Discussion in 'General ME/CFS Discussion' started by Sushi, Apr 18, 2013.
Posted with permission from the author who is in medical school (English is his second language):
One thing I might add is that several pathways likely to be active in CFS and ME might produce peroxynitrite, massively increasing oxidative stress, and perhaps an initial trigger for dropping glutathione to critical levels which are hard to replace if you have a genetic defect limiting glutathione synthesis.
What a lot of hypotheses miss though is explaining the high prevalence of EDS. To me this points to gut involvement, with increased bacterial and other toxins entering the body, overwhelming and further depleting liver glutathione and other detox mechanisms.
Further, glutathione is critical to mitochondrial function. Its needed to fold aconitase, a critical mitochondrial enzyme, and probably other enzymes too. Any enzyme that requires folding to a final shape (conformation) and is then imported to the mitochondria might be defective. I know that aconitase is a nuclear protein that is imported into mitochondria, but I bet there are others. Deficiency in functioning enzymes (but not necessarily quantity of total enzyme) will not affect the mitochondria much at rest, but will limit the maximum energy available.
Thanks for the post Alex; could you say what you mean by EDS please?
Allyson Ehlers-Danlos Syndrome, in all its variations including those not discovered yet: EDS.
Great thanks Alex, yes I think i has been overlooked to to a great extent; I understand they are re- classifyinghte types again too as more people get diagnosed; i think they used to think you had to be hypermobile to have it and that is now aparently ot the case so many people who havee stiff muscles for whatever reason have been excluded, erroneously.
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