Brain and nerve cell death in celiac disease from eating wheat gluten

How Celiac disease and gluten ingestion results in neurological injury is not well understood. It is however now well recognized that celiac disease and gluten are related to a variety of brain and peripheral nerve problems. According to a new study, nerve cell death, known in medicine by the term apoptosis, occurs in celiac disease not just from the presence antibodies against nerve cells in the blood of people with celiac disease with neurologic problems but from other factors in the blood, especially gliadin and tissue transglutaminase antibodies, and in people without obvious neurological problems. The presence of antibodies to gliadin and tissue transglutaminase in the blood are associated with nerve cell death in the absence of anti-nerve antibodies.

The complicated nature of the process that gluten ingestion and celiac disease results in neurological damage can be appreciated by the reading the study by Cervio et al. from the University of Bologna, Italy, published in the July 2007 issue of Gastroenterology. Their very detailed and difficult to understand article describes the very elegant yet extremely sophisticated study they performed. The study they conducted attempted to determine if it is the anti-nerve antibody, known as antineuronal antibody, that causes the degenerative damage to the brain and nerves seen commonly in celiac disease. They tested whether the blood of people with neurological disease with and without celiac disease and with and without antibodies to nerve cells could cause nerve cell death in cells studied outside the body. They compared the effects of blood from people with celiac disease with these antibodies but without neurological symptoms, people with celiac disease without antibodies and without neurological symptoms, and people with neurological disease but not celiac disease.

They did find that the blood from those people with celiac disease with neurological symptoms that had antineuronal antibodies caused the greatest nerve cell death but interestingly they found that blood from people without the antibodies including people with celiac disease without neurological could cause substantial nerve cell death. They conclude that the blood of people with celiac disease without these anti-nerve cell antibodies “may bear a neurotoxic potential”. They go on to state that this “may be ascribed to several factors such as the wide array of other autoantibodies contained in the sera, namely the combination of both antigliadin and anti-tTG antibodies.” Within the article mention is made of the effect on both central nervous system (brain) and enteric nervous system (gut).

I find the possibilities quite intriguing and curious in that there is accumulating evidence that irritable bowel syndrome is a disorder of the enteric nervous system, possibly related to altered gut permeability (leaky gut) associated with altered gut flora (bad bacteria and yeast). In addition this effect in some patients may be related to increase mast cells (mastocytic enterocolitis) resulting from some stimulus such as stress or gut infection. Furthermore, a recent study indicates that gluten free diet is effective in many people with diarrhea predominant IBS when they have elevated gliadin antibodies in the blood especially if they are positive for the high risk celiac disease white blood cell protein pattern HLA DQ2. However, as in much of medicine, the ability to connect these dots is limited by a research process that is quite cumbersome, highly political, pharmacy industry funded, and carried out by scientists focused on their particular area of interest, experience and funding. We will explore the gluten-IBS link in the next post. Stay tuned as we continue our journey.

Reference:

Cervio E. et al. Sera of patients with celiac disease and neurological disorders evokes a mitochondrial-dependent apoptosis in vitro. Gastroenterology July 2007; 133: 195-206.


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Gluten sensitivity confirmed by genetics and blood tests in irritable bowel syndrome

Gluten sensitivity is very common, much more common than celiac disease. However, both celiac disease and gluten sensitivity are often missed, ignored or misdiagnosed. It is widely accepted celiac disease affects approximately 1% of people worldwide. It is commonly accepted that between 3-4% of people previously diagnosed with irritable bowel syndrome (IBS) have undiagnosed celiac disease. Dr’s. Rodney Ford, Ken Fine and I believe that many more than this are gluten sensitive. We believe that the presence of an elevated serum gliadin antibody is indicative of gluten sensitivity in most people. We concede that such individuals often do not have “true celiac disease” as it is now strictly defined by presence of HLA DQ2 or DQ8, a positive IgA endomysial antibody test or tissue transglutaminase IgA antibody with characteristic small bowel biopsy. However, our experience is that such individuals commonly present with symptoms identical to those with celiac disease and these symptoms respond to a gluten free diet. Now, researchers from Germany provide their scientific data that validates what we have observed and have been writing about. In the July 2007 issue of Clinical Gastroenterology and Hepatology, Wahnschaffe et al., from Germany report that gluten sensitivity causes symptoms meeting criteria for diagnosis of diarrhea predominant irritable bowel syndrome (d-IBS) that responds to a gluten-free diet.

They confirmed their earlier studies that found approximately one third of patients with d-IBS have IgG anti-gliadin and/or tissue transglutaminase antibodies in absence of villous atrophy and celiac disease specific antibodies. In this study they confirmed that those positive for HLA DQ2 with elevated AGA IgG or TTG IgG respond to a gluten-free diet with significant improvement of d-IBS symptoms. Also of interest is their mention in the paper that they had previously noted a subgroup of d-IBS identified by presence of DQ2 who had increased antibodies to gliadin or tissue transglutaminase in duodenal aspirate (similar to those Fine reports in stool). They state that these people “might actually have latent/potential celiac disease and could profit from a gluten free diet.” In conclusion I quote the authors as follows “…serum IgG antibodies against gliadin or tissue transglutaminase in combination with HLA DQ2 expression are useful markers to identify a subgroup of patients with d-IBS who are likely to respond to a gluten-free diet.”

This study published in the peer reviewed clinical journal of the American Gastroenterological Association is, in my opinion, a landmark article confirming the broader spectrum of gluten sensitivity and benefit of continuing to use gliadin antibodies as a screening blood test for both very early celiac disease as well as non-celiac gluten sensitivity. The paper also provides support for the concept that the presence of gliadin and tissue transglutaminase antibodies in the intestinal fluid (duodenal aspirate or stool) indicates gluten sensitivity. The presence of these antibodies appears to be sign of gluten sensitivity at a much earlier state than the presence of such antibodies or more specific celiac disease antibodies in the blood, before advanced intestinal injury has occurred.

In my clinical experience, if gliadin antibodies are also normal in the blood but the suspicion of gluten sensitivity is high, especially if the patient has HLA DQ2 or DQ8, then stool antibody testing may be helpful. Also, duodenal biopsy is often helpful, especially if any of the celiac disease related antibodies are elevated, the patient has risk factors, or they have suggestive symptoms of gluten sensitivity, regardless of the blood test results.

I have found many but not all of my patients with suggestive symptoms of gluten sensitivity who have “normal” celiac blood work have elevated stool gliadin IgA antibodies (Enterolab), with or without elevated tissue transglutaminase IgA antibodies, especially those with HLA DQ2 or DQ8. These individuals invariably respond to a gluten free diet. I myself am such a person. I have also found many of these individuals have intestinal biopsies demonstrating increased numbers of intraepithelial lymphocytes, the earliest finding in celiac disease.

I have submitted an abstract of my findings to one our national GI societies. Dr. Ford has also submitted such data for publication. However, since we are both clinically based and are reporting our single gastroenterologist experiences, and we are now known to have a bias that non-celiac gluten sensitivity exists, our reports lacks the power or impact of larger research center based studies such as this study from Germany. Since Dr. Ken Fine has yet to publish his experience with stool antibody testing, though he has publicly disclosed preliminary results, stool antibody testing is not widely accepted but instead is considered suspect or unproven by most “celiac experts”. However, we are now seeing more research, especially from Europe, that supports the existence of a distinct clinical entity we are calling non-celiac gluten sensitivity (NCGS). This condition clearly affects a much larger group of people than the “hidden epidemic of celiac disease” believed to occur in one in one hundred people in the world. The next questions may not be does NCGS exist but exactly how common is it? Is it one in ten or closer to one in three? Stay tuned to www.thefooddoc.com for more exiting news about celiac disease and non-celiac gluten sensitivity as we journey together in search of a healthy gut, healthy life.

Copyright ©2007 The Food Doc, LLC www.thefooddoc.com

Reference:
Wahnschaffe U. et al. Predictors of Clinical Response to Gluten-Free Diet in Patients Diagnosed With Diarrhea-Predominant Irritable Bowel Syndrome. Clinical Gastroenterology and Hepatology July 2007 5; (7): 844-850.

Acid reflux or allergic esophagus? Is expecting doctors to routinely biopsy the esophagus like waiting for your cat to bark?

Heartburn is the cardinal symptom of acid reflux . This may result in damage to the esophagus causing difficulty swallowing. However, so can allergic esophagus also known as eosinophilic esophagitis.

Recent studies confirm both may be present though allergic esophagus may be missed. This is because of the unawareness of this fact by some gastroenterologists and the common practice to presume acid reflux is the cause. If acid reflux is presumed and the visual and historical clues of acid reflux missed then a biopsy of the esophagus that confirms the characteristic finding microscopically of an abnormal number of the allergy cell, eosinophil, in the esophagus may not be done by the doctor. As a result the role of food allergy in the patient’s symptoms will be not be appreciated.



Adding to the confusion is the knowledge of many pathologists and endoscopy doctors that eosinophils are commonly present in the lower esophagus when acid reflux injury has occurred. However, typically the number of eosinophils is few. The number of eosinophils may not be high enough to separate acid reflux from acid reflux in some patients. A recent study found another allergy cell known as the mast cell, help differentiate allergic esophagitis from acid reflux esophagitis. This study also provides further support that some people have both acid reflux and allergy.

Eosinophils are not normally present in the esophagus but are seen in small numbers under the microscope in biopsies of esophagus due to acid reflux. A count of more than 15-20 eosinophils per high power field (HPF or 40x) is the usual range considered diagnostic of acid reflux though some pathologists use 24 or more. In reflux, up to 7 eosinophils per HPF is considered typical.

Kirsch et al. found a significantly higher number of eosinophils (on average 55/HPF) in acid reflux , along with the presence of mast cells, compared with reflux. However, though 96% of the acid reflux biopsies showed IgE on cells so did 41% of those with acid reflux . This is consistent with some earlier studies that have suggested some people with acid reflux , especially those with more than 7 eosinophils per HPF, also have an allergic component.

This may also explain the failure of acid blocking medications alone to relieve the symptoms acid reflux in some people. The study also again highlights the growing evidence of the importance of biopsies when the gastrointestinal tissue visually appears normal. Without biopsies of normal appearing tissue in people with symptoms microscopic evidence of food allergy or sensitivity is commonly missed. Now that special stains are available for seeing previously difficult to see the allergy cell known as the mast cell, we are finding that this cell is commonly present in gastrointestinal tissue in people with symptoms who have previously been told that they had a normal exam.

Unfortunately, far too many gastrointestinal doctors are still failing to biopsy normal appearing tissue. Sometimes, it feels like despite the accumulating evidence of the importance of biopsies despite normal appearing tissue that seeing change in gastrointestinal doctors habit is like waiting for your dog to bark. Sadly, many people with irritable bowel syndrome have been told they have normal exams when they may have increased mast cells in their intestines and could be offered disease directed curative therapy rather than therapy directed at reducing symptoms combined with the unhelpful “you’re going to have to learn to live with it”.

Are we doing the same or worse with many people with chronic acid reflux symptoms? Post me a comment to let me know your thoughts and experiences. To your healthy gut, healthy life, The Food Doc.

Copyright © 2007, The Food Doc, LLC, All Rights Reserved.
www.thefooddoc.com

Reference: Kirsch R et al. “Activated mucosal mast cells differentiate eosinophilic (allergic) esophagitis from gastroesophageal reflux disease” Journal of Pediatric Gastroenterology and Nutrition 2007; 44:20-26.

Leaky gut and the innate immune system explained

Our innate immune defense response is an automatic and a non-specific system. It consists of the barriers such as the skin and the intact intestinal wall of the digestive tract. The intact intestinal wall is similar to a fence or wall. It is patrolled by certain immune cells that are like security guards or rent-a-cops, guarding the body. This includes white blood cells circulating in the blood or present in the intestinal lining. Circulating white blood cells typically include cells known as neutrophils, eosinophils, and natural killer T lymphocytes. Lining the intestinal wall (skin and respiratory tract) are other white blood cells and immune cells such as basophils, dendritic cells, phagocytes and macrophages. In the intestine white blood cells present in small numbers may be mobilized to the area for specific threats. These include eosinophils, mast cells, lymphocytes and neutrophils. These latter cells are increased in such conditions as eosinophilic esophagitis, eosinophilic colitis, eosphinophilic gastroenteritis, mastocytic enterocolitis, celiac disease, lymphocytic colitis and bacterial infections of the gut such as E. coli associated enterocolitis and other infectious colitis.

The intestinal lining is normally an intact barrier except when signaled to allow some bigger particles through such as certain proteins or other nutrients. The intestinal tract lining has a single layer of cells of the epithelial cell type. These cells are joined tightly, shoulder to shoulder, through a scaffolding of proteins, such as occludens. These tight junctions can open up on signal, from proteins such as zonulin. Certain normal signals permit the opening of the gaps between the lining cells, the paracellular spaces, or decrease the tight junctions resulting in increase intestinal permeability transiently. However, abnormal stimuli can trigger opening of the tight junctions resulting in abnormally increased intestinal permeability or leaky gut. When tight junctions open up wall of the gut may become abnormally permeable or leaky allowing it to be penetrated by foreign proteins including bacteria, viruses, molds, parasites and intact food proteins or lectins. Impairment of gut wall integrity or barrier function is an abnormal innate immune defense. It is like an insecure border, fence or wall.

Various immune cells of the innate response can release chemicals to contain or destroy invaders if they are near the area of an impaired barrier or they recognize that an invader is trying to get through just like a border patrol or roving security guard. Some of the tissue based immune cells destroy the invaders by actually eating them (phagocytes, eating cells and macrophages, large eating cells). They also are able to clean up left over debris and promote healing in a non-specific manner.

Certain good bacteria, such as acidophilus, lactobacillus and bifidobacter, residing in our gut actually help maintain our intestinal wall barrier function, act as antibiotics killing bad bacteria and inhibit other bacteria and yeast from taking over our system. Probiotics containing such bacteria like VSL#3 and Flora Q help promote and maintain a healthy intestine and intact gut wall.

Certain foods, such as gluten can increase gut permeability through the innate immune system. If you have the right genetic pattern (HLA DQ2 or DQ8) an abnormal adaptive immune response can result in serious intestinal injury that defines Celiac disease. However, an abnormal innate immune response can occur non-specifically in anyone resulting in gluten intolerance or sensitivity with all its associated symptoms or illness. Certain bacteria or yeast such as Saccharomyces cerevisiae (Brewer’s or Baker’s yeast, dietary yeast) can trigger an abnormal adaptive immune response in genetically predisposed people resulting in Crohn’s disease or colitis. To learn more about the immune system subscribe to this blog as we explore this further in future postings. Also visit www.thefooddoc.com to learn how to achieve and maintain a healthy gut, healthy life.

Copyright © 2007 The Food Doc, LLC. All Rights Reserved. www.thefooddoc.com

Celiac disease and gluten may be linked to allergic condition of esophagus, eosinophilic esophagitis

Eosinophilic esophagitis may be a manifestation of celiac disease and gluten sensitivity. Bua et al. from Italy report three patients aged 7, 17 and 19 years old, who were discovered to have eosinophilic esophagitis during evaluation for celiac disease. Biopsies of the lower esophagus obtained at the time of endoscopy performed to obtain duodenal biopsies to confirm celiac disease revealed eosinophilic esophagitis. All three had positive specific antibodies and small bowel biopsies diagnostic for celiac disease. However, they also had eosinophils greater than 20 per high power field found on esophageal biopsies though they were not symptomatic for eosinophilic esophagitis. I have also found eosinophilic esophagitis in patients with celiac disease and non-celiac gluten sensitivity. Like Bua, I believe there is a link to gluten and eosinophilic esophagitis.

Two of the three patients in the Italian report failed to resolved their eosinophilic esophagitis on follow up biopsies. However, both were teenagers who had known or suspected non-compliance with a strict gluten free diet. This is substantiated by both having persistently positive celiac blood tests and abnormal small bowel biopsies. On the other hand, the younger patient had laboratory and small bowel biopsy evidence of compliance with a gluten-free diet that was also associated with resolution of the findings of eosinophilic esophagitis on follow up esophageal biopsy.

How eosinophilic esophagitis occurs is not completely understood. Food allergies are known to play a role in a large number of patients but not all. Food sensitivity is suspected in others but not proven. The authors claim that this is the first report of association of eosinophilic esophagitis and celiac disease though there none of the patients reportedly had any esophageal symptoms.

Mast cells and eosinophils are reported to have a role in celiac disease. Lavo et al. reported in 1989 that gliadin causes increase mast and eosinophil chemical release in small bowel of patients with celiac disease given gliadin by intestinal infusion. Horvath et al. reported in 1986 evidence of mast cell release after a single dose of gliadin in children with celiac disease. Lancaster-Smith et al. reported in 1975 that the small intestine in patients with celiac disease and its skin equivalent dermatitis herpetiformis have increased intraepithelial lymphocytes, the characteristic white blood cell seen, and eosinophils after gluten exposure.

It makes sense to routinely obtain duodenal biopsies in people with suspected eosinophilic esophagitis and esophageal biopsies in people with suspected celiac disease not only to avoid missing diagnoses but also to avoid missing an important association not previously recognized. In my experience, eosinophilic esophagitis, mastocytic enterocolitis, and lymphocytic colitis occur in patients who are gluten sensitive and those who have celiac disease. In some patients more than one of these conditions is present and is only found because of my habit of obtaining biopsies routinely from all major areas of the GI tract during endoscopy. This common link to gluten in eosinophilic esophagitis and celiac disease has now been reported by others and the onus in on me to report my observations. I intend to do since we have been collecting our data. If you aren’t already one of my patients but have been diagnosed with more than one of these conditions, send me an email at thefooddoc@thefooddoc.com. Learn more about eosinophilic esophagitis and celiac disease at my website www.thefooddoc.com where we explore a healthy gut, healthy life on-line.

Copyright © 2007 The Food Doc, LLC. www.thefooddoc.com

References:

Bua J. et al. Eosinophilic oesophagitis and coeliac disease: is it just a causal association? Gut 2007 56; 1029-1030.

Lavo B. et al. Challenge with gliadin induces eosinophil and mast cell activation in the jejunum of patients with celiac disease. Am J Med. 1989 Dec;87(6):655-60.

Horvath K. et al. Mast cell degranulation after a single dose of gliadin in the jejunum of patients with coeliac disease. Acta Paediatr Hung. 1986;27(4):311-6.

Lancaster-Smith M. et al. The cellular infiltrate of the jejunum in adult coeliac disease and dermatitis herpetiformis following the reintroduction of dietary gluten. Gut 1975 Sep; 16(9): 683-8.

Genetics of Food Allergy and Food Sensitivity

Can genetics explain if you are allergic to some pollens or foods? White blood cell patterns determined genetically and designated as HLA DQ and DR genes have been identified with an increased risk of pollen, dust, latex, and food allergies. The intriguing part of this story is that there is an advantage to knowing your HLA DR and DQ type when evaluating your risk for pollen allergies and their associated food allergies or cross reactions.

We all have proteins on the surface of our cells that are genetically determined. These patterns are easily detectable by testing cells from blood or from the mouth. Specific patterns have been associated with increased risk for autoimmune conditions, gluten sensitivity and celiac disease. Now it appears certain DQ or DR patterns are associated with food and pollen allergies as well.

Boehncke, et al. from the University of Frankfurt reported in 1998 that certain white blood cell types known HLA class II genotypes or HLA DQ and DR genetic patterns were found more frequently in people with certain pollen associated food allergies. HLA-DQB1*0301 is present in more people with grass pollen allergy. Those with HLA-DRB1*08, an inherited white blood cell protein pattern linked with a grass pollen allergy, have six times the increased risk of peanut allergy.

Those who have inherited the HLA-DRB1*12 white blood cell pattern are 13 times higher at risk for carrot allergy. Birch pollen associated hazel nut allergy is linked to HLA-DRB1*01, DQA1*0101, and DQB1*0501. Hazel nut, almond, walnut and apple are the most common food allergies associated with birch tree pollen. Allergies to those foods are commonly associated with birch tree pollen in other studies. To download a printable table that lists the common foods that cross-react with various pollens, dust, and latex allergens go to the Food Doc resource page.

In 2004, Wang et al. from China published that the inherited white blood cell type DQA1*0302 is found in more people with Artemisia pollen-induced allergic rhinitis. This is hay fever due to the weed Mugwort also known as Sagebrush. Mugwort allergy is associated with several oral allergy food reactions including those from apple, celery, hazelnut, pistachio, lettuce, almond, peanut, and carrots.

The OAS literature contains numerous reports of food allergy or intolerance reactions associated with specific pollen, dust, mold or latex allergies. One of the best examples is ragweed pollen allergy. It is associated with a higher risk of food allergy or intolerance to only a few foods. These include foods in the gourd family (cucumbers and melons) and bananas. On other the hand, Birch tree pollen allergy is associated with sensitivity to many foods. The list includes those foods in the Rosacea family (apples, pears), tree nut family (hazelnut, almond, walnut), potatoes, and carrots. Reactions include classic allergic reactions such as skin rashes (atopic dermatitis, hives), wheezing (asthma), runny nose (allergic rhinitis), as well as the burning mouth OAS symptoms and other food intolerance symptoms.

It is helpful to establish a baseline symptom score. This can be done on-line or by printable symptom survey form at the Food Doc resource page. A detailed food symptom diary before a trial of elimination diet is also extremely helpful. An elimination diet before accepting diagnoses of IBS, fibromyalgia, unexplained neuropathy or headaches, and chronic fatigue syndrome is recommended. Any symptoms not readily explained or improved with other diagnoses and treatment should be considered to be possibly due to a food reaction until proven otherwise. This new information about the link of white blood cell protein patterns, HLA DQ types, suggests that we should consider having genetic testing done as well. Learn more at www.thefooddoc.com.

Selected Bibliography

Boehncke, et al. Clin Exp Allergy. 1998 Apr;28 (4):434-41.

Fine KD et al. Am J Gastroenterol. 2000 Aug;95(8):1974-82.

Wang et al. Otolaryngol Head Neck Surg Feb; 130(2): 192-197.

Copyright 2007 The Food Doc, LLC. All rights reserved. www.thefooddoc.com

Gluten free salad dressing packets great for restaurants

Trying to maintain a strict gluten-free diet can be frustrating. Hidden sources of gluten lurk everywhere. Salad dressings commonly contain wheat or gluten. It is nearly impossible to determine if restaurant salad dressing is safe. It is one of the many challenges of eating out for those of us on a gluten free diet. Gluten-free salad dressing packets however are an excellent option. Unfortunately many people on a gluten-free diet are unaware they are available.

Skipping croutons that are put on most salads is just the first challenge. If your experience is like my patients and mine, it is common to have salads brought out with croutons despite specifically instructing the restaurant staff to leave them off. After pointing out the mistake some restaurant staff simply pick them off the salad before bringing it back to you. You then discover dreaded gluten breadcrumbs after you have eaten part of the salad realize you have been “glutened”. For many like my wife and several of my patients who are severely gluten sensitive, such a accidental gluten exposure sets off a cascade of diarrhea, painful abdominal bloating, fatigue, bone and joint pains, and headaches over the next several days

Because of the fear of hidden gluten, many give up a healthy and generally safe gluten free meal option because of uncertainty of the salad dressing. However, if you can avoid the crouton fiasco, you can maintain a gluten-free diet while eating salad at restaurants or other gluten uncertain situations, by bringing your own salad dressing. If you are like my wife, who has Celiac disease, carrying a very large purse to accommodate small children and our family's gluten free lifestyle, it is nothing to carry a collection of emergency gluten-free snacks. Carrying a bottle of salad dressing is a bit more of challenge. For gluten-free salad dressing there is another option to the giant handbag. Carrying packets of Annie’s Naturals gluten-free salad dressing is an excellent option. The Cowgirl Ranch Dressing by Annie’s Naturals taste great and comes in a generous 1.5 ounce single packet that doesn’t require refrigeration. The packets are not cheap at 79 cents each but they are great to have for salads at restaurants. They are great for dipping gluten free chicken nuggets strips and fresh vegetables.

I highly recommend you try the gluten-free Annie’s Natural Cowgirl Ranch Dressing. Order some of their easy to carry and use packets. They also offer gluten-free Caesar and Balsamic Dressing packets. They have several other gluten-free dressings but not all their salad dressing are gluten-free so check their products at www.anniesnaturals.com and as always, read labels closely. My website www.thefooddoc.com has launched. We are still working the web development team to clear up some needed adjustments including the final forms of the site guide and symptom assessment tool. I appreciate your patience if you have been to check it out and noted some kinks. They will be fixed within the next week and we will be rolling much more very soon. So, stay tuned to the Food Doc and our journey to a healthy gut, healthy life.

Copyright © 2007, The Food Doc, LLC, All Rights Reserved.

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Why wheat gluten is not safe to eat

Despite reassurances by the grain industry that the current high gluten wheat flour and grains making up much of our current diet are safe for those without celiac disease, it isn't true according to new research. Scientific evidence is accumulating explaining why many eating such a diet are ill and feel better on a gluten free diet even when they don’t have celiac disease. Are you one of them? Researchers from Spain describe an abnormal immune response to gluten in humans whether they have celiac disease or not.

Gliadin, a protein produced from the digestion of gluten, increases intestinal permeability. This effect is noted in intestinal tissue regardless if someone has celiac disease. In those with celiac disease the gut injury from gluten is worse and produces a leaky gut that lasts longer than in those without celiac disease. The ability of gluten to damage the intestine more severely is clearly linked to certain white blood cell patterns that are inherited. The leaky gut persists in people with celiac disease as long as they continue to eat gluten-containing foods because of a genetic predisposition tied to white blood cell protein patterns designated DQ2 and DQ8. Those with these patterns are at much higher risk for gluten induced intestinal injury.

White blood cells carrying DQ2, DQ8 or both patterns can develop an abnormal adaptive immune response to gluten (gliadin). Most people carrying these patterns do not have both abnormal innate and adaptive immune responses to gluten resulting in celiac disease. However, many people with and without these patterns have symptoms that are worse while eating gluten and better on a gluten free diet. Why is that?

Bernado et al. from Spain help with the explanation of how gluten can do this. In their report in the May 2007 issue of Gut 2007 the report evidence of an altered innate response to gluten (gliadin) in people WITH AND WITHOUT celiac disease. They propose that an abnormal innate immune response is common in patients with and WITHOUT celiac disease regardless of genetic make up, that is DQ 2 or DQ8 status. They report that there is an abnormal innate immune response to gluten producing chemicals in the intestine resulting in injury (and therefore leaky gut and symptoms).

However, abnormal adaptive immune response results in more severe intestinal injury (abnormal small intestine biopsy) and abnormal specific blood tests (endomysial and tissue transglutaminase antibodies) now required for the formal diagnosis of celiac disease. It is often forgotten that before these tests were available, the diagnosis of celiac disease was based on symptoms and response to a gluten free diet. Celiac disease as defined as the presence of villous atrophy on intestinal biopsy and abnormal EMA and tTG antibodies is almost entirely restricted those with DQ2 and DQ8. Why is this?

Increased intestinal permeability due to activation of intra-epithelial lymphocytes in DQ2 or DQ8 positive individuals is known to cause severe intestinal injury that further increases gut permeability from gluten. However, not everyone with these genetic patterns develop celiac disease. In the absence of these white blood cell patterns, it is rare to develop severe intestinal injury and positive specific blood tests.

I believe however, it is quite clear that gluten (gliadin) causes leaky gut even in normal people. This likely due to activation of immune cells that release chemicals called cytokines that injure tissue and cause symptoms. Immune activation of lymphocyte white blood cells and intestinal injury commonly results in elevated gliadin antibodies and non-specific intestinal biopsy abnormalities in people who don’t have celiac disease but respond to a gluten free diet.

Though such individual do not and may never meet diagnostic criteria for celiac disease despite the presence or absence of DQ2/DQ8 genetics, many of these do have improved symptoms, normalize their gliadin antibodies and any intestinal biopsy abnormalities when offered a gluten free diet trial. Withholding, discouraging or failing to suggest a trial of gluten free diet from such people because they do not meet diagnostic criteria for celiac disease or or are DQ2 and DQ8 negative seems cruel. Considering the accumulating scientific notwithstanding the experience of many people who are better on a gluten free diet, it is unwise to not consider gluten as a reversible cause of illness. It is however, better to undergo appropriate evaluation before starting a gluten free diet to avoid missing the diagnosis of true celiac disease.

The new information coming from celiac disease research indicates to me that gluten may not be good for you regardless if you have celiac or not. But I already knew that from personal and professional experience. If you are not sure if gluten is bad for you or want more information about the differences between the innate and adaptive immune response, see the research page on my website
www.theFoodDoc.com and my other articles.

References:

Bernado D. et al. Is gliadin safe for non-coeliac individuals. Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides. 2007 56:5; 889


Drago S. et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestine cell lines. Scand J Gastroenterol. 2006;41(4): 408-419.

Maiuri L. et al. Association between innate responses to gliadin and activation of pathogenic T cells in coeliac disease. The Lancet. 2003;362(9377):30-37.

The Food Doc is dedicated to helping you achieve a “healthy gut, healthy life”.

Copyright © 2007, The Food Doc, LLC, All Rights Reserved.
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Expert on Food Allergies, Intolerance, and Sensitivity Launches The Food Doc Website

The Food Doc website has launched! After months of waiting, people all over the world are visiting website created by Dr. Scot Lewey, a digestive specialist with personal experience and professional expertise with food allergies, food intolerance and food sensitivity.



The website features Dr. Lewey's review and insights on the latest research and news. There is an e-store, downloadable printable materials and slides. Also available to subscribing members are unique applications such as an on-line symptom diet diary with symptom survey tracking ability, and an interactive symptom assessment tool. The site includes a virtual office for secure on-line consults with the Food Doc. Additional articles and features are already on the way.





We encourage you to go to www.thefooddoc.com now and begin taking advantage of the on-line tools and doctor authored helpful information you can trust. Drop us a note after you do to let us know what you think. Send us your suggestions and e-mail the site to friends. The Food Doc is dedicated to helping you achieve a “healthy gut, healthy life”.

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