Posted on 02/22/2014 7:00:16 PM PST by Seizethecarp
Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune system dysfunction or specific pathogenic agent. However, no single causative agent has been found. In this speculative article, I describe a new hypothesis for the etiology of CFS: infection of the vagus nerve. When immune cells of otherwise healthy individuals detect any peripheral infection, they release proinflammatory cytokines. Chemoreceptors of the sensory vagus nerve detect these localized proinflammatory cytokines, and send a signal to the brain to initiate sickness behavior. Sickness behavior is an involuntary response that includes fatigue, fever, myalgia, depression, and other symptoms that overlap with CFS. The vagus nerve infection hypothesis of CFS contends that CFS symptoms are a pathologically exaggerated version of normal sickness behavior that can occur when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria.
(Excerpt) Read more at medical-hypotheses.com ...
Here is a more detailed article about this vagus nerve hypothesis on a ME/CFS research blog(hat-tip to this blog):
“One Theory To Explain Them All? The Vagus Nerve Infection Hypothesis for Chronic Fatigue Syndrome”
VanElzakker proposes that an infection triggers ME/CFS, but if his theory is right the most important thing about that infection is not what it is but where it is. That ‘where’ is the biggest nerve in the body; the vagus nerve – a ‘wandering nerve’ that stretches over much of our torso and sends its roots into most of the organs of the body.
The vagus nerve isn’t just any nerve; it’s the nervous system’s immune conduit to the brain. VE believes that an infection there doesn’t need to be large to cause havoc in the brain; it just needs to be present.
In some ways, vagus nerve appears, in fact, to be ripe for infection in ME/CFS. As it ‘wanders’ through the body it comes into contact with virus havens such as the esophagus, stomach, lungs and spleen, all of which have likely at one time or another harbored the herpesviruses (HHV6, HHV-5 [cytomegalovirus], HHV-4 [Epstein-Barr virus]) that have been thought to be associated with ME/CFS for decades.
Most humans carry several of these herpesviruses in latent form unless some stressor or biological event allows them to become reactivated.
VanElzakker believes that upon reactivation these viruses replicate and move outside the nerves where they run into glial cells that attempt to gobble them up. The glial cells perk up remarkably in the presence of viruses, releasing all manner of pro-inflammatory and neuroexcitatory compounds (proinflammatory cytokines [IL-1B, IL-6, TNF-a], glutamate, prostaglandins, nitric oxide and free radicals. ) - See more at: http://simmaronresearch.com/2013/12/one-theory-explain-vagus-nerve-infection-chronic-fatigue-syndrome/#comment-5430
I’ve read that the vagus nerve may constitute another brain.
With all the chemical additives and hormones and GMO we stuff in our food and let polute our waters, I wonder if any of that has to do with syndromes like CFS and Fibromyalgia?
BOOKbump
Good article, the trouble is, what happens is Vagus doesn’t always stay in Vagus!
I don’t think it’s new news that people who are fatigued, stressed, and depressed tend to have health problems becasue these things can break down your immune system. Maybe this is a detailed explanation of how it happens, but the cause-effect thing doesn’t seem to be new news.
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*snicker*
“I’ve read that the vagus nerve may constitute another brain.”
The vagus nerve is involved in a lot of “autonomic” processes that are semi or totally autonomous:
http://en.wikipedia.org/wiki/Vagus_nerve
The vagus nerve supplies motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, notable ones being:
Cricothyroid muscle
Levator veli palatini muscle
Salpingopharyngeus muscle
Palatoglossus muscle
Palatopharyngeus muscle
Superior, middle and inferior pharyngeal constrictors
Muscles of the larynx (speech).
This means that the vagus nerve is responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, and quite a few muscle movements in the mouth, including speech (via the recurrent laryngeal nerve) and keeping the larynx open for breathing (via action of the posterior cricoarytenoid muscle, the only abductor of the vocal folds). It also has some afferent fibers that innervate the inner (canal) portion of the outer ear, via the Auricular branch (also known as Alderman’s nerve) and part of the meninges. This explains why a person may cough when tickled on the ear (such as when trying to remove ear wax with a cotton swab).
With CFS (the defined syndrome, of just “chronic fatigue”) the body appears to be trying to fight of a pathogen somewhere in the body. Chemical additives and hormones, etc., aren’t pathogens and haven’t been found to provoke the same cytokine responses in the body seen in CFS as far as I know.
“Often, mild to mild/heavy exercise for 20-30 minutes a day helps dissipate chronic fatigue.”
A person with simple “chronic fatigue” who responds favorably to what is called “graded exercise training” or GET does NOT have true CFS in my understanding.
People with CFS, the identified syndrome, have something called post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE). They can suffer a relapse after even moderate exercise that mysteriously starts 24 to 48 hours AFTER the exercise and can last for a week or longer.
I have experienced this for the last 13 years!
People with CFS must scrupulously minimize their activities (called pacing) and limit their exercise to avoid debilitating relapses.
Here is a video lecture from the NOVA University’s CFS research center on excecise and CFS. They have found that CFS sufferers do best when they limit specific exercise to 2 minutes:
Here is a link to numerous NOVA CFS lectures from the opening day their opening day of their new CFS research center and clinic in January 2013:
http://www.nova.edu/nim/past-events.html
“Maybe this is a detailed explanation of how it happens, but the cause-effect thing doesn’t seem to be new news.”
CFS patients appear to be responding to a pathogen but no pathogen has been found in the blood to date.
What is new in this article is the hypothesis that the pathogen is attacking multiple organs not from the blood but from within an infected vagus nerve!
Post of the day!
Interesting, informative and : )
And one of the sneakiest and most mutatable infections comes from Chronic Lyme Disease—an infection the CDC is loathe to discuss.
Interesting, and again, seems to support and give a more detailed explanation as to why frayed nerves and stress cause disease.
“Just curious, do people that have CFS suffers from seizures more often than the general population?”
I have seen no increased correlation between CFS and actual seizures in the research, although a person could also have seizures just as they could also have any other condition.
What I have seen and do experience personally is debilitating orthostatic intolerance (intolerance of sitting or standing) which results on loss of blood to the brain.
This causes fainting (syncope) or near-fainting (pre-syncope).
For people with CFS this is usually caused by either POTS (Postural Orthostatic Tachycardia Syndrome) or neurally-mediated syncope (aka neurocardiogenic syncope).
As you can see there is a lot of jargon.
Here is the Wiki-page on POTS:
http://en.wikipedia.org/wiki/Postural_orthostatic_tachycardia_syndrome
Here is the Wiki-page on neurally-mediated syncope (also aka vasovagal response):
http://en.wikipedia.org/wiki/Neurally_mediated_syncope
So no seizures with CFS but when the brain stops working it
might as well be!
The way that othostatic intolerance is confirmed is by using a “tilt-table” test conducted by a cartiologist in a lab where they can revive you if you pass out (in agony). I made a little joke with the MD that the tilt-table test is like being crucified, only without the nails. He joked back to me that they had stuck two IV’s into me, one in each arm, so it was getting close!
Here is the Wiki page on tilt-table test:
http://en.wikipedia.org/wiki/Tilt_table_test
“A tilt table test, occasionally called upright tilt testing,[1] is a medical procedure often used to diagnose dysautonomia or syncope. Patients with symptoms of dizziness or lightheadedness, with or without a loss of consciousness (fainting), suspected to be associated with a drop in blood pressure or positional tachycardia are good candidates for this test.
“The procedure tests for causes of syncope by attempting to cause syncope by having the patient lie flat on a special table or bed and then be monitored with ECG and a blood pressure monitor. The table then creates a change in posture from lying to standing.”
“Interesting, and again, seems to support and give a more detailed explanation as to why frayed nerves and stress cause disease.”
Stress has been shown to be correlated to the onset of a large subset of CFS cases due to compromise of the immune system caused by stress. The resulting vulnerability makes possible attack by either new pathogens or the reactivation of old pathogens in the body that the immune system can no longer keep in check.
However, there is a large subset of CFS cases where there is NO link to stress but rather a sudden onset after a viral disease in perfectly healthy non-stressed people many of whom were athletes in top condition.
At the NOVA clinic I am currently being screened for antibodies of a range of viral infections and also with PCR testing to detect specific DNA of possible reactivated viruses or new pathogens.
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