To give you a sweeping generalization of the currently competing theories of ME etiology:
- ME is due to a chronic infection of the CNS
- ME is due to some infectious 'trigger', but said trigger is long since conquered by the immune system, which remains hyperactive ever after - or, hyperactive and then depleted
- ME is due to an inborn error of metabolism, immune dysfunction, or a pituitary disorder
- ME symptoms are due to an overabundance of ROS/NOS species
- ME is 'really' some other, better-understood disorder (or a number of them)
- ME is some combination of all of the above: for example, a person with an inborn error of metabolism or immunology contracts Lyme, which goes on to infect the vagus nerve; meanwhile, the immune system responds via processes that generate ROS/NOS as byproducts in an endless, positive-feedback loop of hyperexcitatory immunological action.
Two general documents that may be helpful:
First of all, here is the blog post regarding the document I put together that summarizes ME: Myalgic encephalomyelitis: a multi-system disorder. There is a pdf attached at the bottom of the post; it would probably be wise to access it from there, if you should wish to print it out. It really doesn't encompass the entire illness; it is a primer written for patients to hand to their physicians, especially those who are combating a diagnosis of depressive disorder instead.
Here is a summary of the Canadian Consensus document that defined myalgic encephalomyelitis as a clinical entity in 2013. It contains the clinical definition and diagnostic criteria for ME, although it is actually a summary of the original document, which was much longer. This is geared towards clinicians.
Three pieces of primary literature that may be helpful:
Here is the widely-read Hornig study from earlier this year that showed patterns in immunological markers in people with ME in the first three years of illness vs long-time patients: Distinct plasma immune signatures in ME/CFS are present early in the course of illness.
Here is the laudable Julie Newton study showing abnormal glucose uptake in the muscle cells of patients with ME. Abnormalities of AMPK activation and glucose uptake in cultured skeletal muscle cells from individuals with Chronic Fatigue Syndrome
Michael Maes works from the understanding that ME is the result of ROS and NOS gone out of control; he also posits that the same process is occurring in other neurological diseases. He's very prolific, but the most recent, helpful thing I've read from him is a paper on lipid peroxidation: The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.
And finally, something from a patient advocacy group:
Here is the survey data regarding the effect of pacing therapy, cognitive behavioral therapy, and graded exercise therapy on ME patients. It's very long, but it's important to note the first chart on page 4: using 'graded exercise therapy' in which the technique is to ramp up physical activity regardless of perceived setbacks, 74% of patients noted a worsening of their symptoms, long-term. Many ME patients continue to fight against a prevailing narrative that it is possible to 'exercise oneself well'.
I'm sure that's more than enough to get started with! Thank you so much for being
[supportive / kind / not a raving egomaniac / actually interested in research / not a terrible human being.]