Bob this thread hits a nerve. Well said!
Harry, I also can attest to the "battle fatigue" of hoping for a cure for years and years. It gets really tiresome to get all excited once again, only to find it does not work more than somewhat and at a significant health cost. And I have been on the immune bandwagon for long enough to have come to the conclusion that in fact there is a basic flaw in the model or we'd have better progress than we do. My mother has RA and is severely disabled with obviously grossly deformed joints. She has taken eveery suppressive therapy available for 40 years as it came out as she is aggressively losing the battle
But the comment by GWA
None of the other diseases that are speculated to be autoimmune are being effectively treated or cured either
caught me because I unfortunately have RA as well as MS, and I agree. RA has been, like MS, speculated for decades as an "autoimmune disease". However, unlike MS the inflammation is both very painful and visible as it is in joints and they become hot, swollen and visibly red when the immune system is actively working there. People cannot stand the pain of it so they demand something to stop inflammation, whereas the MS patient is not likely to know they are having lesions occur at all unless thye are in a critical area so are not "demanding' anything most of the time. In RA, anti inflammatories reduce the pain and inflammation effectively, and newer therapies cause immunosuppression aggressive enough to stop the pain and visible "flares" (equivalent to an MS exacerbation) on a long term basis.
HOWEVER..it is KNOWN that in spite of this active reduction in inflammation and immune suppression the joint damage continues under the radar without the red joints pain and easily visible signs of the damage occurring. People gradually become disabled even though seemingly managed well and pain free.
from here <shortened url
METHODS: In this multicenter prospective followup study, a cohort of 195 patients with early, clinically active RA was randomly assigned to treatment with a combination of methotrexate, sulfasalazine, hydroxychloroquine, and prednisolone or with a single DMARD (initially, sulfasalazine) SNIP-. At 5 years, the corresponding percentages were 28% and 22% (P not significant). The median Larsen radiologic damage scores at baseline, 2 years, and 5 years in the combination-DMARD and single-DMARD groups were 0 and 2 (P = 0.50), 4 and 12 (P = 0.005), and 11 and 24 (P = 0.001), respectively CONCLUSION: Aggressive initial treatment of early RA with the combination of 3 DMARDs for the first 2 years limits the peripheral joint damage for at least 5 years. Our results confirm the earlier concept that triple therapy with combinations of DMARDs contributes to an improved long-term radiologic outcome in patients with early and clinically active RA.
That's a rather technical quote but it essentially says that in RA treatment with *three* suppressing therapies at the same time *limits* damage and improves out comes but note it does not *stop* joint destruction, as the final numbers show. People still had some joint destruction. Since these drugs have significant side effects, this is a high price for this benefit, though in the RA patient reduction of pain improves quality of life today.
The question in RA has become if suppression only limits joint destruction, is it the immune system causing the damage or is there something we are missing?
recently Margaret Hammerschlag MD of the American CDC made this comment
One of the major characteristics of Chlamydia spp. is its ability to cause prolonged, often subclinical infections. Chronic, persistent infection with Chlamydia pneumoniae has been implicated in the pathogenesis of several chronic diseases initially not thought to be infectious, including asthma, arthritis and atherosclerosis.
if these autoimmune diseases are infectious, either bacterial or viral, does this not explain the lack of efficacy in the decades long suppression of immunity? And if one of these diseases is infective not autoimmune, how likely is it that the other so called autoimmune diseases are actually correctly characterized?
In my mind this is the issue and cure of any kind cannot come until we get the cause correctly described. It is clear the suppressing immunity results in SOME benefit if the RA and it's very visible and well studied joint damage as a plausibly good model for how nerve damage happens in MS. I believe this is why we see some improvements in immunosuppressed patients: the damage seconday to the inflammation itself is stopped so the damage over all is slowed down, just as we see in RA joints, but it is not stopped altogether because it is not the cause of the disease. I sincerely hope that soon we see someone stumble onto the right clue that brings this monster down like a house of cards.........
my bias is also that it is probably infective.....JMHO