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CELIAC & ARTHRITIS (& also fibro...)

Sunday, February 04, 2007

Arthritis and Celiac Disease

Copyright © 1995-2006
Scott Adams,
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 that 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. Eating a food, either an unusual food eaten for the first time or sometimes a regular food eaten in excess usually brings on the joint inflammation. 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 nonspecific 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.

End Notes/Sources:

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. Stool Testing info

Thursday, February 01, 2007

From Clan Thompson's newsletter:

1. CELIAC DISEASE: Just the Tip of the Iceberg

A Report on Dr. Kenneth Fine's Conference in Dallas - March 4, 2006

by Lani K. Thompson

Twenty percent of all Americans have some auto-immune problem - and "it's almost certainly related to gluten sensitivity", Dr. Kenneth Fine told a group of doctors, nurses, nutritionists, celiac patients and other interested people who attended his "Intestinal Health...and Beyond" Conference in Dallas, TX between March 3-5. That's because there's an increased risk of other auto-immune diseases developing in a person with celiac disease when the diagnosis is made later in life, as it often is in America.

Dr. Fine's lecture was called "Early Diagnosis of Gluten Sensitivity Using Fecal Testing: Report of an 8-Year Study" and it was the focal point of the weekend. In it, he discussed the spectrum of gluten sensitivity vs. celiac disease, the shortcomings of blood tests and biopsies for gluten sensitivity, and how stool testing has overcome these shortcomings and revealed the problem to be more extensive than previously known.

Celiac Disease, also known as celiac sprue, is an autoimmune disorder. In order to develop celiac disease, a person needs to have the celiac gene, some kind of "trigger" or activation of the gene, and be eating gluten. People with celiac disease can't eat gluten, a grain-based protein found in wheat, rye, barley, and oats. When they do, the protein sets off an immune response that causes damage to their small intestine. Symptoms of celiac disease vary widely, as do their severity. Some people don't have any symptoms at all. Others may experience diarrhea, bloating, abdominal cramping, anemia, fatigue, muscle cramping, pain in the bones or joints, unexplained weight loss, weakness, decreased ability to clot blood, osteoporosis, depression, mood changes, and more. There is no cure, but the disease can be treated with a gluten free diet. However, not everyone who gets better on the gluten free diet has celiac disease, said Dr. Fine. "Celiac sprue is just the tip of the iceberg of gluten induced disease".

"We now know, not only is there this spectrum of change in the intestine and in the symptoms, but that we can actually identify people who seem to be gluten sensitive but never have the villous atrophy" that is seen in full blown celiac disease, he told his audience. Reports of gluten sensitivity with no villous atrophy - or intestinal damage - have been around since the early 1980's, but when the antitissue transglutaminase Ab test was developed in the 1990's, doctors thought it could rule in and rule out all disease. "Blood tests allowed us to pick up more disease, and in more people," Dr. Fine said.

However, he continued, Celiac Sprue is really the end disease and it is only in the end stages of this disease that doctors have 100% reliability of the tests currently used to diagnose it. A positive biopsy or blood test result means you have the disease, but a negative result does not mean you are fine. In fact, each of the two blood tests that are commonly used to make a diagnosis are only accurate 59% of the time and, in celiacs with only partial villous atrophy, the antigliadin and anti-endomysial antibodies tests were only able to detect the disease 31% of the time.

Celiac disease was first written about by Aretaeus the Cappadocian in 100 AD. However, not much was known about the disease until the past few decades. Now some doctors think that undiagnosed celiac disease may be as common as 1 in 130 people. Before he founded the Intestinal Health Institute and, Dr. Fine studied microscopic colitis, an inflammatory disease of the colon in which the body's immune system starts to attack the bacteria living in the colon. Colitis can cause the body's immune system to react to gluten.

Dr. Fine used slides to show how the pathology of microscopic colitis is virtually identical to celiac sprue. When the pathology occurs in the small bowel, it's celiac disease. When it occurs in the large bowel, it's microscopic colitis. However, because the patient doesn't usually have fully developed celiac disease, diagnostic tests, like blood tests, are usually negative. The first study Dr. Fine ever did, as a young researcher, was to try to figure out why there seemed to be an overlap between the different syndromes of microscopic colitis and celiac sprue.

What he discovered was that 64% of people with microscopic colitis have the celiac-like genes of the HLA which is DQ2 and most of the others had another set of genes that had never before been reported in an inflammatory condition associated with gluten sensitivity.

"We had an apparent celiac-like gene genetic predisposition and, perhaps, a new set of genes making their first appearance," Dr. Fine said. When they looked at the small bowel biopsies, they found they were abnormal in 70% of the patients...but it was not celiac disease. There was no villous atrophy and, when they looked at the blood, there were no more antigliadin antibodies than there are in the general population.

"So, here I was scratching my head. What were all of these celiac genes doing in these microscopic colitis people? Why does the biopsy look like celiac disease?" He found a study comparing the presence of antigliadin antibodies inside the intestine to antigliadin antibodies in the blood.

Patients with celiac disease showed these antibodies in both the blood and the small intestine. Normal people had no antibodies in their blood or in their small intestine. Celiacs who followed a gluten free diet for one year tested negative for antibodies in the blood but positive for antibodies in the intestine. So, when there is mild intestinal damage, there are antigliadin antibodies in the intestine.

This was such an important finding that researchers developed a technique to try to detect the antibodies without having to insert a long tube into the small intestine. They had the patient swallow a short tube that went into the stomach, pumped twenty gallons of fluid through to clean everything out, then looked for the antigliadin antibodies. This was considered a relatively non-invasive screening test for celiac sprue and was used for many years!

"You have to get inside the intestine to see what's going on immunologically," Dr. Fine said. A less invasive way to do this is through fecal analysis. Fecal analysis is superior to blood testing because it is more sensitive to the presence of the offending proteins.

Comparison of Test Results for the Presence of Antigliadin Antibodies

Patient Group Blood Test Fecal Analysis
Untreated Celiacs 76% 100%
Microscopic Colitis 9% 75%
Sympomatic People 12% 57%
Asymptomatic People 11% 29%

"That was an extremely important finding in my career. What this meant was a minimum, 29-30% of the general population and 50-75% of people with irritable bowel syndrome, microscopic colitis, perhaps other forms of inflammatory bowel disease and autoimmune disease" have these antigliadin antibodies in their stool.

In a follow-up study, Dr. Fine looked at 7336 patients. 99.4% of them were sick and/or symptomatic and 60% of his patients tested positive for gluten sensitivity.

42% had autoimmune disease
21% had irritable bowel syndrome
20% had a family history of celiac disease or gluten sensitivity
6% had microscopic colitis
2% had chronic fatigue
8% had weight loss, headaches, autism, ADD, or other disorders.

Of the patients in this study, 57% of them had the celiac gene and only 0.07% had no predisposing gene at all. In the general US population, 42% of people have the celiac gene and only 0.4% have no predisposing gene at all.

"Who should be screened?" asked Dr. Fine. There are certain people at greater risk of developing gluten sensitivity. They include: people with microscopic colitis, Crohn's Disease, Ulcerative colitis, Irritable Bowel Syndrome, relatives of those with gluten sensitivity, those with hepatitis C, Down's Syndrome, Gastroesophageal reflux disease, seizure disorders, short stature in children, autoimmune liver disease, dermatitis herpetiformis, Type I diabetes, Rheumatoid arthritis, Sjogren's syndrome, Lupus, Autoimmune thyroid disease, Aids, Peripheral neuropathy, and autism.

Unlike other tests for gluten intolerance, Dr. Fine's new stool test is not invasive and his own research shows that it's more sensitive than other tests, too. It can help identify gluten sensitivity before significant intestinal damage is done, before other complications and autoimmune diseases can develop, and before gluten intolerance becomes full-fledged celiac sprue.

(Note: Slides from Dr. Fine's keynote address from the conference have been posted at Click on the "Research and Education" link for the slides and a related essay. To obtain a DVD of the conference, you may email requests for them to Include your name, mailing address (U.S. mail) phone number (to contact you when they are completed), and email address. The Intestinal Health Institute will contact you when they are ready. The cost is $49.95 + S/H.)


About Dr. Kenneth Fine: Dr. Fine is the Medical Director and Director of Operations for Reference Laboratory, the Director of Operations and Director of Medical Research for Intestinal Health Institute and Director of Operations and Chief Consultant for FinerHealth and Nutrition. You can visit him online at, or


Let us ...

Monday, January 22, 2007

"Let us not become weary in doing good, for at the proper time we will reap a harvest if we do not give up."

Galatians 6:9



Saturday, January 20, 2007

I got this shortly after my diagnosis, I believe it was written by a pharmacist.



After a diagnosis of Celiac Disease is made, additional follow up tests are recommended. These include:
i Blood work for vitamin and mineral deficiencies
i Thyroid Screen (note: Patients on thyroid replacement and other medications may need frequent monitoring for dosage adjustment once their absorption improves.)
i Bone density scan
i Liver enzymes

Note: Calcium and Iron status will improve in most individuals even without supplements once the intestine heals. Several doctors recommend NOT prescribing drugs such as Fosamax and Evista until after the intestine heals and more calcium is being absorbed from the diet.
Healing progress on the gluten-free diet may be monitored by re-testing whichever diagnostic blood test was initially highest, at an interval of 6 - 12 months. Children are likely to heal within a few months; adults may take a few years, and some may never totally heal.


Most individuals will experience a significant decrease of symptoms within a few weeks or months of starting a gluten free diet. However, some individuals may continue to experience significant digestive problems or may have a relapse of symptoms. Some possible explanations are summarized below:

Hidden Gluten Exposure
Look for any possible sources of gluten exposure. Binders in medication, cross contamination, misunderstanding of the strictness required of the diet, etc. should be explored. Repeat blood tests might give an indication of continued gluten exposure, however these may not be sensitive enough to note low level exposure.

Lactose Intolerance
Especially during the healing phase of CD, intolerance to lactose, a protein found in dairy products, may be seen. Enzymes needed to digest lactose are manufactured by the intestinal villi, which have been damaged by exposure to gluten. Often once the villi have regrown, symptoms of lactose intolerance will subside. Testing includes Lactose H2 breath testing. Suggested treatment includes using an over-the-counter lactose enzyme (Lacaid, ___) used when ingesting dairy products. Re-colonizing the small intestine with beneficial bacteria (see probiotics, below) is also recommended.

Small Bowel Bacterial Overgrowth
In a report published in the American Journal of Gastroenterology, Vol. 98, No. 4, 2003 of 15 persons with continuing symptoms, 10 showed evidence of overgrowth of bacteria within the small bowel. Testing included Lactulose H2 breath testing. Suggested treatment includes the non-systemic, prescription antibiotic, Rifaximin (800 mg. per day for one week). Note that the antibiotic used is called Rifaximin in England and Xifaxam in the U.S. Digestive function should also be evaluated as the underlying cause of SBBO.

Yeast Overgrowth
Some individuals report continuing symptoms due to overgrowth of yeast. Testing includes blood antibody testing for Cadida. Suggested treatment includes ½ tsp Nystatin powder (mix with water), twice a day and 200 mg Ketoconizole once per day for 2-3 months. Monthly liver function testing during treatment is recommended. Nystatin powder may be ordered, by prescription, through Belmar Pharmacy at 303-763-5533. Digestive function should also be evaluated as the underlying cause of yeast overgrowth. Dietary changes may also be considered.

Other Food Sensitivities
Additional IgG food sensitivities may be seen. An IgG sensitivity is different from the IgE allergies most allergy doctors check for. Common food sensitivities include dairy casein, corn, soy and eggs. York Labs tests for both IgG and IgE reactions to other foods, by mail, without a prescription. See: Treatment includes avoiding the food, and food rotation. There are some reports of a reduction of food sensitivities when digestive function improves.

Digestive Function
Multiple problems with digestive function may be found. A complete evaluation should be done. One source for a comprehensive stool analysis may be obtained, by mail and by prescription, at Great Smokies Diagnostic Laboratory ( ).

Intestinal motility
Increased intestinal motility may contribute to continuing diarrhea. Try reducing motility by using a fiber supplement like Benefiber or Citracel. Cholestid, a prescription drug used for lowering cholesterol, also may slow motility, particularly in individuals who have had their gall bladder removed. It acts by binding to bile salts.

Decreased stomach acid
Low stomach acid (hypochlohydria) may interfere with the effectiveness of one’s own digestive enzymes and may create an environment that encourages yeast or bacterial overgrowth. Additional information may be found in the book “Why Stomach Acid is Good for You” by Wright & Lenard. Testing may be done using the Heidleberg Capsule or Gastrocap tests. Supplemental Betaine HCl, bitters, digestive enzymes and probiotics, available at a health food store, may be helpful.

Beneficial bacteria
Probiotics are very helpful for regaining the balance of the intestinal flora. Use ones that have multiple kinds of bacteria. The ones found in the refrigerated section of health food stores will have the highest level of bacteria. Kefir, raw kimchee and raw sauerkraut (found in the refrigerated section at Vitamin Cottage) also have high levels of active cultures.

Digestive enzymes
Pancreatic enzymes assist with more complete digestion, discouraging unhealthy bacterial growth. Recommendations have been made for the vegetable based enzymes from Kirkmann ( and for Enzymedica’s ( V-Gest (formerly “Carbo”) and Digest capsules. Animal derived enzymes are available by prescription. Experiment to see what works best. To avoid heartburn, start by sprinkling ½ capsule on food & increase as needed and tolerated. Be sure to carefully check the Gluten-Free status of all enzymes. It is common for the Maltase to be made from barley.

Carbohydrate intolerance
Some individuals do not digest carbohydrates and sugars well. The undigested carbohydrates encourage the growth of harmful yeasts and bacteria. More information on a diet low in carbohydrates may be found in the book “Breaking the Vicious Cycle” by Gottschall. She recommends eliminating all complex carbohydrates to kill off the bad bacteria.

Other Possibilities
Parasites and other bacterial problems
Check for parasites and other bacterial problems, including Giardia lamblia and Ascaris lumbricoides. Just because an individual has CD, doesn't mean they can't have the bugs that a normal person with diarrhea may have!

Other autoimmune diseases
At least 1/3 of the people diagnosed with CD as adults will also have another autoimmune disease. Many report a significant improvement in their other autoimmune disease after beginning a gluten free diet. However, some individuals with CD may develop other autoimmune diseases even after beginning a gluten free diet.


Goal setting ...train hard and expect success!

Saturday, January 06, 2007

from my email newsletter (just wanted a reminder):

Zig Ziglar once said that, "A goal casually set and lightly taken will be freely abandoned at the first obstacle."

You might want to back up and read that quote again, maybe even write it down or print it out, because this one hits the bull's-eye!

This truly explains why New Year's resolutions almost never work, and why so few people can keep off the pounds after they get rid of them.

Goal setting should not be casual or lightly taken. Goal setting is an important and serious matter. This is not a game - this is your life, and you only have one life to live.

Goal setting is also not a one time event - it is an ongoing process
of literally "re-wiring your brain." With the discovery of brain plasticity, we now know that this is science fact, not self-help fiction.

Make the time to set REAL goals, today! Take it seriously, do it
scientifically, re-write your goals every day, think about them constantly, get emotionally involved with them and then take massive action

Do it and this will be the most successful goal-achieving year of your life

Train hard and expect success.

Tom Venunto


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