakker seems to indicate it is more of an over active vagus nerve caused by an infection, or a lingering sickness response that was initially provoked by an infection or trauma of some sort.
So Driscoll is talking about efferent signalling on the vagus nerve, which uses ACh as a neurotransmitter at pre and post ganglionic neuron junctions. Van Elzakker is talking about afferent vagal signals from peripheral organs to the brain, which it looks like might use a different neurotransmitter such as glutamate.
 
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Remy

Administrator
So Driscoll is talking about efferent signalling on the vagus nerve, which uses ACh as a neurotransmitter at pre and post ganglionic neuron junctions. Van Elzakker is talking about afferent vagal signals from peripheral organs to the brain, which it looks like might use a different neurotransmitter such as glutamate.
Thank you, that helps!

So are the afferent vagal signals overactive? And the efferent ones potentially underactive? Is that possible?
 

weyland

Well-Known Member
So are the afferent vagal signals overactive?
Van Elzakker hypothesizes that they are overactive due to infection of the nerves themselves, leading to an exaggerated sickness response in the brain.

And the efferent ones potentially underactive? Is that possible?
Yes, I believe it's probably possible as they are two different nerve pathways potentially using different neurotransmitters. As with serotonin in ME, research has shown a similar exaggerated response to cholinergic substances implying that there might be upregulated AChR expression due to lack of normal adequate ACh release.
 

Remy

Administrator
@weyland, do you understand how some of these devices that are supposed to work by "increasing vagal tone" actually do work? Are they able to differentiate between the afferent/efferent?
 

weyland

Well-Known Member
@weyland, do you understand how some of these devices that are supposed to work by "increasing vagal tone" actually do work? Are they able to differentiate between the afferent/efferent?
Sorry, I don't. I've been quite curious about how these might work myself.
 

Remy

Administrator
So I found this about the VNS devices...looks like they are working on the afferent part of the nerve (toward the brain) a la Van Elzakker.

But if Van Elzakker is saying that the afferent nerve is overactive due to chronic or past infection, would stimulating them with a VNS just make things worse?

On January 28, 2013 researchers at the University of Glasgow in Scotland announced that they are hoping to help victims of stroke to overcome physical disabilities by helping their brains to 'rewire' themselves using a Vagal Nerve Stimulator (VNS). Lead researcher Dr Jesse Dawson, a stroke consultant and clinical senior lecturer in medicine, described the vagus nerve by saying, "That nerve is one of the major nerves that goes to the brain. By stimulating the nerves, you can cause upstream changes in the brain without having to go into the brain."

It is hoped that the device will stimulate release of the brain's own chemicals and help the brain form new neural connections which might improve participants' arm mobility. In 2005, the FDA approved the use of VNS for treatment-resistant depression, although it’s use remains controversial... VNS is also used to treat epilepsy and tinnitus.
Dr Dawson added: "Evidence from animal studies suggests that vagus nerve stimulation could cause the release of neurotransmitters which help facilitate neural plasticity and help people re-learn how to use their arms after stroke, particularly if stimulation is paired with specific tasks.” The link between vagus nerve stimulation and neuroplasticity is strong. By focusing on creating healthy vagal tone you can trigger similar neuroplastic changes from the bottom-up. Creating a mindset of grace under pressure can be reinforced through the powerful mind-body connection of the vagus nerve.
 
Yea I mean there is vagus nerve involvement but is not the primary infection site..infection works the opposite way. Starting in lower spinal cord working its way up through neuron pathways of the spinal horns into the ganglion nerves, maybe including upper end of vagus nerve. Infection may not even make it up that far..Vagus/Ganglion nerves might just be affected negatively by the screwed up spinal cord impulses.
CFS is a gut infection occasionally spreading to heart and spinal cord. Once spinal cord and CNS become damaged, ME phase begins..Can happen very quickly or can take a decade or more.
 
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Remy

Administrator
Gah, I'm confused again.

In reading an article about insulin resistance, it says:

One of the causes could be found in a dysregulation of the CNS (central nervous system) centers controlling energy and glucose homeostasis as well as insulin
secretion. According to this view, the regulation of the autonomic nervous system is altered with a resulting increase in parasympathetic and a decrease in sympathetic efferent tone: the organism’s metabolic balance is shifted to the anabolic side, there is a hypersecretion of insulin and a sequence of events follows which leads to the insulin resistance syndrome (2, 3, 4).
So is this the same thing that VanElzakker hypothesizes happens in MECFS? Or exactly opposite?
 

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