XMRV cuadra teoría Konynenburg metilación.

[EndSFC]

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Thank you for your interest!

At this point, I think that the GD-MCB hypothesis is still viable to describe the pathogenesis and pathophysiology of ME/CFS. It really has always been a pathogenesis and pathophysiology model. I've always included several possible etiologies (root causes) in this model, any combination of which can deplete glutathione, and from there on, the model goes on to describe how the biochemistry gets disrupted and what the detailed mechanisms are that give rise to the symptoms. Among the etiologies has been what I have called "biological stressors," and these include the pathogens (bacterial, viral, fungal and parasitic) as well as vaccinations, blood transfusions, and a diet deficient in essential nutrients. XMRV would fit there. Whether it's a "first cause" or whether it is exacerbated by something else, such as inflammation caused elsewhere or EBV or other viral infections, remains to be seen, I think.

I do think it is becoming more clear that the partial methylation cycle block is intimately involved with expression of viral and retroviral genes, and that glutathione depletion favors viral and retroviral activity. There appears to be a vicious circle mechanism by which the viruses promote these problems and also benefit from them. I think it's a very exciting time for the development of the understanding of the pathogenesis and pathophysiology of ME/CFS. I'm also intrigued by how the gut-related stuff seems to be coming together with the rest of it.
Here's some stuff to think about: some people have gluten or casein sensitivity, and this interferes with cysteine absorption by the gut. This does two things: it denies the body cysteine, which is the rate-limiting amino acid for making glutathione, and it gives cysteine to the gut bacteria. The latter promotes growth of bacteria that can ferment cysteine, and convert it to hydrogen sulfide. This then is absorbed into the blood and causes lots of problems, including promoting mito dysfunction and impacting the hypothalamus (the latter according to Dr. de Meirleir).

Of course. not everyone has casein and gluten sensitivities, but this is just one way these things are coming together. I think there is a pretty clear connection between GD-MCB and mito dysfunction directly, too, and this brings in the work of Myhill et al. My view is that Pall's work comes out of the methylation cycle partial block, though he disagrees with this. I think Cheney's heart work, the diastolic dysfunction, comes out of mito dysfunction in the heart muscle cells, though he may not agree with this. And Dick Deth's work is supporting the connection between oxidative stress and the inhibition of the methylation cycle. He and I are very much on the same page. Shoemaker's work may tie in by the depletion of glutathione by mold toxins, which has been observed for at least some of them. Also, the ongoing activation of the innate immune system as a result of toxins that the adaptive immune system in some people cannot recognize because of their HLA genotypes would place an ongoing demand on glutathione, I think. It's going to be quite a story when all of this is linked together with all the I's dotted and the T's crossed. What makes it challenging is that some different things are going on in different people. They all do seem to channel together into a partial methylation cycle block, though.

Best regards,

Rich

[gerardo]

Muy interesante ENDsfc

Me explico así mi respuesta casi inmediata que tuve a la acetilcisteina. Es posible que no estuviera absorbiendo bien la cisteina.

Desde que sigo el ciclo de metilación no tomo acetilcisteina creo que ya con este no me mejoraba más la acetilcisteina, pero puede que haga el experimento de tomarla unos días a ver que pasa

Un saludo