From the Journal of Nature and Science (open access), October 2016.
Elevated Energy Production in Chronic Fatigue Syndrome Patients.
Nick Lawson(1), Chung-Han Hsieh(1), Dana March(2), Xinnan Wang(1*).
1) Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA.
2) Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
* Corresponding Author. Email: firstname.lastname@example.org
Chronic Fatigue Syndrome (CFS) is a debilitating disease characterized by physical and mental exhaustion. The underlying pathogenesis is unknown, but impairments in certain mitochondrial functions have been found in some CFS patients.
To thoroughly reveal mitochondrial deficiencies in CFS patients, here we examine the key aspects of mitochondrial function in blood cells from a paired CFS patient-control series.
Surprisingly, we discover that in patients the ATP levels are higher and mitochondrial cristae are more condensed compared to their paired controls, while the mitochondrial crista length, mitochondrial size, shape, density, membrane potential, and enzymatic activities of the complexes in the electron transport chain remain intact.
We further show that the increased ATP largely comes from non-mitochondrial sources.
Our results indicate that the fatigue symptom in this cohort of patients is unlikely caused by lack of ATP and severe mitochondrial malfunction. On the contrary, it might be linked to a pathological mechanism by which more ATP is produced by non-mitochondrial sources.