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Parkinson's disease, the gut, & the vagus nerve: Vagotomy and subsequent risk of Parkinson's disease

Bob

Senior Member
Messages
16,455
Location
England (south coast)
I came across this on Twitter, via Erica Verrillo.

News Article...

Parkinson's disease may begin in the gut
Parkinson's disease begins in the gastrointestinal tract, large study indicates
June 23, 2015
http://www.sciencedaily.com/releases/2015/06/150623103609.htm
"Our study shows that patients who have had the the entire vagus nerve severed were protected against Parkinson's disease. Their risk was halved after 20 years. ..."
The research has presented strong evidence that Parkinson's disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain. Many patients have also suffered from gastrointestinal symptoms before the Parkinson's diagnosis is made.

"Patients with Parkinson's disease are often constipated many years before they receive the diagnosis, which may be an early marker of the link between neurologic and gastroenterologic pathology related to the vagus nerve ," says Elisabeth Svensson.
Read more:
http://www.sciencedaily.com/releases/2015/06/150623103609.htm


Research paper:

Vagotomy and subsequent risk of Parkinson's disease
Elisabeth Svensson, Erzsébet Horváth-Puhó, Reimar W Thomsen, Jens Christian Djurhuus, Lars Pedersen, Per Borghammer and Henrik Toft Sørensen
Annals of Neurology
29 MAY 2015
DOI: 10.1002/ana.24448
http://onlinelibrary.wiley.com/doi/10.1002/ana.24448/abstract
Abstract

Objectives
: Parkinson's disease (PD) may be caused by an enteric neurotropic pathogen entering the brain through the vagal nerve, a process that may take over 20 years. We investigated the risk of PD in patients who underwent vagotomy, and hypothesized that truncal vagotomy is associated with a protective effect, while super-selective vagotomy has a minor effect.

Methods: We constructed cohorts of all patients in Denmark who underwent vagotomy during 1977-1995 and a matched general population cohort, by linking Danish registries. We used Cox regression to compute hazard ratios (HRs) for PD and corresponding 95% confidence intervals [CIs], adjusting for potential confounders.

Results: Risk of PD was decreased in patients who underwent truncal [HR = 0.85, 95% CI= 0.56–1.27; follow-up of >20 years: HR = 0.58, 95% CI: 0.28–1.20] compared to super-selective vagotomy. Risk of PD was also decreased following truncal vagotomy when compared to the general population cohort [overall adjusted HR = 0.85, 95% CI 0.63–1.14; follow-up >20 years, adjusted HR = 0.53 [95% CI: 0.28–0.99]. In patients who underwent super-selective vagotomy, risk of PD was similar to the general population [HR = 1.09, 95% CI: 0.84–1.43; follow-up of >20 years: HR = 1.16, 95% CI: 0.80–1.70]. The statistical precision of the risk estimates was limited. Results were consistent after external adjustment for unmeasured confounding by smoking.

Interpretation: Full truncal vagotomy is associated with a decreased risk for subsequent PD, suggesting that the vagal nerve may be critically involved in the pathogenesis of PD. This article is protected by copyright. All rights reserved.
 
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Ecoclimber

Senior Member
Messages
1,011
The media has been reporting back since 2009 that gut flora is the cause for MS, Obesity, Behavior, Mental illness, heart disease and just about every other disease known to mankind. Unfortuanately, there are 100 trillions microbes living in the intestinal tract.The permutations are astronomical given 500-1000 species and still more that have not been identified.

This is a totally a new frontier, Microbiome. This is why the Microbiome Project was authorized by the NIH to the tune of $668 million dollars ( except for ME/CFS...the NIH just couldn't peal off a measly $1million for Lipkin's microbio project ) and spread across research institutes in the U.S. to identify possible causation with known diseases. I have not heard of serious consideration in targeting the gut flora in research projects for these diseases unless it is within the Microbiome Project but we are looking way down the road for any significant break throughs in my opinion.

2010
Biologists at the California Institute of Technology (Caltech) have demonstrated a connection between multiple sclerosis (MS) -- an autoimmune disorder that affects the brain and spinal cord -- and gut bacteria.
http://www.sciencedaily.com/releases/2010/07/100719162643.htm

2015
http://www.express.co.uk/life-style...reat-Alzheimers-multiple-sclerosis-Parkinsons
 
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Hip

Senior Member
Messages
17,809
We investigated the risk of PD in patients who underwent vagotomy, and hypothesized that truncal vagotomy is associated with a protective effect, while super-selective vagotomy has a minor effect.

I wonder whether this reduction in Parkinson's incidence is due to the fact that the vagus nerve is the main route for carrying inflammatory signals from the body peripheries (like the gut) into the central nervous system (CNS), because in the CNS, these inflammatory signals trigger the release of pro-inflammatory cytokines from microglial cells in the brain.

So if the vagus nerve is cut, these inflammatory signals from peripheral locations like the gut may not reach the brain, meaning that the overall level of inflammation in the brain may be reduced, especially in people with some mild chronic gut inflammation. This reduction of brain inflammation due to a cut vagus may conceivably be the factor that protects against the development of Parkinson's disease, as brain inflammation releases several toxic factors such as superoxide.



I wonder what would happen if you performed a truncal vagotomy on an ME/CFS patient. Might cutting the vagus nerve in this way cure or improve ME/CFS? Michael VanElzakker thinks that inflammatory signals traveling along the vagus nerve to the brain are the cause of ME/CFS symptoms, by virtue of the fact that these inflammatory signals will ramp up brain inflammation and instigate sickness behavior.

If VanElzakker's theory is right, then blocking these signals from traveling along the vagus could be an effective treatment for ME/CFS.

I have often thought that using a local anesthetic (by injection) on the vagus, to temporarily block the inflammatory signals sent along this nerve, might be a very interesting experiment to perform on an ME/CFS patient. Would temporarily anesthetizing the vagus nerve, just like a dentist does to the nerves in your mouth, make ME/CFS symptoms disappear for a few hours?

I can't imagine it would be difficult to anesthetize the vagus nerve. Provided the vagus nerve was only anesthetized below the heart (so that heart function is not affected), then I would think this should be safe. It would be like a temporary truncal vagotomy. If temporarily anesthetizing the vagus helped ME/CFS, then a permanentl truncal vagotomy might be considered.



It would also be interesting to know if the incidence of ME/CFS is lower in patients that have had truncal vagotomy. If so, this would tend to indicate the involvement of the vagus nerve in generating ME/CFS symptoms.

Dr John Chia has shown that 82% of all ME/CFS patients have a chronic enterovirus infection of the parietal cells of the stomach (the stomach acid-secreting cells). Now it just so happens that the vagus nerve is directly connected to these parietal cells (since the vagus helps activate these cells to release stomach acid). This chronic enterovirus infection could be sending inflammatory signals to the brain via the vagus, giving rise to the symptoms of ME/CFS.
 
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