Energy

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.

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  • One hypothesis is cell mitochondria are shutting down production as a firewall against oxidation stress and the neuroinflammatory damage caused if normal ATP production from mitochondria permitted normal activity levels.

    A safety switch is thrown forestalling an inflammatory cascade by down regulating ATP production under stress signalling at a cellular level, result fast track flat battery we all know.

  • Non-mitochondrial sources jnsci.org/files/article/201...

  • Can u write the above so we can understand what ur trying to say with out all the medical terms, I suffer with this, would like ur help, but HAVNT got a medical degree to understand what u r saying