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ME/CFS Metabolomic Study Points to a Potential Cause of Mitochondrial Dysfunction


Senior Member
Another write up by Cort on Healthrising.

The low plasmalogen levels implicated small organelles in the cell called peroxisomes. These organelles, which have not been highlighted in ME/CFS before, are the site of plasmologen synthesis. They help maintain the cellular membranes, reduce oxidative stress, and perhaps most importantly, break down very-long-chain fatty acids to metabolic intermediates that the mitochondria can use to produce ATP. Without the peroxisomes breaking down those fatty acids, the mitochondria won’t have the fuel they need to produce ATP.

And for those playing with supplements the consequence of these low organelles is

  • Low plasmalogen levels inhibit the breakdown of long-chain fatty acids to compounds the mitochondria needs to produce ATP. (The low plasmalogen levels implicate the peroxisome organelles in the cell).
  • Low levels of carnitine may be interfering with ATP production.
  • Reduced levels of unsaturated phosphatidylcholines (PCs) may interfere with mitochondrial functioning by impairing the flow of proteins into the cell.
  • Low choline levels may indirectly impact mitochondrial functioning by impairing the production of PCs.

Suggesting taking Carnitine, PCs and Choline may be beneficial.



Senior Member
See previous thread where this study was posted (Jan 2022). Probably best to continue this discussion there instead..?

Even earlier thread where a previous version of the same paper (with a different title) was discussed in greater detail (July 2021): "Dysregulation of the Kennedy Pathway and Tricarboxylic Acid Cycle in ME/CFS (Che et al., 2021)"

The full text of this pre-print paper: "Evidence for Peroxisomal Dysfunction and Dysregulation of the CDP-Choline Pathway in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome"