Rusin, Andrej, Li, Megan, Cocchetto, Alan et al. · Medical hypotheses · 2021 · DOI
This paper explores the idea that ME/CFS may be caused by damage to mitochondria—the energy-producing parts of cells—possibly triggered by radiation exposure or other environmental stressors like viruses or toxins. When mitochondria cannot produce enough energy, cells throughout the body struggle, and neighboring tissues try to compensate, which may explain why ME/CFS patients experience widespread symptoms like fatigue and immune problems.
This work addresses a critical gap by proposing testable mechanisms connecting environmental exposures to the well-documented mitochondrial dysfunction observed in ME/CFS patients. If validated, the proposed biomarkers could enable objective diagnostic tools and identify disease subtypes, potentially leading to targeted interventions.
This paper does not prove that radiation exposure causes ME/CFS, nor does it establish that mitochondrial dysfunction is the primary (rather than secondary) driver of the disease. As a hypothesis paper reviewing existing literature rather than reporting original experimental or clinical data, it cannot demonstrate causation or validate the proposed biomarkers in patient populations.
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 →
Spotted an error in this entry? Report it →