Ross, Stephanie Maxine · Holistic nursing practice · 2024 · DOI
This review examines how problems with mitochondria—the energy-producing parts of our cells—might contribute to ME/CFS. The study explores the theory that when mitochondria don't work properly, cells can't produce enough energy, which could explain the severe fatigue and exhaustion that ME/CFS patients experience. Understanding this connection may help researchers develop better treatments aimed at restoring cellular energy production.
Identifying mitochondrial dysfunction as a core mechanism in ME/CFS could redirect clinical research toward therapies targeting cellular energy metabolism and bioenergetics. This mechanistic understanding may help distinguish ME/CFS from other fatigue-related conditions and validate the biological nature of the disease for patients and clinicians.
This review does not establish that mitochondrial dysfunction is the primary cause of ME/CFS or prove causation—it presents a mechanistic hypothesis based on existing evidence. The study cannot demonstrate treatment efficacy or determine whether mitochondrial abnormalities are primary defects or secondary consequences of disease processes. Clinical applicability and patient outcomes remain to be tested through prospective intervention studies.
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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