Rheumatoid Arthritis, how it happens

[@Rene-uz3eb]

The 11:05 2007 paper. They admitted physician assessment and measurement of the 1 year delayed group and the initial group were comparable, and time curves were very similar, but then fall back on some random threshold metric that most usefully split patients for their purposes which they then use as a basis to, incredibly, claim that the 1 year delay probably caused irreversible damage (and you better take your drugs and stay on them) So somehow they measured some difference in the ACR scores when all the global effectiveness graphs they have show no difference. The study group selection is also not justifiable at all. First, they chose 1 of the 2 equivalent drug trial groups after 1 year, already allowing for a selection bias (ie which ever one by chance did better against the placebo group). But it gets worse. The run in period resulted in a dropout of 25% of patients, and the all important 10 year extension only had 30% of patients left. Not only can you sweep under the rug whatever you want with this setup, it should be pretty clear that the people asked to do a 10 year extension when they only got a placebo before is going to think differently than a group simply asked to extend a therapy they experienced already for a year.

[@Rene-uz3eb]

Some more on the todo list to verify, wherever the speaker even leaves references.

[@Rene-uz3eb]

Classical controlled chronic disease: treat early or else destruction. Every single inflammatory marker is going up in that 7 year period so I don't think you can pin it on self antibodies. Given that nothing new has come out on citrillunated proteins, not even the function of the ones for which there are antibodies, at the least I suspect that antibodies binding to them would not aggravate the disease (whats the harm of removing some byproduct protein). Most likely imo ancillary peripheral tolerance failure due to chronic cell damage originating around the cartilage cells (nutritional insufficiencies etc). And just to point it out: all disease modifying RA drugs contain sulfur, coincidentally. Note that the antibody stats 36:23 show there are 10x more flu T-cells in non-flu patients than there are citru T-cells in RA patients! Case closed. This can't be relevant. Also let me point out why research looking for drug targets is so limiting: by definition a drug disables some specific protein or mechanism, or promotes one vs others, in both cases undermining what the body is trying to do..in every instance of this thinking it is always based on: the illness means the body is broken and we are going to have to fix it. Never mind that evolution would laugh in your face at the idea (at the thought that a large percentage of people have broken bodies). How about providing the input the body is actually designed for allowing it to fix the actual problem

[@smokindave100]

Anti CCP antibody's are found in people without RA. It's rare but people with PR also can test positive.

[@No2theBS]

Caused by leaky gut but there's No money in that for the drug company's

[@sheiladyck5863]

And I just went to order my Xaljanz after having RA for 6 years, and found out that this drug was $13,000 a month, my copay would have me pay $801.04!! I was finally positively diagnosed with RA via an MRI out at Mayo Clinic in Rochester three weeks ago. I was given an assistance program phone number through the Xaljanz Company after fighting with our Blue Cross Blue Shield Insurance Company when my husband and I already pay almost $3,000 a month for health insurance - no way was I going to pay $801.04 per month for this drug!!!! I now will have a $0 copay. Also I have NEVER smoked a day in my life!!!

[@lh1514]

Dr.Brooke Goldner. She has the answers.