How do you reconcile the test results that myself and others like you have of positive Coxsackie and Echovirus tests (Mine were actually Coxsackie A7,A9,A11,A21. Very high titers too. Plus high nagalese), with the recent series of studies showing hypo metabolic function, with the possibility that the enterovirus may not be the causal factor of the disease?
Hi
@eljefe19, glad you decided to join the forum.
I think it could be reconciled if enterovirus, or other viruses linked to ME/CFS, such as EBV, are triggering an autoimmune response that targets and disables mitochondria, or some related area of the energy metabolism.
The rituximab studies indicate that there is likely autoimmunity going on in ME/CFS (and the two orthostatic intolerance conditions common found in ME/CFS, namely orthostatic hypotension and POTS, have also been linked to autoimmunity); so there is a good argument for an autoimmune basis of ME/CFS.
So actually what we need to do is reconcile three areas: the large amount of studies that have shown enterovirus is linked to ME/CFS, with the fact that ME/CFS likely involves autoimmunity, with the fact that energy metabolism seems to be dysfunctional in ME/CFS.
The idea that viruses may trigger an autoimmune response that targets the energy metabolism would reconcile these three areas, and explain a lot of what we already know about ME/CFS.
I am similarly over anxious and moody with no clear reason why, along with lots of neuro and body inflammation. I take NAG, Flax, Low dose amisulpride, etc.
Did these supplements help your anxiety to any degree?
My ability to focus is destroyed by this illness, and so your well sourced and formatted posts are a tremendous help.
Glad that these posts have been a help to you.
In fact it's only by slow methodical writing of my posts, and making a clear layout, that I am able to understand the material myself!
I have the same brain fog problems, and ADHD too, which makes reading text difficult for me, and I find the process of writing posts with a clear layout helps me get to grips with the material I am trying to learn.
How do you reconcile the is microglial activation harmful or helpful debate?
The
three brain autopsies that so far have been conducted on deceased ME/CFS patients all showed some degree of enterovirus infection in the brain. So if brain infection is common in ME/CFS, you might expect some chronic microglial activation, just in order to keep the infection in check.
There are two main modes of microglial activation: the
classical mode, which is the "kill" mode that destroys pathogens, but which is also neurodestructive and causes collateral damage. (One major destructive factor in the classical mode may arise when microglia activate an enzyme called NADPH oxidase. This enzyme generates superoxide in order to kill pathogens, but the superoxide probably also causes some mild collateral damage.)
There is also the
alternative mode of microglial activation, which is the "repair and heal" mode, and presumably this alternative mode would normally kick after microglia in the classical mode have completely killed the brain infection.
But if the brain infection is chronic and cannot be fully eradicated, it's hard to say what might be going on. I have not seen any research on this. Perhaps the microglia might remain in the classical mode, but at a low level of activation, just to keep the infection in check.
I don't think neurological damage from microglial activation will be major factor in most cases of ME/CFS, as not many patients show brain lesions on their MRI scans.
Also, consider the fact that some patients report very occasional periods where they spontaneously obtain temporary but complete remission from symptoms for period of a few days. If ME/CFS were caused by major damage to the brain, such remissions would be hard to explain. Those remissions suggest that there is nothing much physically wrong with the brain.
It seems more likely that some chronic immunological dysfunction is driving the brain symptoms; then when you get a few day where the immune system rights itself for a short time, the temporary spontaneous remissions occur.
I compiled a large list of microglial activation inhibitors in
this post. There is also section in that post for supplements that favor the neuroprotective alternative mode of microglial activation, over the neurodestructive classical mode.
Of particular interest is apocynin from the herb Picrorhiza kurroa, which is a potent NADPH oxidase inhibitor, and has been shown to promote the neuroprotective alternative microglial mode of activation.
It may be worth experimenting with these microglial activation inhibitor supplements; however, assuming there is a low level brain infection in many ME/CFS patients, I should think that you will always have some degree of classical microglial activation, as this will be needed just to keep the infection under control.
I should say I follow your posts religiously.
Not a good idea! Better to be a bit skeptical and questioning!
