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 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.[1]

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 infections, low gut motility/SIBO, new exposures to 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.

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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.