Hi, kdp.
Yes, cell membranes are also made of phospholipids. There are several types of phospholipids. Cardiolipin is one of them, and it is found almost exclusively in the mitochondrial membranes, and mainly in the innner mitochondrial membrane. Its role or roles are the subject of ongoing research, and at least one of them seems to be involved with the process of apoptosis, i.e. the organized type of cell death.
Most of the oxidizing free radicals in the cell are produced in the mitochondria, so when there is oxidative stress (i.e. an excess of oxidizing free radicals, in my hypothesis due to glutathione depletion), the mitochondrial membranes sustain the most damage.
Yes, there are toxins in the mitochondria in CFS, as has been shown by the testing done by Dr. John McLaren Howard of Acumen Lab in the UK. Some of them may be able to diffuse through the mitochondrial membranes in response to a concentration gradient. Others may be actively imported by transporter proteins into the mitochondria. In my hypothesis, they remain there because glutathione is depleted, so that the normal detox processes that would take them out are not operating properly.
I haven't heard of any research results suggesting an interaction between XMRV and the mitochondria. As I understand it, XMRV produces its complementary DNA from its RNA, and this DNA then becomes part of human nuclear DNA molecules.
I'm aware of research conducted by Garth Nicolson and Rita Elliethorpe showing that NT Factor repairs mitochondrial membranes, causing the electrical potential across the membrane to move toward normal. As far as I know, other treatments that supply phopholipids or unsaturated fatty acids (omega-3 and omega-6) would be beneficial for these membranes, also. NT Factor is a nested liposomal treatment, and nested liposomes are more likely to be able to deliver phospholipids to the mitochondria, because they are able to penetrate other membranes in order to get to the mitochondria.
One concern I have about supplying additional phospholipids or unsaturated fatty acids in CFS is that the oxidative stress may damage them. In lipid oxidation, there is a chain reaction process that can produce lipid peroxides in large quantities if oxidative stress is present. I think it is wise to counter the oxidative stress either simultaneously while supplying the lipids, or prior to doing so. In the Simplified Treatment Approach that I've suggested, phospholipids are supplied at the same time that supplements are given to lift the partial methylation cycle block, which allows glutathione to come up, thus countering the oxidative stress. I believe that in Dr. Kane's protocol, glutathione is given intravenously as part of the protocol, while phosphatidylcholine is also given in separate IVs.
Dr. Cheney's views about which supplements are beneficial and which are not in CFS are based on his short-time measurements (of the order of a minute or a few minutes) of changes in the IVRT parameter in echocardiography, in response to applying a small amount of each supplement transdermally. In my view, this approach is not an accurate way to judge the benefit of supplements, because many biochemical changes take longer than a few minutes. I think this approach interrogates only the first step or steps in the metabolism of a substance applied in this way, and the overall effect of a substance will depend on its more complete metabolism and the effects of that on the cells. I have expressed this view to Dr. Cheney several times, but I don't think he has changed his mind about this. I'm not aware of anyone else who is using this approach to judge the merits of supplements. Dr. Cheney has not submitted this method to any formal peer review, as far as I know.
Best regards,
Rich