What’s worse than having terrible, daily pain? Having daily pain and thinking you’re also developing cancer because of your medications.
Health.com has reported that RA is linked to increased risk for eight different kinds of cancer. Whether the statistics are very low or not, this is pouring salt in the wounds of RA sufferers.
Meanwhile, I see a terrible delay in the treatment of RA catching up with the data available. To learn more about the cause and treatment, please have a look at my website and then go and do your own research on medline. Don’t expect your Rheumatologist to tell you that it is likely his profession will either cease to be or be converted over to a subspecialty of gastroenterology.
Here is the most recent analysis of the issue. If you don’t read medicalese, just skip to the bottom sentence. Here is the cause and possible cure for RA.
Autoimmun Rev. 2010 Feb;9(4):216-23. Epub 2009 Nov 4.
Ebringer A, Rashid T, Wilson C.
Rheumatoid arthritis (RA) is a crippling joint disease affecting over
20 million people worldwide. The cause of RA is most probably linked to the
triad of microbial trigger, genetic association and autoimmunity and can be
explained using the philosophical method of Karl Popper or Popperian sequences.
Ten “Popper sequences” have been identified which point to the
urinary microbe Proteus mirabilis as the cause of RA: Popper sequence 1
establishes that HLA-DR4 lymphocytes injected into a rabbit evoke specific
antibodies against Proteus bacteria. Popper sequence 2 establishes that
antibodies to Proteus bacteria are present in RA patients from 14 different
countries. Popper sequence 3 establishes that antibodies to Proteus bacteria in
RA patients are disease specific since no such antibodies are found in other
conditions. Popper sequence 4 establishes that when RA patients have high
titres of antibodies to Proteus such bacteria are found in urinary cultures.
Popper sequence 5 establishes that only Proteus bacteria and no other microbes
evoke significantly elevated antibodies in RA patients. Popper sequence 6
establishes that the “shared epitope” EQR(K)RAA shows “molecular
mimicry” with the sequence ESRRAL found in Proteus haemolysin. Popper
sequence 7 establishes that Proteus urease contains a sequence IRRET which has
“molecular mimicry” with LRREI found in collagen XI of hyaline
cartilage. Popper sequence 8 establishes that sera obtained from RA patients
have cytopathic properties against sheep red cells coated with the
cross-reacting EQR(K)RAA and LRREI self-antigen peptides. Popper sequence 9
establishes that Proteus sequences in haemolysin and urease as well as the self
antigens, HLA-DR1/4 and collagen XI, each contain an arginine doublet, thereby
providing a substrate for peptidyl arginine deiminase (PAD) to give rise to
citrulline, which is the main antigenic component of CCP, antibodies to which
are found in early cases of RA. Popper sequence 10 establishes that antibodies
to Proteus come not only from sequences crossreacting to self antigens but also
from non-crossreacting sequences, thereby indicating that active RA patients
have been exposed to infection by Proteus. The ten Popper sequences establish
that RA is most probably caused by Proteus upper urinary tract infections,
which can possibly be treated with anti-Proteus therapy.
Copyright 2009 Elsevier B.V. All rights reserved.
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