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    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

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The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure


Senior Member

It's basically what I've believed ME is, just in higher, professionally supported, detail: that glial cells affect pretty much all aspects of body function, and get locked into an abnormal state.

"Finally, and possibly most importantly, astrocytes and microglia are unique among all cellular compartments in their flexible response to stress, which includes the formation of “stress memories”: Following pro-inflammatory stimulation glia remain in a reactive state and become hyperresponsive to subsequent stimulation because primed neuroglia respond at a different threshold than homeostatic neuroglia. Also, once repetitively stimulated by challenges, the “activation” threshold may decrease and with it the ability of the glial cells to revert to homeostatic physiological functions. In this context-dependent flexibility, neuroglia may be a prime candidate to explain the unique phenomenon of PEM (see section “Post-exertional malaise”). It may also explain why ME/CFS patients clinically deteriorate over time if they chronically exceed their “energy envelope” and why “pacing,” i.e., the strict observation of energy limits, so far remains the only effective “therapy” for ME/CFS."

Optimistic bit: "It has indeed been suggested that, if a cure for ME/CFS was found tomorrow, the vast majority of ME/CFS patients may rise out of their misery biologically unharmed"