Rheumatoid Arthritis, Molecular Mimicry, and Diet as a Possible Therapy

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Rheumatoid Arthritis, Molecular Mimicry, and Diet as a Possible Therapy

by

Ron Hoggan

Rheumatoid arthritis (RA) is an autoimmune disease where the body attacks

its own cartilage and joint linings. It is characterized by swelling and

pain. The synovial membrane at afflicted joints goes through several

abnormal stages of autoimmune damage, ultimately destroying the cartilage

and fusing the bones with fibrous tissues that may ossify, eliminating

joint mobility (1).

This is all very interesting, but it fails to capture the real nature of

RA. It is darned painful, and can be very frustrating. Every practitioner

seems to have a different answer that either doesn't work, or has so many

side effects that it is only marginally worthwhile to take the prescribed

medications. And it sometimes seems that there is a new answer every week.

But there is a new paradigm in autoimmunity. It offers a profoundly more

hopeful perspective than has been possible in the past. If the notion of

molecular mimicry is substantiated in RA, which seems likely, given the

recent exponential increase in researchers' interest in this area. By my

count, more than 80% of the research connecting RA with molecular mimicry,

as reported on Medline, has been reported during the last decade.

Some researchers are looking for a protein, or partial protein (peptide),

from a chronic infectious agent that might reside in the gut, and regularly

be transported across a permeable intestinal wall into the circulation.

Others are searching for a specific bacterium or virus that has an amino

acid sequence that would serve as a trigger for production of antibodies

against that " invader " . The assumption is, of course, that the antibodies

in question would attack tissues with similar sequences of amino acids in

their protein structures. The immune system would start out mounting an

attack against a foreign substance, and wind up attacking the collagenous

tissues at the joints, as in RA.

There is considerable interest in this area, and I believe it warrants

exploration. However, I am disposed to the application of the theory of

molecular mimicry, to RA, in a little different manner. Infectious agents

often come and go. Yet autoimmune diseases usually progress, either

steadilly, or through cycles of remission and relapse. This may be an

important flaw in the application of the theory of molecular mimicry to

infectious agents.

What foreign proteins find their way into the blood on a continuous basis?

There is clear evidence that some of the alcohol soluble proteins from

farinacious grains are regularly absorbed into the blood (3). Since these

grains serve as a daily staple in the diets of virtually everyone living in

the industrial world, such grains are a likely prospect for initiating and

perpetuating a dynamic of molecular mimicry leading to rheumatoid arthritis.

On the strength of this evidence alone, a gluten-free diet should be given

an empirical trial with every RA patient, but there is much more evidence

suggesting the need for such a trial. It has been reported that celiac

disease, a disease characterized by an intestinal inflammatory response to

farinacious grains, is associated with endocrine or connective tissue

disorders (4) and that celiac disease is overrepresented in connective

tissue disease, including RA (5). This lends further implicit support to

the notion that gluten-containing grains may be a factor in at least some

cases of RA. In fact, one group reported that 37% of their RA patients

demonstrated elevated antibodies against gliadin (6). Although it is

important to note that the presence of these antibodies are often not

predictive of celiac disease the following conclusion warrants careful

reading:

" CONCLUSION. Despite the increased AGA positivity found distinctively in

patients with recent-onset RA, none of the RA patients showed clear

evidence of coeliac disease. AGA positivity in early RA may indicate a role

of the gut immune system in the initiation of RA. " (6)

Perhaps the most compelling evidence for a causal relationship between

gluten and some cases of RA may be found in the reports that in patients

where both celiac disease and RA are diagnosed, the gluten free diet is

often an effective treatment for both conditions (8,9)

Not surprisingly, this new understanding serves as something of an

indictment of some current practices in the treatment of RA. Koot et al.

conclude their report with the following statement: " The elevated IgA

antigliadin titre in the RA group might be ascribed to the use of NSAIDs,

which are harmful to the gut, but the immunological trigger effect of

gluten cannot be ruled out " (10). It is important to manage pain, but it is

also important to limit any self-perpetuating impact of analgesics.

The theory of molecular mimicry offers new hope to those who suffer from

RA, and there is a compelling alternative to waiting for the current search

to exhaust the field of infectious agents, and begin to investigate dietary

antigens as a possible trigger and perpetuating factor in RA. ELISA testing

offers to identify specific dietary antigens that may be at work in RA. In

a large number of cases this will likely include gluten, but may not be

restricted to gluten alone. Milk protein is also relatively new to the

human diet, and may also need to be excluded. Caseins, proteins found in

dairy products, are structurally similar to gluten, and are also likely

candidates for inciting autoimmune dynamics through the dynamic of

molecular mimicry. In other cases, perhaps additional dietary antigens will

also need to be removed from the diet.

For further information on ELISA testing:

http://www.betterhealthusa.com/home.htm

or

http://www.immunolabs.com/

Sources

1. Tortora & Grabowski _Principles of Anatomy and Physiology_ 1996

Harper, N.Y. p. 234

2. Tiwana H, et al. Cross-reactivity between the rheumatoid

arthritis-associated motif EQKRAA and structurally related sequences found

in proteus mirabilis. Infect Immun. 1999 Jun;67(6):2769-75.

3. Husby S, et al. Passage of undegraded dietary antigen into the blood of

healthy adults. Quantification, estimation of size distribution, and

relation of uptake to levels of specific antibodies. Scand J Immunol. 1985

Jul;22(1):83-92.

4. Reunala T, et al. Diseases associated with dermatitis herpetiformis. Br

J Dermatol. 1997 Mar;136(3):315-8.

5. Lepore L, et al. Prevalence of celiac disease in patients with juvenile

chronic arthritis. J Pediatr. 1996 Aug;129(2):311-3

6. Paimela L, et al. Gliadin immune reactivity in patients with rheumatoid

arthritis. Clin Exp Rheumatol. 1995 Sep-Oct;13(5):603-7.

7.Lepore L, et al. Anti-alpha-gliadin antibodies are not predictive of

celiac disease in juvenile chronic arthritis. Acta Paediatr. 1993

Jun-Jul;82(6-7):569-73.

8. Carli P, et al. [inflammatory rheumatism and celiac disease in adults.

Coincidence or pathogenic relationship]? Presse Med. 1995 Apr

1;24(13):606-10. French.

9. Collin P, et al. Rheumatic complaints as a presenting symptom in

patients with coeliac disease. Scand J Rheumatol. 1992;21(1):20-3.

10. Koot VC, Van Straaten M, Hekkens WT, Collee G, Dijkmans BA, " Elevated

level of IgA gliadin antibodies in patients with rheumatoid arthritis "

_Clin Exp Rheumatol_ 1989 Nov;7(6):623-626

http://www.gluten-free.org/hoggan/ra.txt