An exciting hypothesis from a neuroscientist could explain chronic fatigue syndrome
It could explain the disappointing Lipkin Chronic Fatigue Initiative pathogen study results. It shows how an infection could trigger ME/CFS and then – poof – seemingly disappear. It includes two hot research topics in ME/CFS; the autonomic nervous and immune systems. It explains how sickness behavior could occur in ME/CFS without high cytokine results. It even includes the sensory nerves – another not research topic in fibromyalgia.
It may incorporate more aspects about ME/CFS into it than any other hypothesis.
Plus it suggests some new treatment possibilities.
It’s called the Vagus Nerve Infection Hypothesis for ME/CFS and it’s got a lot of people excited.
ME is caused by a dysfunction of the autonomic nervous system. The gas pedal is depressed (sympathetic nervous system). This results in a vicious circle in which the body can not relax and recover (parasympathetic nervous system). The problem may be in the vagus nerve, but there are more locations imaginable. I think the problem lies in the area which is called medulla oblongata. It does not necessarily have to be an infection, an autoimmune problem or damage is also obvious. But Michael B. VanElzakker is on the right track. I hope his theory is examined scientifically. I therefore expect to find in the spinal fluid a clue. I look forward to the results from the study by Lipkin and Peterson.
Yes, I wonder when we’re going to hear about the spinal fluid results…
Your theory sure fits my experience Gijs…I hope this area gets lots and lots of research.
This rings true for me – I have POTS and I have palpitations which I thought were heart related and had a holter monitor which found nothing serious. I believe the palpitations are in fact an overstimulated vagus nerve firing off, as they feel like an electric jolt in the centre of my chest – they are worse after eating or with stomach gas or when changing positions – all of which would put pressure on the vagus nerve. I know lots of people have them but I also have cold sores, including one in my nose that has been there for 3+ months!! I hope the research continues to be fruitful.
Cort as you will know I’m a long time skeptic of persistent viruses having a role in CFS but I must admit this seems like an excellent theory and one that aligns in with my own views of a central role for neuroinflammation / microglia in CFS.
Great article thanks, and a happy 2014!
Thanks Matthias…and a good 2014 to you as well. 🙂
Very interesting article and very interesting research. I really look forward to more information as it becomes available about his research.
Wondering how the 2 day CPET results would be explained by this theory? My foggy brain isn’t tying it together for me. Any ideas?
Wow, how interesting.
It could possibly fit with my illness experience. I had a bad but typical case of mono, got well, and then a year later it reactivated while I was living in an apartment with an (unknown to me) toxic mold problem. What if the stress on my (genetically susceptible to mold toxins) body of being exposed to mold toxins allowed the herpesvirus to go deeper into my nervous system and end up at my vagus nerve somehow?
What if people who are genetically susceptible to Lyme bacteria toxins end up with chronic Lyme infections because the bacteria get to their vagus nerve somehow? It could tie Dr. Shoemaker’s discoveries into this theory.
Oh, I had an idea.
What if the herpesvirus or enterovirus infection is retreating to the vagus nerve to get away from biological neurotoxins?
Like, suppose a person gets mono as a teenager, and then gets well. So she’s walking around with herpesvirus dormant in her. Then later in life she gets Lyme disease and the virus reactivates and moves to her vagus nerve to get away from the toxins the Lyme bacteria make.
Or suppose a person gets mono while living in a moldy building, and the infection retreats to the vagus nerve for safety.
Could a research scientist please do an experiment to find out if this could happen?
What would happen if you put a bunch of herpesviruses in a petri dish, and then put some mold toxins in with them. Would the viruses all run screaming to the other side of the dish? Or whatever medium is appropriate to use. Maybe a nerve?
Thanks for listening.
Forebearance