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I am a firm believer that the immune system plays a role in RSD. I personally believe that my immune system was taxed before my surgery for a number of reasons, and therefore my immune system wasn't able to deal with surgery effectively. This may seem like a stretch, but I've been looking at the similarities with Autism (although obviously the symptomology is different, both are neurological). There are a lot of people with autism that have an improvement in symptoms after doing things to clean up their immune systems detoxing, changing diet getting rid of yeast, gluten, casien, cleaning up their gut--getting rid of bad bacteria and introducing the "good" and even getting rid of parasites, going organic so it's one less thing for the immune system to deal with (processing pesticides), taking different supplements. If this can help with a neurological problem like autism (which was thought to be "incurable," than why not RSD, if it really is related to an immune problem? I actually did try quite a bit of this, as I was reading "Mother Warriors" as I was going through HBOT. I'm not sure how much it played a role in my improvement compared to everything else I've tried, but I AM better now. I haven't stuck with the diet, though, after I began to feel better.
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To Millerprof -
Hi. I can't find where I first saw it, but a few years back I came across an article that suggested that when folks were already under high stress - that is carrying a heavy load of C-reactive proteins, among other things - they were at greater risk of getting CRPS from injuries, analogously to how they would be more likely to develop recurrent colds and other minor infections. That said, the research on autoimmunity takes this one step farther, to one of a number of mechanisms whereby CRPS may actually be
maintained in the body.
And anecdotally, a number of women of this and the old BT forum have reported that their CRPS went into remission during pregnancy, which is consistant with research showing that the body changes it's immune reponse during pegnancy so as to avoid attacking the fetus as a hostile "other." As an example of the general concept, take a look at:
"Autoimmune disease during pregnancy and the microchimerism legacy of pregnancy," Adams Waldorf KM, Nelson JL, Immunol Invest. 2008; 37(5): 631-44.
Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA. adamsk@u.washington.edu
Pregnancy has both short-term effects and long-term consequences on the maternal immune system. For women who have an autoimmune disease and subsequently become pregnant, pregnancy can induce amelioration of the mother's disease, such as in rheumatoid arthritis, while exacerbating or having no effect on other autoimmune diseases like systemic lupus erythematosus. That pregnancy also leaves a long-term legacy has recently become apparent by the discovery that bi-directional cell trafficking results in persistence of fetal cells in the mother and of maternal cells in her offspring for decades after birth. The long-term persistence of a small number of cells (or DNA) from a genetically disparate individual is referred to as microchimerism. While microchimerism is common in healthy individuals and is likely to have health benefits, microchimerism has been implicated in some autoimmune diseases such as systemic sclerosis. In this paper, we will first discuss short-term effects of pregnancy on women with autoimmune disease. Pregnancy-associated changes will be reviewed for selected autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus and autoimmune thyroid disease. The pregnancy-induced amelioration of rheumatoid arthritis presents a window of opportunity for insights into both immunological mechanisms of fetal-maternal tolerance and pathogenic mechanisms in autoimmunity. A mechanistic hypothesis for the pregnancy-induced amelioration of rheumatoid arthritis will be described. We will then discuss the legacy of maternal-fetal cell transfer from the perspective of autoimmune diseases. Fetal and maternal microchimerism will be reviewed with a focus on systemic sclerosis (scleroderma), autoimmune thyroid disease, neonatal lupus and type I diabetes mellitus.
PMID: 18716941 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
That said, I am also a firm believer that reversable changes in the brain itself play a significant role in the maintenance of CRPS, a view the is supported by the success of a number of treatments including mirror imaging therapy, high dose NDMA-receptor antagonists (ketamine) and even - I would still dare to submit - RUL ECT.
Mike