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Animal studies indicate that fatigue/flu-like symptoms go gangbusters when the vagus nerve gets infected. In fact, it’s possible the flu-like symptoms associated with infections wouldn’t even exist without the vagus nerve. Rodents with their vagus nerves cut don’t act sick even after they’ve been infected with a pathogen; the fevers, fatigue, the desire for isolation – are gone.
I'm a little puzzled by the idea that the cytokines are only localized and not in the blood. Immune studies have shown both immune cell abnormalities (NK cell abnormalities for one) and abnormalities in circulating cytokines. It seems that these significant results are contrary, or at least unexplained, by the theory of a hit-and-run infection of the vagus nerve
Yes, I think I get that. The thing is, abnormal cytokine patterns are found in the blood in a significant group of CCC/ICC-defined patients, aren't they? Are you thinking that these are somehow getting there from the spinal fluid? Since I don't know much about the immune system, I guess it's not surprising that I don't get how abnormal spinal fluid cytokines can be normal in the blood.Cort explains this in the comments rather well. No cytokines are needed in the blood to invoke a major brain response, only at the vagus nerve. That nerve sends the signal to the brain (probably) that orchestrates the brain response.
However do be aware that the brain is connected to spinal fluid, and abnormal spinal fluid cytokines may be normal in the blood. Lipkin is looking into this.
Thanks, Alex. I read the article, but I'm really struggling cognitively lately. I appreciate you clearing that up for me.Hi @SOC, the article covers this. Whether or not abnormal cytokines are in the blood might (an hypothesis) be due to the location of the infection. If the vagus nerve is infected in the spine then only spinal abnormalities are likely to be found, but if its in the body then it can get into the blood.
Also the brain response may change our immune system with unpredictable consequences for the most part.
There is far too much of this model that is still speculative. I wish the science were done tomorrow. Maybe if I wish real hard at New Year?
So which is it - are we trying to stimulate the vagus nerve, calm down the overactive vagus nerve or something else? I don't get it.
These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.
So this is saying that we want to stimulate the vagus nerve to produce acetylcholine.
But what if the vagus nerve isn't producing acetylcholine properly anymore because it is overstimulated already? In that case, wouldn't we want to calm it down?
And how to tell the difference?
If it's the second scenario, could glial damage show up on a scan?