Morris, Gerwyn, Maes, Michael · Current neuropharmacology · 2014 · DOI
This study proposes that ME/CFS involves a harmful cycle where the body's immune system becomes overactive and produces damaging molecules called oxidative stress. These problems can be triggered by infections, gut bacteria leaking into the bloodstream, or problems with the energy-producing parts of cells called mitochondria. Once started, this cycle feeds on itself, causing brain inflammation, reduced blood flow to the brain, and damage to cells throughout the body.
Understanding that ME/CFS may involve interconnected cycles of immune activation and oxidative damage could explain why the condition is so persistent and multifaceted. This framework suggests that breaking these cycles—through targeting infections, reducing oxidative stress, or modulating immune function—might be therapeutic approaches worth investigating.
This is a theoretical review that synthesizes existing knowledge rather than presenting new experimental results, so it does not provide direct empirical proof of causation. The study does not establish which triggering factors are primary versus secondary, or whether O&NS and immune activation are causes or consequences of ME/CFS. It also does not demonstrate that targeting these pathways will effectively treat the disease.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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