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  • Joan Rothchild Hardin

Chronic Fatigue Caused by Vagus Nerve Infection?


Source: Dr. Jockers

If you have Chronic Fatigue Syndrome (CFS), you know its difficult to get a definitive diagnosis.  Confusingly, its symptoms resemble many other health conditions and there’s no single test for identifying it. You also know its symptoms seriously interfere with living your life as you’d like.

The principal characteristic of Chronic Fatigue Syndrome (CFS) is extreme fatigue. The fatigue may worsen with physical or mental activity but doesn’t lessen with rest. CFS is also sometimes referred to as myalgic encephalomyelitis (ME) or systemic exertion intolerance disease (SEID).

People with CFS – and other energy-sapping chronic conditions as well – often use Spoon Theory to describe their experience of being chronically exhausted and the limitations that imposes on their lives. Spoon Theory is a clever metaphor created by Christine Miserandino, a woman with both lupus and Chronic Fatigue Syndrome, to explain to friends and family what it’s like to have limited and unreliable energy. (MEpedia, 2017).

Check out her website butyoudontlooksick.com for more information.


Source: MEpedia

AUTOIMMUNE CONDITIONS & DISEASES

Lupus, by the way, is a chronic autoimmune disease “in which the body’s immune system becomes hyperactive and attacks normal, healthy tissue. Symptoms include inflammation, swelling, and damage to the joints, skin, kidneys, blood, heart, and lungs.” (Brazier, 2018)

There’s still ongoing discussion about whether CFS is also an inflammatory, autoimmune condition. Considerable research indicates that chronic low level inflammation in the body leads to the constellation of symptoms described as Chronic Fatigue Syndrome. (Dellwo, 2018 A)


Source: vliquidassets.com

This is my shorthand description of how autoimmune conditions and diseases develop: Chronic imbalance in the contents of the gut microbiome (gut dysbiosis) -–> leaky gut -–> chronic low level inflammation in the body, which eventually -–> one or more autoimmune diseases

Autoimmune diseases develop when the body’s immune system produces an inappropriate immune response against its own tissues. Because the vast majority of our immune system (70-80%) is located in the composition of our gut microbiome, this is where we need to focus to understand how we come to develop an autoimmune disease (probably more than one) and also how to reverse these types of diseases.

When the immune system stops recognizing as “self” something that’s a normal constituent of the body, it starts producing autoimmune antibodies that attack the body’s own cells, tissues and/or organs. This produces chronic inflammation that damages these body parts and leads to full blown autoimmune diseases.

See my post AUTOIMMUNE DISEASES: How they develop and how to put them in remission for more information. (Hardin, 2014)

A MORE THOROUGH EXPLANATION OF CHRONIC FATIGUE SYNDROME

Michael B. VanElzakker, PhD


Source: Simmaron Research

Researcher Michael B. VanElzakker, now a neuroscientist affiliated with Massachusetts General Hospital, Harvard Medical School and Tufts University, has proposed a more specific explanation for how Chronic Fatigue Syndrome develops.

In a 2013 paper, Chronic fatigue syndrome from vagus nerve infection: a psychoneuroimmunological hypothesis, VanElzakker described his novel psychoneuroimmunological hypothesis as the VAGUS NERVE INFECTION HYPOTHESIS (VNIH).

In the 2013 paper he pointed out that Chronic Fatigue Syndrome researchers mostly agree that CFS symptoms seem to reflect an intense, ongoing immune response, possibly due to a viral infection. They therefore were focusing their research on trying to uncover the specific pathogenic agent in plasma and blood cells responsible for the syndrome – without success. (HHV-6 Foundation, 2018)

Instead, VanElzakker proposed that CFS develops from an infection of the vagus nerve.

Herpesvirus infections of the trigeminal nerve cause shingles.  Do human herpesvirus infections of the vagus nerve cause chronic fatigue syndrome?


Source: Simmaron Research

“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.”

His Vagus Nerve Infection hypothesis of CFS contends that the syndrome’s cluster of 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.

“Drawing upon relevant findings from the neuropathic pain literature, I explain how pathogen-activated glial cells can bombard the sensory vagus nerve with proinflammatory cytokines and other neuroexcitatory substances, initiating an exaggerated and intractable sickness behavior signal.”

Following this new hypothesis, it’s possible any pathogenic infection of the vagus nerve could cause CFS, resolving the ongoing controversy about identifying  a single pathogen.

VanElzakker’s hypothesis integrates two of the most important actors in CFS, the autonomic nervous system and the immune system, offering an explanation of what causes the brain to receive a non-stop stream of messages instructing it essentially to shut down the body by producing fatigue, pain and other disabling symptoms. It proposes that “nerve loving viruses trigger a difficult to detect  immune response which produces the fatigue and other symptoms present in chronic fatigue syndrome.” (Cohen, 2019)

The VNIH focuses on sensory nerves, “an increasingly hot topic in ME/CFS/FM” and coincides with an established model of fibromyalgia. If this hypothesis is correct, it will change how Chronic Fatigue Syndrome is viewed, researched and treated. (Johnson, 2013)

VanElzakker’s work on CFS has zeroed in on the human herpes viruses – with the human herpes virus 6 (HHV-6) at the top of his list of suspects. (HHV-6 Foundation, 2018)

See Human Herpesvirus 6 (HHV-6): Its Role in Disease – Links to Numerous Diseases for a list of diseases associated with HHV-6 types A and B.  (Dellwo, 2018 B)

Histological slide of the human herpes virus-6 (HHV-6)showing infected cells


Source: Wikipedia

The following two paragraphs from the HHV-6 Foundation’s article CFS: a herpesvirus infection of the vagus nerve? discuss, in fairly technical terms, VanElzakker’s theory  of how a human herpesvirus-6 infection of the sensory vagal ganglia or paraganglia could produce the intense symptoms found in people with Chronic Fatigue:

“During infection, the sensory vagus nerve sends a signal to the brain to initiate “sickness behavior,” an involuntary response characterized by fatigue, fever, myalgia, depression, and other symptoms that are often observed in patients with CFS. However, VanElzakker proposes that when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria, these symptoms would be exaggerated. He notes that many of the symptoms of sickness behavior (such as fatigue, sleep changes, myalgia, cognitive impairment, depression and zinc depletion) are also mediated by proinflammatory cytokines and observed in CFS.

“Herpesviruses and certain intracellular bacteria establish latency in the vagus nerve and reactivate during periods of stress or illness, causing the release of proinflammatory cytokines. HHV-6 is a highly neurotropic virus and potent inducer of cytokines such as IL-6 and NFkB, which many groups have proposed as an etiological theory for the role of HHV-6 in neurological conditions such as seizures and epilepsy. If this low-level “chronic” infection is localized to the vagus nerve it would be undetectable in the plasma, but could be demonstrated through analyzing tissue biopsies of the vagus nerve, VanElzakker suggests. HHV-6 is well-known for invading the hippocampus and other parts of the limbic system, and also establishes residence in the human sensory ganglia along with other neurotropic herpesviruses including HSV-1 and VZV.” (HHV-6 Foundation, 2018)

THE VAGUS NERVE

The vagus nerve, historically called the pneumogastric nerve, is the 10th cranial nerve and interfaces with the parasympathetic control of the heart, lungs, and digestive tract. The vagus nerves are paired but are normally referred to in the singular. It’s the longest nerve of the autonomic nervous system in the human body. (Wikipedia, 2019)

As the two branches of the vagus nerve make their way between the brain and the gut, they connect to every organ they pass along the way.


Source: Dr. Vittoria Repetto’s Blog

THE VAGUS NERVE & THE GUT MICROBIOME CONNECTION


I’ve been intrigued by the vagus nerve since discovering it’s a key player in the Gut/Brain Axis – the constant, two-way communication taking place between our brains and our guts.


Source: First for Women

From my 2015 post How the Gut Microbiome Influences the Brain – and Vice Versa:

“Maybe you’re used to thinking of the brain in your head as your only brain – but your body actually has TWO BRAINS: In fact, the ‘brain’ in your gut does a lot more than digest your food. While this brain doesn’t produce thoughts, it contains its own independent nervous system along with more neurotransmitters and serotonin than the brain in your head.

“Sheaths of neurons are embedded in the walls of the entire alimentary canal. Technically known as the enteric nervous system, this gut brain measures about 9 meters (29.5 feet) from esophagus to anus and contains about 100 million neurons, more neurons than exist in either the spinal cord or the entire peripheral nervous system. Equipped with its own reflexes and senses, this second brain can control gut behavior independently of the brain. Here’s a single example to  give you an idea of the importance of the gut brain for the entire body:  About 90% of the fibers in the vagus nerve, the largest of the visceral nerves, carry information FROM the gut TO the brain – but not the other way around.” (Hardin 2015)