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Quitting Challenge After 2 Days! Omg

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I started a post about chicken nuggets....today and I decided to start a new one.

I was out shopping started getting severe abdominal pain, racing pulse...and decided no more challenge.

I check my blood pressure...109 over 77 pulse was 95...

Right there lower bp racing pulse....either dehydration or an alergic reaction...or auto immune reaction.

I just can not subject myself to it....omg.....and I will write the doc a note tomorrow when I fax the labs.

I am not....going to gluten myself at all...


I can't beleive the reaction from m ybody...

Quod me nutrit, me destruit

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Excellent decision.......when the reaction is that obvious it simply isn't worth it.

I am a German citizen, married to a Canadian 29 years, four daughters, one son, seven granddaughters and four grandsons, with one more grandchild on the way in July 2009.

Intolerant to all lectins (including gluten), nightshades (potatoes, tomatoes, peppers, eggplant) and salicylates.

Asperger Syndrome, Tourette Syndrome, Addison's disease (adrenal insufficiency), hypothyroidism, fatigue syndrome, asthma


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if you have not done a entrolab test, you should look into one that way you can go back onto the diet and still get accurate test results. enterolab.com

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I have had way positive IGA, TTG, and highly elevated Complement levels, and crp.

I have also had a CT scan, that shows som intestinal damage that they are coining non-specific colitis or somehting generic like that...

Quod me nutrit, me destruit

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Guest ~jules~

I am new here and just wondering what the gluten challenge is all about. Is it pretty self explanitory, or is there more to it?

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Thats what I thought, pretty much. But why?

That perhaps seemingly niaeve question really sums it up!

In its simple and crudest form a gluten challenge is where you deliberatly try and damage an important internal organ which may never repair fully so that someone can take a sampleof it while damaged and confirm its damaged.

Longer answer ....

I think its a historical question and also a need to fulfill a "gold standard" to fit a label in part by Dr's and in part by patients.

From the writings of Dr James S. Steward, Consultant Physician, West Middlesex University Hospital, Isleworth, Middlesex.

"After the 1939-45 war came a fundamental discovery which proved to be the main advance in the treatment of coeliac children and adults alike. This discovery was made and described in detail by a Dutch paediatrician, Professor Dicke, in his doctoral thesis for the University of Utrecht in 1950. He showed how coeliac children benefited dramatically when wheat, rye and oats flour were excluded from the diet. As soon as these were replaced by wheat starch, maize flour, maize starch or rice flour the children's appetite returned and their absorption of fat improved so that the fatty diarrhoea disappeared."

The next step was the isolation of various parts of wheat and identification of one of its two main proteins (gluten) as the culprit.

This is where things start to get confused.

" The original observation which, together with Processor Dicke's discovery, led to our present understanding of the nature of the coeliac condition was made by Dr. J. W. Paulley, a physician in Ipswich, and reported to the British Society of Gastroenology in Birmingham in the same year as Professor Dicke's discovery. Dr. Paulley described an abnormality of the lining of the small intestine found at the operation in an adult coeliac patient. This abnormality consisted of an inflammation, the exact nature of which is still being investigated.

The existence of this inflammatory change was confirmed in several patients by Dr. Paulley and was then found by many doctors in this country, the United States and elsewhere to be the most essential single feature on which the diagnosis of the coeliac condition could be based. Its importance to the patient is that it results in a loss of the microscopic projections or villi which are partly responsible for providing the lining membrane of the small intestine with a large surface area. It is from this mucous membrane lining that the absorption of food into the bloodstream takes place." Fig 1 Healthy ViliImage

From this point on research and diagnosis of coeliac disease focused largely on the intestine and the degradation of the villi which line it. The invention of the gastric biopsy and subsequent modification for the intestine provided a easily measurable metric. The destruction of the villi can be clearly seen in the photomicrographs opposite. However According to netdoctor.co.uk "Half of adults with coeliac disease do not have any symptoms from the bowel." Other common symptoms include depression and damage to the nervous system. Ultimately several other autoimmune diseases are also linked with coeliac disease. The focus on the villi has caused a certain neglect of other areas and most of those who do have recognisable damage to the villi also suffer other symptoms. The common digestive symptoms are summarised below.

Common (classic) disgestive related symptoms

* Anaemia (iron deficiency)

* Bloating and flatulence

* Diarrhoea and/or constipation

* Fatigue, weakness and lethargy

* Nausea and vomiting

* Stomach cramps

* Weight loss

Fig 2 Villi being destroyed Image

However a large percentage of people who react to the protein in wheat, barley and rye also suffer wide ranging autoimmune and neurological problems.

Ataxia is caused by damage to the nervous system. It manifests itself as poor muscle coordination or earlier loss of feeling usually beginning in extremeties.

Depression is also well documented but another difficult to measure property.

Many celiacs spend years with a mystery illness.

They go from MD to MD and are often referred to a psychiatrist as hypochondriacs.

Many of the symptoms mimic symptoms of other far more frightening diseases both autoimmune and cancers.

Because of the history of diagnosis and the fact most celiacs end up with a GI there is a huge bias towards looking at the disease form a GI perspective. Looking at it in an overall perspective the damage from the villi is a symptoms of the disease NOT the disease. The actual mechanism of the disease is far from understood but known to involve the bodies own antigens mistakenly attacking gluten and also and cells it is attached to.

The accuracy of blood testing is often questioned.

This is largely IMHO because comparisons are run against single tests, not a full celaic suite

This link also discusses the whole biopsy question ...http://jccglutenfree.googlepages.com/diagnostictesting


Diagnosing celiac disease: a comparison of human tissue transglutaminase antibodies with antigliadin and antiendomysium antibodies.

Baudon JJ, Johanet C, Absalon YB, Morgant G, Cabrol S, Mougenot JF.

Hopital d'Enfants Armand Trousseau, Paris, France. jean-jacques.baudon@trs.ap-hop-paris.fr

OBJECTIVE: To evaluate and compare the sensitivity and specificity of the new serologic marker human antitissue transglutaminase antibodies (IgA anti-tTG) with those of antiendomysium (IgA EMA) and antigliadin antibodies (IgA and IgG AGA) for the diagnosis of celiac disease (celiac disease). METHODS: The level of IgA antibodies to tTG in serum was determined by an enzyme-linked immunosorbent assay (ELISA) test using recombinant human tTG as the antigen; IgA EMA, by indirect immunofluorescence; and IgA and IgG AGA, by ELISA. Sixty-eight serum samples from 59 patients with celiac disease were studied-30 patients had untreated celiac disease, 22 were on gluten-free diets, and 16 had been reintroduced to gluten-and compared with serum samples from 116 children examined for failure to thrive, short stature, various digestive diseases, or other non-celiac disease conditions. RESULTS: Twenty-eight of 30 patients with celiac disease had anti-tTG (the 2 patients whose results were negative were 1 patient with IgA deficiency and 1 infant); 27 of 30 patients had IgA EMA (1 child was IgA anti-tTG positive and IgA EMA negative); 18 of 30 had IgA AGA; and 28 of 30 had IgG AGA. On gluten-free diets, 4 of 22 patients had anti-tTG but none had IgA EMA or IgA AGA. On normal diets, 15 of 15 children who had relapsed had anti-tTG; 9, IgA EMA; 4, IgA AGA; and 8, IgG AGA (1 child did not relapse). In subjects without celiac disease, 3 of 116 had anti-tTG; 12, IgG AGA; and 1, IgA AGA, but none had IgA EMA. In the 3 children who had anti-tTG, celiac disease could be excluded. The positive predictive value of IgA anti-tTG was 90% and the negative predictive value, 98%. In comparison, results for IgA EMA were 100% and 97%, IgA AGA 94% and 90%, and IgG AGA 70% and 98%, respectively. CONCLUSION: The presence of human anti-tTG is a reliable indicator for the diagnosis and follow-up of celiac disease.

In other words a combination of these tests gives very high accuracy.....

In comparison one can look at biopsy.

Firstly we have the concept of "latent celiac" which means everything but a biopsy is +ve.


This IMHO doesn't mean villi are not being damaged but that the body repairs them just as fast.

This doesn't mean no damage is being done. villli tend to die off and be adsorbed and renewed every few days anyway... this is normal for everyone... IMHO celiac spue is when they are killed off faster than they can be replaced.

Someone made a really good analogy here (I forget who and I'm sorry)

Its like going to see a surgeon who is blindfolded ... you have a few spots on your back and the Dr. has to locate and find them using a long flexible tube and a tiny hole in the blindfold ....obviously the more you are covered the higher chance of locating them.

"Sometimes the damage is so severe that it is quite obvious to the naked eye at endoscopy," says Hal Winfield, R.N., director of educational programs at the center.

In other words in exceptional cases villi damage can be seen under endoscopy.

In the rest the Dr. is simply looking for an inflamed area where the sample can be taken, stained and viewed under a microscope anmd a good Dr. will take samples from several.... areas and experience obviously helps but its only increasing the chance of finding the damaged or missing villi and these can be unevenly distributed.

So far this is about biopsy BEFORE gluten-free diet.

A gluten challenge is when you have been gluten-free and then deliberatly eat gluten for a period of time in order to be retested.

Now the first precept is that on a gluten-free diet villi damage is slowly repaired. This seems to be generally true but in the case of older and otherwise sick patients this recovery might be partial.

So in the case you have been gluten-free long enough that almost total repair has occured the idea is to eat gluten over a long enough period to damage the villi enough to be sampled and identified as damaged.

The amount of gluten and time periods are not agreed upon... some "experts say 1 month" and others say 6 months.... and it obviously depends to a large extent on the patient themselves, their health, age and how aggressive their immune system is.

The bottom line is to maximise the chance of a positive biopsy you need to do deliberate damage over a extended period of time to an important organ.

Dr Fine (enterolab) particualrly argues against this and thinks diagnosis and treatment before significant and possibly irrepairable damage is better than deliberatly waiting for the damage to occur.

From a non medical standpoint I fail to see a flaw in this.

The arguaments FOR biopsy state reasons like "a gluten-free diet is expensive" (needn't be and more importantly a biopsy is expensive... its just if you have insurance someone else is paying) and ruling out other diseases.

OK this last one is a valid reason for a biopsy BUT how is it valid to go on a gluten challenge?

Again from a non-medical POV but if you are looking for other things like potentially cancer isn't it easier when the whole intestine isn't inflamed?

And secondly finding damaged villi in no way excludes other auto immune diseases, many celaics develop more than one and many of these diseases might not be in the intestine at all.

To me this sums it up...

One thing is for sure, if you think you will ever want to have a biopsy done...the time to do it is BEFORE you begin experimenting with a gluten free diet. You must be consuming gluten for the biopsy to be accurate.

Also: Follow-Up to the Catassi Study -- Scandinavia

Colin, et al, published a follow-up study to the Catassi (Coeliac Disease in the Year 2000:Exploring the Iceberg - University of Ancona, Italy) in the Scandinavian Journal of Gastroenterology 28(7):595-8, 1993, which demonstrated that approximately one third of the patients from the Catassi Study who had raised antibodies but no villous atrophy, did have villous atrophy when tested two years later. These results raise the number of diagnosed celiacs from the Catassi, et al study to over 1 in 200.

If you still find this confusing... join the club!

Fere libenter homines id quod volunt credunt. (JC, De Bello Gallico Liber III/XVIII)

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That perhaps seemingly niaeve question really sums it up!

In its simple and crudest form a gluten challenge is where you deliberatly try and damage an important internal organ which may never repair fully so that someone can take a sampleof it while damaged and confirm its damaged.

The short answer suffices! :(

Seriously, gfp, thanks for all the research. I may print some of this as a handout for stupid doctors.


Enterolab results: ...two genes for gluten intolerance ...casein intolerance

other sensitivities: corn, eggs, soy, potato, tapioca


Sensitivity to high EMFs [electromagnetic frequency] (limits my time in front of the computer)

Living a healthier, happier life.


If I take the wings of the morning, and dwell in the uttermost parts of the sea, even there shall thy hand lead me, and thy right hand shall hold me.Psalm 139: 9,10

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Guest nini

Thanks Gfp also... I printed it out and will use it as reference material during our gluten free food demo's that I will be doing this weekend and next week with Dr. Joe Esposito (licensed dietician and Dr. of Chiropractic)... it will give me plenty of ammo and talking points! thanks!

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