Subject: Arthritis - arthrit.txt [1/1]

From: [email-masked] (larry withers)
Date: 8 Sep 1995 17:37:05 GMT

Arthritis
Arthritis may be an allergic response to 
materials in the food supply.  Diet revision may be 
helpful in reducing the activity of inflammatory 
arthritis and in some instances may halt the 
progression of the disease.

There are many patterns of arthritis. A group of 
related joint and connective disorders have been 
called rheumatic diseases. All these diseases are 
immune-mediated, and all are expressions of 
inflammation in connective tissues. Inflammation 
damages joints and surrounding tissues resulting 
in loss of function and deformities. Variations in 
the patterns of these diseases reflect the many 
possibilities for immune damage to disturb and 
distort structure and function. Severity ranges 
>from  mildly painful, chronic activity to drastic, 
disabling disease. Rheumatoid arthritis, often 
severe and disabling, is the dominant rheumatic 
disease which can attack all joints in the body. 

Rheumatoid arthritis is often considered to be 
an autoimmune disease. Our idea is that no disease 
is just internally generated and must involve 
outside contributions. Arthritis is often associated 
with inflammatory bowel disease. The 
mechanisms of food allergy link abnormal 
Gastrointestinal Tract (GIT) function with 
immune attacks on connective tissue. In all 
arthritic patients, normal GIT function should be 
rigorously sought by adaptive dietary adjustments. 

Simple allergic arthritis is a definite entity that is 
often not recognized as a food allergy. Typically, 
a dramatic, acute, and painful swelling develops 
in one or more joints asymmetrically. The joint 
inflammation is usually brought on by eating a 
food, either an unusual food eaten for the first 
time or sometimes a regular food eaten in excess. 
This presentation is similar to and often confused 
with gout. Any food can cause allergic arthritis. 
Staple foods such as milk, eggs, and wheat (rye, 
oats, barley), coffee, beef, pork,  and food 
additives are the most common food triggers. 
Carinini and Brostroff reviewed the concepts of 
and evidence for food-induced arthritis.  They 
stated: 

"Despite an increasing interest in food allergy 
and the conviction of innumerable patients with 
joint disease that certain foods exacerbate their 
symptoms, relatively little scientific attention has 
been paid to this relationship. Abnormalities of 
the gastrointestinal tract are commonly found in 
rheumatic disease...Support for an intestinal 
origin of antigens comes from studies of patients 
whose joint symptoms have improved on the 
avoidance of certain foods antigens, and become 
worse on consuming them. These have included 
patients with both intermittent symptoms, 
palindromic rheumatism and more chronic 
disease." 

In another study, 33 of 45 patients with 
rheumatoid arthritis improved significantly on a 
hypoallergenic diet. The authors concluded:  

"Increasing numbers of scientific studies 
suggest that dietary manipulation may help at 
least some rheumatoid patients and perhaps the 
greatest need now is for more careful and well-
designed research so that preconceptions may 
be put aside and role of diet, as a specific or 
even a non-specific adjunctive therapy, may be 
determined."

Unfortunately, dairy products, wheat and its close 
relatives, oats, barley, and rye, have proved to be a 
major problem in the diets of our patients. There 
are many possible reasons for cereal grains to 
become pathogenic. Hypersensitivity mechanisms 
triggered by grain proteins,  collectively called 
"Gluten",  are the likely cause of the illnesses 
related to  intake of cereal grains. Gluten is a 
mixture of individual proteins classified in two 
groups, the Prolamines and the Glutelins. The 
prolamine fraction of gluten concerns us the most 
when grain intolerance is suspected. The 
prolamine, Gliadin, seems to be a problem in 
celiac disease; gliadin antibodies are  commonly 
found in the immune complexes associated with 
this disease.   Recently marketed grains, spelt and 
kamut, are wheat variants (despite claims to the 
contrary)  and are likely to cause problems similar 
to other wheat varieties.  

A wheat gluten mechanism has been studied in 
rheumatoid arthritis patients. The clinical 
observation is that wheat ingestion is followed 
within hours by increased joint swelling and pain.  
Little and his colleagues studied the mechanism, 
as it developed sequentially following gluten 
ingestion.  Dr. Parke and colleagues concurred 
with this explanation of the gut-arthritis link in 
their report of three patients with celiac disease 
and rheumatoid arthritis.  The mechanism 
involves several stages:

GIT must be permeable to antigenic proteins or 
peptide fragments, derived from digested gluten.  
The food antigens appear in the blood stream and 
are bound by a specific antibody (probably of IgA or 
IgG, not IgE class), forming an antigen-antibody 
complex, a circulating immune complex (CIC)

The antigen-antibody complex then activates the 
rest of the immune response, beginning with the 
release of mediators - serotonin is released from the 
blood platelets. Serotonin release causes 
"symptoms" as it circulates in the blood stream and 
enhances the deposition of CICs in joint tissues.

Once in the joint, the immune complexes activate 
complement, which in turn damages cells and 
activates inflammation. More inflammation results in 
more pain, swelling, stiffness, and loss of mobility. 

Arthritis is usually treated with salicylates or 
related anti-inflammatory drugs generally 
referred to as NSAIDs. These drugs alleviate the 
terrible pain of active arthritis but do not 
favorably affect the outcome of the disease. All 
anti-arthritic medication can produce asthma or 
chronic rhinitis and a variety of allergic skin 
rashes. Gastrointestinal surface irritation, 
bleeding, and ulceration are routine problems of 
anti-arthritic medication.

The first attack of joint swelling and pain should 
be treated as an urgent problem to be solved. 
Inflammation may damage joints. Often NSAIDs 
and physiotherapy are the only treatments 
prescribed and inflammation is given every 
opportunity to ravage tissues. We have seen 
countless patients, just treated with NSAIDs, who 
progressed rapidly to a severe disabling disease, 
often with poor pain control. In unlucky patients, 
severe deformities of joints accumulate in the 
first few months of a severe attack. There is a  
trend to recommend more aggressive treatments, 
using drugs that impair the immune response. The 
best drug is prednisone, but it is seldom used 
because it has long-term side effects which scare 
both physicians and patients. Prednisone is often a 
magic drug that relieves terrible pain and 
suffering often in the first 48 hours of therapy. 
Beyond prednisone, there is a grab bag of immune 
suppressant drugs to treat arthritis -chloroquine, 
penicillamine, gold  and methotrexate have 
emerged as the favored drug therapies.  All these 
drugs have impressive side effects and great 
potential for toxicity. 

Our preference is to try to stop the inflammatory 
activity as soon as possible with diet revision. All 
inflammation is likened to a fire. You get out the 
fire-extinguishers and go to work. No matter what 
pattern the immune attack assumes, our standard 
defense can be tried first. The Core Program 
method of diet revision is used. Food is replaced 
with an elemental nutrient formula, ENFood, for 
a clearing period of 10 to 20 days. Prednisone 
and/or NSAIDs are drug options during the 
clearing period and then the dosage is reduced  
after pain and swelling have subsided.  
Improvement is followed by slow food 
reintroduction (see Core Program). Each 
returning food is carefully screened for arthritis-
triggering effects. You hope that food allergy 
caused the problem and that food control can be 
successful controlling the disease in the long-
term. Nothing is lost by taking this approach and 
complete control of the disease can sometimes be 
obtained. If strict food control proves to be 
inadequate, then other drug treatments can be 
instituted.
  Carinini C, Brostroff J. Gut and joint disease. Annals of 
Allergy 1985;55:624-625.
  Darlington et al. Lancet Feb 1 1986;236-238. 
  Keiffer M et al. Wheat gliadin fractions and other cereal 
antigens reactive with antibodies in the sera of of celiac 
patients. Clin Exp Immunol 1982;50:651-60. 
  Little  C, Stewart AG, Fennesy MR. Platelet serotonin 
release in rheumatoid arthritis: a study in food intolerant 
patients. Lancet 1983;297-9.
  Parke AI et al. Celiac disease and rheumatoid arthritis. 
Annals of Rheum Dis 1984;43:378-380.
  Voorneveld CR, Rubin LA  Disease-modifying 
antirheumatic drugs: early use is better. Medicine North 
Amer. Oct 1991 3177-3184