Hi, all.
For what it's worth, quite a few PWCs have sent me their results from these tests. I find them interesting. They document in detail that there is mito dysfunction in ME/CFS. There are a few differences in detail from one PWC to another, such as which toxins are present, but generally they all show the same types of problems, if the person has ME/CFS.
In my opinion, the mito dysfunction in ME/CFS originates from glutathione depletion and a partial block in the methylation cycle.
The glutathione depletion allows oxidative stress to build up in the mitochondria, and it also allows buildup of toxins. The oxidative stress and the toxins interfere with the production of ATP, which is the main product of the mitochondria. Low ATP affects the energy supply to the membrane ion pumps, and that allows calcium to rise and magnesium to drop.
The partial methylation cycle block decreases the rate of production of carnitine and coenzyme Q10, both of which are needed by the mitochondria. Creatine production also requires methylation, and creatine is used to transport, store and exchange energetic phosphate groups supplied by ATP. Methylation is also required to convert phosphatidyl ethanolamine to phosphatidyl choline, and the proper amounts of each are needed for the inner mito membrane. All of these are found to be deficient in ME/CFS. I think that low methylation capacity is the reason.
So in my view, if you want to help the mitochondria, you must deal with the partial methylation cycle block, which in turn will allow glutathione to come up.
I think that doing what Dr. Myhill suggests to remove toxins can be helpful as well, and supplying her package of mito support nutrients (magnesium, B vitamins, carnitine, CoQ10 and ribose) can also be helpful. But it's also necessary to get at the root of the problem in order to restore the mito function, and that's where the methylation cycle treatment comes in.
I don't think that Dr. Myhill and Dr. McLaren Howard have bought into my explanation for the origin of the mito dysfunction in ME/CFS, but they do measure red blood cell total glutathione. This does not reflect intracellular glutathione levels in the tissues very well, but nevertheless, they often do find low RBC total glutathione. When it goes low in the RBCs, it is likely very low in the tissue cells, because the RBCs are normally net producers and exporters of glutathione. When they are low, everybody is low!
I also note that Dr. Myhill does use something similar to the methylation protocol I have suggested in some of her patients. I just don't think that she makes a direct connection between the methylation cycle problem and the mito dysfunction, but in my opinion, they are very much linked together in a cause and effect relationship.
Best regards,
Rich
