Issie
Well-Known Member
Here's the tricky part of the immune system. I have hypogammaglobulinemia (underactive immune system) which means amongst other things pneumonia could kill me. I can't fight it. Of the 20 something strains tested on me I only had antibodies to 6 and not enough to fight. I had to acknowledge that the doctor told me this could kill me if I get it. I also have my immune system attacking me (overactive). I have alopecia and vitiligo. I have chronic Lyme and co-infections and another protozoa - that my immune system is not detecting. I have HyperPOTS, MCAS, EDS and there are others. (But you get the idea. Very complex.) So on one hand it's over active and on the other hand underactive. It's a balancing act between what to do. But, seems what I'm doing is working. I'm more functional than Ive been in over 30 years. I have been mostly house bound and in a wheelchair with parts of my illnesses. Im now having a life. Some of us can come back from this. Its more than one thing. There are many pieces to this puzzle. But, they all make up the whole. But, the bottom line is if the Autoimmune system was working properly ----the body would detect things it should and the body would function as optimally as is possible given our imperfect state. Addressing inflammation and the immune system has been what is working for me.Definitely one of the more likely options, given that we can have remissions and that there is such a large gender disparity. But other culprits might be chronic infection, or some weird new form of immune dysfunction which we don't even have a framework to comprehend yet. One problem with treating for presumed autoimmunity, when the specific cause of ME/CFS is not yet clear, is that the treatments aimed at doing that in a non-targeted manner are basically suppressing the immune system. That can be dangerous if the cause is actual infectious, or if it is featuring both infectious and autoimmune components, as it could allow infections to run wild when the immune system is deliberately surpressed.
And then there's the issue of figuring out if everyone has the same disease. Do 67% of ME patients have a strictly autoimmune disorder, while the other 33% have a primary or secondary chronic infection? Is there a different cause or additional infective component in severe patients versus mild? We need answers, research, funding
Issie