Celiac Disease (CD) is an autoimmune digestive disease that damages the villi of the small intestine. The diagnosis and treatment focused only on the intestinal lining. No other areas of the body are considered to be affected by gluten exposure despite multiple medical journals reporting most reactions to gluten are purely neurological.

Before gastrointestinal symptoms like upset stomach appear, neurological damage may already be done, according to the Center for Peripheral Neuropathy. The Gluten Free Society calls gluten a “potential neurotoxin.” Gluten damage may cause everything from unexplained dizziness to numbness in the hands and feet.

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Celiac Disease and Gluten Sensitivity have become synonymous. Most Celiac information excludes the possibility of nerve damage. The focus is solely on the gut.

The “Interlaken Criteria” 

In order to be diagnosed with Celiac disease, the medical community requires you to meet the following  Interlaken Criteria specifications:

Three important elements:

  • Gluten is the triggering agent for celiac disease.
  • There must be a remarkable & easy identifiable mucosal lesion.
  • However, since that lesion could have other causes, the medical community urges doctors not to diagnose CD until it could be proven that gluten was indeed the cause of the mucosal atrophy.

These steps must manifest to meet the Interlaken Criteria:

  • Complete clinical remission on a gluten-free diet
  •  Followed by the documentation of the normalization of the lesion
  •  Its recurrence once gluten was reintroduced into the diet

These criteria were formalized in 1969

  •  “Interlaken criteria” which for over 40 years served worldwide as the accepted diagnostic standard.
  •  The criteria included a gluten re-challenge for confirmation of the diagnosis of CD.
  •  After their publication in 1990, the revised ESPGHN criteria were adopted
    •  Re-challenge was applied only in special situations
      •  Doubt about initial diagnosis
      •  Suboptimal response to gluten elimination from diet
      •  Children <2 years).

Interlaken Criteria + Intestinal Damage

  1. Do you feel worse eating gluten?
  2. Do you feel better avoiding gluten?
  3. Do you feel worse reintroducing gluten?
  4. Did an endoscopy or biopsy reveal an easily identifiable mucosal lesion?
  • If you answer yes to all 3 questions and have “visible” intestinal damage, you may be diagnosed with Celiac Disease.
  •  Answer No to any of the 4 and you may not be diagnosed or considered to have Celiac Disease despite having adverse reactions to gluten.

When You Do Not Meet the Interlaken Criteria.

I have had many patients tell me they were examined by a Gastroenterologist or Celiac Specialist, but were not diagnosed with Celiac Disease. Many were not able to show anti-gliadin antibodies, while others had a reaction but no visible damage to their lining. Two years ago, my own Gastrointestinal Effects profile showed no antibodies for my lower digestive tract but salivary antibodies were positive. How would the specialist explain that? Most likely they would fault the tests with out taking into account physical symptoms. Every time I eat gluten I feel like I am drowning. I have named it Leaky Lung. As to the colon, with constant exposure the immune system can become fatigued to the point of not being able to produce antibodies.

Concerned about your Health?

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The medical community is looking for a visible or macroscopic damage. You may have Microscopic Colitis. They will say it looks irritated but not enough to diagnose Celiac Disease. They will also ignore the other overlapping conditions noted below.

Microscopic Colitis AKA: Lymphocytic colitis, Collagenous colitis, and Lymphocytic duodenosis

The term “microscopic colitis” includes lymphocytic colitis (LC) and collagenous colitis, bearing common clinical presentation distinguishable only by examination of colonic biopsies.[i] There is an association of lymphocytic colitis with HLA-DQ2 genes.[ii] The HLA-DQ genes account for the overlap of celiac and microscopic colitis. Celiac disease was present in 16% of patients with lymphocytic duodenosis.

In the absence of a positive celiac diagnosis, lymphocytic duodenosis was most commonly associated with drugs (21%), infection (19%), immune dysregulation (4%), inflammatory bowel disease (2%), microscopic colitis (2%), sarcoidosis (1%) and IgA deficiency (1%).[iii] Conditions such as celiac disease, IBS, and thyroid diseases were found to be related to Microscopic Colitis.[iv] Mild to moderate immune cell inflammation of the small intestine, often accompanied by deterioration of the gastrointestinal lining, is frequent in patients with the microscopic colitis syndrome.[v]

Celiac Disease vs. Gluten Sensitivity

Celiac Disease Gluten Sensitivity
Antigliadin Antibodies + Antigliadin Antibodies +
Transglutaminase + Transglutaminase
Small Intestine Biopsy + Small Intestine Biopsy
Endomysial Antibodies + Endomysial Antibodies
Fecal Fat Microscopy + Fecal Fat Microscopy

The most important idea to understand is that you can have gluten sensitivity without having Celiac Disease. You don’t have to have a positive HLA-DQ gene to have gluten sensitivity. A positive HLA-DQ means you are more likely to develop sensitivity to gluten.

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The damage to the gastrointestinal lining sought in Celiac disease may be Autoimmune Gastrointestinal disease. Many suffer from the unhappy trilogy of anemia, Autoimmune Thyroid Disease and Autoimmune Gastrointestinal Disease making treatment very confusing.

Studies have reported that anemia was observed in 82% of patients with both Autoimmune Thyroid Disease (AITD) and Autoimmune Gastrointestinal disease (AIGD) but only in 22% of patients without AIGD. In the patients with AITD studied, about one third had AIGD, which was diagnosed while they were young

The presence of anemia, even microcytic, is suggestive of undiagnosed AIGD. The increased frequency of chronic anemia in patients with autoimmune thyroid disease (AIGD) is essentially due to the presence of autoimmune gastrointestinal diseases occurring at the same time.

The classical paradigm of autoimmune pathogenesis involving a specific genetic makeup and exposure to environmental triggers has been challenged by the addition of a third element: the loss of intestinal barrier function.

This new paradigm implies that, once the autoimmune process is activated, it is not self-perpetuating; rather it can be modulated or even reversed by preventing the continuous interplay between genes and environment.

Concerned about your Health?

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Autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by Re-Establishing Intestinal Barrier Function.

Re-Establishing Intestinal Barrier Function.

The reestablishment of intestinal barrier function is a four part simultaneous treatment process. The four parts are:

  • Quenching the inflammation.
  • Re-regulating the immune system.
  • Restoring the structural and function components for gastrointestinal sequencing and digestive chemistry, i.e. chewing is the first step to proper digestion of food.
  • Restoring dysfunctional metabolic processes, i.e. anemia, blood sugar, neurotransmitters, etc.

[i] Simondi D, Pellicano R, Reggiani S, et al. A retrospective study on a cohort of patients with lymphocytic colitis. Rev Esp Enferm Dig. 2010 Jun;102(6):381-4.

[ii] Fernández-Bañares F, et al. Predisposing HLA-DQ2 and HLA-DQ8 haplotypes of coeliac disease and associated enteropathy in microscopic colitis. Eur J Gastroenterol Hepatol. 2005 Dec;17(12):1333-8.

[iii] Aziz I, Evans KE, Hopper AD, Smillie DM, Sanders DS. A prospective study into the aetiology of lymphocytic duodenosis. Aliment Pharmacol Ther. 2010 Dec;32(11-12):1392-7.

[iv] Kao KT, Pedraza BA, McClune AC, et al. Microscopic colitis: a large retrospective analysis from a health maintenance organization experience. World J Gastroenterol. 2009 Jul 7;15(25):3122-7.

[v] Fine KD, Do K, Schulte K, Ogunji F, et al. High prevalence of celiac sprue-like HLA-DQ genes and enteropathy in patients with the microscopic colitis syndrome. Am J Gastroenterol. 2000 Aug;95(8):1974-82.

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