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Acquired immune and mitochondrial dysfunction hypothesis
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A stressor of some kind ([[virus]], accident, surgery, chemical or other toxic exposure, other trauma) causes [[mitochondrial disorder]]s and [[immune dysfunction]] in genetically susceptible people. The mitochondrial and immune dysfunction could have been occurring prior to the stressor due to [[infectious agents]], acquired over the lifetime of the affected individual. The mitochondrial dysfunction could cause or contribute to the immune dysfunction.<ref>[http://www.cortjohnson.org/forums/threads/end-me-cfs-severe-patient-study-turns-to-the-mitochondria.3949/ End ME/CFS Severe Patient Study Turns to the Mitochondria - CortJohnson.org]</ref> After the stressor has come and gone, low-level infectious agents living throughout the body reactivate, and [[inflammation]], including [[mast cell activation]], occurs. Inflammation, from [[Reactivated infection|reactivated infections]], [[low gut motility]]/[[Small intestinal bacterial overgrowth|SIBO]], new exposures to [[Toxin|toxins]] (with a more sensitized immune system), et al., affects the body and the brain. Microglial activation in the brain causes [[Hypothalamic-pituitary-adrenal axis]] (HPA) dysregulation. A downward spiral of infectious reactivation, inflammation, [[dysautonomia]], and HPA axis dysregulation is set up, which perpetuates the illness. ==See also== *[[Mitochondrion]] == References == {{Reflist}} [[Category:Medical hypotheses]]
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