ME/CFS is a challenge for the patients, for medical research and ethics, for all of public health, and for society. The intensified hunt for scientific evidence explaining ME/CFS has large consequences for many thousands of people. Many of the published results need repetition. But as shown in this article the signs that autoimmunity and energy metabolic deficiency is involved in the disease have increased. A hypothetical but logical path, from gastrointestinal tract dysbiosis, to formation of pathogenic autoimmune B cells, to inhibition of energy production and deficient cognition, to flares of cytokine production, can be delineated. The natural history indicates that in many cases infections can elicit or worsen this autoimmunity.
The recently intensified research on ME/CFS yielded many biomarker candidates, as mentioned in this study. The main consequence of this work is that the proposition that there is no logical somatic explanatory model for ME/CFS (14) can be refuted. However, like for virtually all autoimmune diseases, the explanatory model has several tentative steps which need further exploration. The elucidation of the molecular nature of circulating metabolic inhibitors in ME/CFS (275) is a central question. If they turn out to be immunoglobulins, they may directly yield diagnostically useful biomarkers and an explanation of the mechanism underlying ME/CFS.
The risk of giving a hypothetical unifying explanation, as in this study, is that hypothesis can be perceived as fact, and that it influences the perception of the disease. But contacts with ME/CFS patients and those who care for them have convinced us that most can handle the uncertainty that hypotheses involve. Without hypotheses we cannot direct the acquisition of further knowledge of ME/CFS.
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Possibly misdiagnosis of my CFS? Extreme weight loss and severe fatigue.