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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Their theory is that when the Rituximab is given, it brings down the B-cells, but when that goes down, so does some other immune parameter of which they haven't identified yet. That doesn't mean that it isn't a known immune parameter, it means they don't know which it might be yet. That is displayed as "x" in the graph.
Anyone got any guesses as to what it might be?
I noticed in the video from Norway they mentioned that they believed the autoantibody target might be the sensory nerves. Do you recall if that was mentioned in the London presentation?
I am currently interested in the possibility that anticardiolipin antibodies are a red herring, or secondary. I suspect we get them for the same reason we get many of the cytokines - bacterial products in the blood. Bacteria make lots of cardiolipin, if LPS is getting into the blood then cardiolipin might be too, although I think bacteria deliberately shed LPS but cardiolipin would only be released from dying bacteria.
On the other hand if we develop antiobodies to bacterial cardiolipin, what impact will that have on us? It could well be damaging, but I am unsure. Are there cells in the body that have a lot of cardiolipin on the surface?
Bye
Alex
Hi, Alex.
In humans, cardiolipin is found in the inner mitochondrial membrane. The elevation of cardiolipin antibodies in ME/CFS may reflect mitochondrial dysfunction and early die-off of cells, with the immune system responding to the fragments. The antibody test developed by Dr. Hokama for ciguatoxin was found to cross-react with cardiolipin, and this may explain why he found a high rate of positives in PWMEs/PWCs.
Dr. Shoemaker reports that people with biotoxin illnesses also have elevated levels of anticardiolipin antibody.
Best regards,
Rich
Hi, Alex.
In humans, cardiolipin is found in the inner mitochondrial membrane. The elevation of cardiolipin antibodies in ME/CFS may reflect mitochondrial dysfunction and early die-off of cells, with the immune system responding to the fragments. The antibody test developed by Dr. Hokama for ciguatoxin was found to cross-react with cardiolipin, and this may explain why he found a high rate of positives in PWMEs/PWCs.
Dr. Shoemaker reports that people with biotoxin illnesses also have elevated levels of anticardiolipin antibody.
Best regards,
Rich
Rich,
Could you clarify something for me? Does your above post mean that you believe the paper from 2009 is incorrect? That's how I am reading your post and I'm just not sure if that is indeed what you mean.
Thanks!
For those needing to review the history of this ancient hypothesis look here:
http://www.ncf-net.org/forum/summer-vol13-1.htm
I find it interesting that the lastest and greatest research in ME/CFS is basically revisiting dated theories that have long ago been discarded by many. Is the concept that ME/CFS is related to a neoplastic disease process in any way supported by successful treatment with an anti-cancer drug? Just wondering.
Is the fact it's an ancient hypothesis necessarily a negative feature? The idea of evolving species had been around long before Darwin developed his theory, sometimes it takes a new discovery or a new way of thinking applied to an old idea to make everything fit together. The concept of autoimmune involvement sounds very logical to me, I can't believe there are still people hanging onto the idea that there is one specific pathogen or group of pathogens causing this illness, XMRV should have been the last nail in the coffin for that line of enquiry.
I don't recall saying that it WAS a negative feature. To the contrary, my guess is that the mystery of CFS has probably already been unraveled, and the answer to a biological cause is already well explained in some small initial study, periodical editorial, or even an internet thread somewhere. If there is a negative feature, it is that the abundance of these small starts, theories, and postulations are not followed up, never adequately funded or translated into a well powered strongly evidence based and scientifically rigorous work.
Perhaps if there were a small tax, say $1 per theory, that must be paid in order to chime in from the peanut gallery and discuss the cause of ME or CFS it might be better. Then, we would have a huge source of income for funding the dearly needed research that will be needed to actually get clarity for the biological causation of the illness.
Hi, Alex and dsdmom.
Alex: Yes, that's what I meant. The cell dies and comes apart, releasing its fragments to the blood plasma, and the immune cells have access to the fragments, including the cardiolipin, and raise antibodies to it. The antibodies don't have to cross membranes.
dsdmom: I'm not sure which paper from 2009 you are referring to. Do you mean one of Dr. Hokama's papers? He is the one who discovered the cross reactivity that I mentioned. His test was an antibody test, and apparently part of the ciguatoxin molecule looks like part of the cardiolipin molecule, so the the antibody test responds to both.
Best regards,
Rich
Hi Rich, at face value your explanation would then mean that anticardiolipin antibodies wont cause damage - which was my point.
http://www.ncbi.nlm.nih.gov/pubmed/17062932?dopt=AbstractCONCLUSION:
The incidence of echocardiographic abnormalities is high in SLE patients, most often in valves and pericardium. The aCL is probably related to valvular damage in SLE patients.