You are thinking black and white
I am simply explaining the details of Michael VanElzakker's vagus nerve infection hypothesis for ME/CFS, or variations thereof.
Certainly the activators of sickness behavior are more complex than just the vagus nerve route that is the central part of VanElzakker's theory.
If you are interested in the complexities of sickness behavior activation by cytokines, then here goes:
First of all, sickness behavior symptoms can be triggered when IL-1β, TNF-α and IL-6 are released within the brain. So brain inflammation, brain infection and microglial activation which releases these cytokines can directly induce sickness behavior. Autopsies of ME/CFS patients have shown enterovirus infections in the brain tissues, so these brain infections could be one source of sickness behavior in ME/CFS.
In addition, there are also at least
four known pathways by which peripheral infection and inflammation in the body can be detected, and the information transmitted to the brain in order to activate sickness behavior.
1 ➤ The vagus nerve pathway detailed earlier is one of the four pathways, and is the main and most important pathway. It is also referred to as the
neural pathway of sickness behavior activation.
The other three pathways by which peripheral infection and inflammation can activate sickness behavior in the brain involve messages conveyed by these inflammatory cytokines in the blood circulation. These three pathways are called the
humoral pathways of sickness behavior activation.
These three other pathways are essentially three different routes that IL-1β, TNF-α and IL-6 in the blood can either cross the blood-brain barrier and enter the brain to activate sickness behavior, or transmit a signal across the BBB to activate sickness behavior.
2 ➤ The first of the three routes is via active transport of the cytokines IL-1β, TNF-α and IL-6 across the blood-brain barrier and into the brain, where they then activate sickness behavior;
3 ➤ the second of the three routes is where these cytokines in the blood activate endothelial cells and perivascular macrophages in the blood vessels of the brain, which then release prostaglandin E2 within the brain, which promotes neuroinflammation and sickness behavior;
4 ➤ and the last of the three routes is where these cytokines (and also LPS) in the blood activate macrophages on the circumventricular organs and the choroid plexus of the brain, which then in turn promotes neuroinflammation and sickness behavior.
So this last route indicates that LPS in the blood, deriving from say a leaky gut, could activate sickness behavior. So in some ME/CFS patients with gut issues, this last route might be part of the picture of how their ME/CFS symptoms / sickness behavior arise.
Source:
Cytokine, Sickness Behavior, and Depression
