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    An Experts Group Meeting About Non-celiac Gluten Sensitivity


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Winter 2014 Issue


    Image Caption: CC--ITU/I.Wood

    This article originally appeared in the Winter 2014 issue of Journal of Gluten Sensitivity.


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    Celiac.com 04/30/2014 - Dr. Catassi and colleagues reported, in the September of 2013 issue of Nutrients, that during the previous 21 months for every ten reports about celiac disease, there was one report of non-celiac gluten sensitivity (1).  They plotted the publication ratio over the last 60+ years, showing that there has been a steady increase of reports on non-celiac gluten sensitivity in the medical literature that has grown proportionally faster than the number of reports about celiac disease, and most of us are aware of the rapid growth made by the celiac literature during that same period. By implication, we may reasonably assume that this reflects a growing interest among physicians and other health care workers.  Catassi and colleagues mention the first meeting of an expert panel in London during 2011, and report on discussions from the December, 2012 meeting of experts in Munich, addressing a wide range of illnesses thought to have some connection with gluten ingestion (1, 2).  An approximately concurrent report by Mooney et al ( including Sanders, one of the above-mentioned experts) (3)  attempts to clarify and extend some of the information from the Catassi et al report, as well as contradicting it on the issue of IgG anti-gliadin antibodies as a potential biomarker for non-celiac gluten sensitivity (1).   This growing trend of interest in non-celiac gluten sensitivity, along with the publications specifically cited here, offer enormous affirmation of the Journal of Gluten Sensitivity and its editorial staff, and we are loathe to criticize it in any way.

    Oats
    However,  in the same report, Catassi and colleagues repeatedly decry the “lack of biomarkers” for non-celiac gluten sensitivity (1). In essence, they  are saying that there is no known laboratory test that will reliably identify this form of gluten sensitivity. Further, while they admit that they have “poor knowledge of the pathophysiology” of non-celiac gluten sensitivity, they seem to assume that oats may be safely eaten by individuals afflicted by this sensitivity. They appear to reflexively exclude oats from any further investigation, as a possible factor in non-celiac gluten sensitivity. Such assumptions appear to be bleeding over into their perceptions of non-celiac gluten sensitivity from their work with celiac disease.    

    The IBS Connection
    Catassi et al also cite one study that reports a rate of 28% of non-celiac gluten sensitivity among IBS patients, and a larger study that reports a rate of 30% of IBS patients who have wheat sensitivity, either with or without other food sensitivities.  This same group reports a prevalence of IBS in northern Europe of between 16%  and 25% of the population (1).  If we take their most conservative numbers,  estimating that IBS afflicts only 16% of the population, and that 28% of that group has  non-celiac gluten sensitivity, then about 4.48% of northern Europeans should have non-celiac gluten sensitivity. Catassi et al  say that the rate could well be above 1% (1). Some might suggest that this is a gross understatement that distorts the data rather than clarifying it. This, too, may reflect a preoccupation with lessons learned from celiac disease, rather than a de novo view of gluten sensitivity.  

    They cite yet another study of a subset of IBS patients in which diarrhea was the predominant symptom, particularly among patients with genetic HLA DQ2 and DQ8 markers, which are associated with celiac disease.  These IBS patients showed compromised bowel barrier function when consuming gluten, presumably as a function of barrier permeability.  They go on to assert that the gluten free diet offers some measure of symptom relief even to those patients whose IBS may be partly or wholly driven by low-fermentable, poorly-absorbed, short-chain carbohydrates, as  gluten proteins may be included in this list of potentially problematic foods.  

    Psychiatric Connections
    Catassi and colleagues also explore schizophrenia and autism  where sub-groups of non-celiac gluten sensitivity have been identified. They report the findings of two studies of schizophrenic patients wherein no benefits were seen after gluten avoidance over the study periods of either 10 days (4) or 5 weeks of treating 8 chronic schizophrenic patients (5).  Catassi et al also mention the mildly positive results from a study of 14 weeks’ duration (6). However, beyond citing one paper authored by Dr. Curtis Dohan, identified as the earliest suggestion of a connection between gluten and schizophrenia, they do not mention the recommendations of Dohan and his colleagues, who called for a minimum study duration of at least six months and as much as a year on a gluten free, dairy free diet before the potential benefits of this diet can be observed in schizophrenic patients.  They also recommended treating newly diagnosed and newly relapsed schizophrenic patients with this diet as they had observed little positive response among the chronic schizophrenic subjects they studied (8, 9, 10, 11). Further,  Catassi et al completely fail to acknowledge the work by Zioudrou and colleagues (12) that identifies a possible source of urinary peptides seen both in many schizophrenics (13, 14) and many patients with autism (15). These peptides have, since their discovery, been recognized as psychoactive (12).  These insights are particularly important in these realms of mental illness and abnormal development, as they offer insights that may someday offer vastly more effective treatments than are currently available.  Again, celiac disease may be coloring the lens through which these experts are looking at non-celiac gluten sensitivity.   

    Catassi and his colleagues go on to acknowledge that IgG class antibodies against gliadin, a sub-group of gluten proteins, as markers for increased intestinal permeability (1) but they fail to acknowledge this protein group as the missing “biomarker” of gluten sensitivity. They say:  “Non-celiac gluten sensitivity is currently a diagnosis of exclusion with the only positive diagnostic criterion being the clinical response to gluten withdrawal. Patients should have negative celiac serology, normal duodenal histology, and negative IgE-based tests” (1).  

    IgG against gliadin offers a biomarker for 19.8% tp 23.5% of the population.  Yet serology is the most common approach to measuring IgG anti-gliadin, and others have made this connection, identifying IgG class anti-gliadin antibodies as “ a measure of the immune response to gliadin” (7). (Gliadin is a sub-group of gluten proteins.)  If  someone is mounting an immune response against gliadin, it is reasonable to say that they are gluten sensitive. So why would Catassi and colleagues back away from the data suggesting that non-celiac gluten sensitivity may afflict from 4.48% to as many as 7.5% of the northern European population, based only on those with diagnosed IBS?  Further, 12%  of healthy blood donors in the United Kingdom  have also been reported to show elevated levels of anti-gliadin antibodies (16).  Taken together, these suggest a rate of non-celiac gluten sensitivity, as identified by IgG class antibodies against gliadin among northern Europeans, of between 16.8% and 19.5%  of the general population.  

    Dr. Sapone and her group have identified and reported on a group of non-celiac gluten sensitive patients (21) who present with what Dr. Sapone and her group have  elsewhere characterized as a function of the innate immune system and comprise between 6% and 7%  of the general population (22).  Only about half of these subjects show anti-gliadin antibodies but since they are not healthy blood donors or IBS patients, we may reasonably predict that between 22.8% and 26.5% of the population has non-celiac gluten sensitivity.  

    And there are likely a lot more cases than are suggested by those numbers.   For instance, about 7% of patients with multiple sclerosis showed IgG class antibodies against gliadin (17),  while more than 20% of patients with Crohn’s disease, and 6.5% of patients with rheumatoid arthritis also showed elevated IgG antibodies against gliadin (18), and Samaroo et al found the same antibodies elevated in the sera of 5.6% of the schizophrenic  patients they studied (19).   And Hadjivassiliou’s group states “IgG antigliadin antibodies have a high sensitivity not only for patients with coeliac disease but also for those with minimal or no bowel damage where the principal target organ is the cerebellum or peripheral nervous system” (20).  

    Cancer
    Perhaps the most distressing part of the Catassi report is where it says “No major complication of NCGS has so far been described; especially autoimmune comorbidity , as observed in celiac disease, has not been reported so far.” In 2007, Anderson et al published a report in which people with non-celiac gluten sensitivity experienced: “ ..... the incidence of malignant neoplasms in patients with celiac disease (positive EMA test) was similar to that of the Northern Ireland population. However,  mortality from malignant neoplasms, NHL [non-Hodgkin’s lymphoma], and digestive system disorders was significantly increased in patients who were gluten sensitive with a negative EMA test” (7).  This same report states that it may be the first investigation of malignancy and mortality among non-celiac gluten sensitive patients (7) and they have found that cancer and increased mortality is higher among those who are gluten sensitive than among those with celiac disease.  

    Why Not IgG Anti-gliadin as Biomarkers?
    You may, like me, be wondering why the Catassi-led group retreated from the use of IgG antibodies against gliadin as a bio-marker for gluten sensitivity, when the consequences of ignoring it are made obvious by the Anderson et al study  mentioned in the previous paragraph, showing increased mortality rates in this group. This result may be due to physicians’ failure to recommend a gluten free diet, reflecting their skepticism regarding this marker.  The Catassi et al skepticism is especially puzzling when at least one of their own members (Sanders) had submitted a report for publication at about the same time, in which he and his colleagues assert a prevalence of non-celiac gluten sensitivity of 12%, among healthy blood donors, based on IgG anti-gliadin antibodies  (3).   We are also left wondering why these experts would ignore the recommendations and insights embodied in the large and earliest body of research connecting schizophrenia and gluten, authored by Curtis Dohan and his colleagues (8-14) while Catassi et al seem to give credence to the negative results reported by investigations lasting only ten days or five weeks?

    I think that Catassi et al have answered this question, but before we discuss that, I’d like to point out that elite athletes have reported improved performance on a gluten free diet (23, 24). They were already performing at the very pinnacle of their sports, yet their experimenting with the gluten-free (and in one case, also a paleo-diet) led to enhanced performance.  That really is quite amazing.  And what about those with IgG AGA who have neurological or other autoimmune diseases?  Also, the girl that Kim and I wrote about in the last issue of this Journal is a perfect example of a patient with autoimmune diabetes, where celiac disease was ruled out, so she was told that she would have to inject insulin for the rest of her life. Yet all she needed was a gluten free diet and very insightful parents who were willing to press physicians to expand their thinking a little.

    I must say that I am very pleased with Catassi et al’s stated recognition of extra-intestinal manifestations of non-celiac gluten sensitivity.  However, their approach is to call for further characterizing  the various groups that respond differently to gluten, based on grouping by specific illnesses. This may miss the larger picture.  Catassi et al acknowledge that “The vast majority of celiac experts initially reacted with a great deal of skepticism to the concept of NCGS existence and the fact that it was a separate entity from celiac disease” (1).  They go on to suggest that we are about at the same place that we were forty years ago with celiac disease.  Perhaps.  

    As it stands, we have celiac disease and we have non-specific anti-gliadin antibodies that signal the lion’s share of cases of non-celiac gluten sensitivity, an increased risk for autoimmunity, a majority of a wide range of neurological diseases that are also more frequent among those with celiac disease, we also have many children with ADHD who recover on a gluten-free diet alone, we have a very large majority of children with learning disabilities who recover on a strict gluten-free diet, we have people who lose weight on a gluten-free diet, we have people who just think that they feel better on a gluten-free diet, and we have elite athletes who perform better on a gluten free diet.  We also have cases of non-celiac gluten sensitivity as characterized by Dr. Sapone et al, where the innate immune system is involved, and we only have anti-gliadin antibodies associated with about half of those individuals.   

    When we see all these fractured pieces scattered about the landscape of gluten induced illness, it is highly likely that we are missing the larger vista that incorporates all of them. But we would have to let go of some sacred cows to see that larger picture. The first sacred cow we should abandon is the idea of celiac disease as a distinct and most important disease entity, and begin to think of gluten induced disease, or to use Rodney Ford’s term, “gluten syndrome”.   I think it is great that non-celiac gluten sensitivity is getting more recognition, but the current lens through which medical researchers view celiac disease and non-celiac gluten sensitivity may be clouded by their reductionist  paradigm.

    The problem, as I see it, is that celiac disease has long been mischaracterized. When Dr. Dicke showed that the gluten free diet reversed celiac disease, few believed him.  He was laughed out of a world conference in New York City and vowed never to return to the USA.  When he and his colleagues searched for a ‘scientific’ way to validate the diet as an effective treatment for celiac disease, they  found intestinal villous atrophy, so the medical understanding of gluten induced illness has evolved, primarily, as an intestinal ailment characterized by villous atrophy.  

    I think that Dr. Rodney Ford’s conception of celiac disease as a sub-group of intestinal and extra-intestinal ailments that first derive from gluten’s assault on neurological tissues (25) is better rooted in the facts, and much more likely to prove true.  Ford’s perspective may well provide a better tool for understanding gluten’s impact on human health - although it impugns major parts of more than seventy years of medical and scientific research into celiac disease. It may even suggest that we were looking in the wrong direction for much of the time. Ford postulates that gluten’s first insult is to neurological tissues. Those who are susceptible to celiac disease may go on to develop intestinal damage as a sequel to the neurological injury. Those who are not susceptible to celiac disease may go on to develop any of a number of gluten-related ailments, depending on their unique genetic makeup, experiences, and exposures (25).  Understandably, Rodney’s conception may be unpopular among some medical practitioners and researchers - but it sure fits the facts better than anything else I’ve seen.   

    Sources:  

    1. Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano  A. Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders. Nutrients 2013, 5, 3839-3853.
    2. http://www.drschaer-institute.com/smartedit/documents/yourlife/dsif_03_2011_uk_internet.pdf
    3. Mooney PD, Aziz I, Sanders DS. Non-celiac gluten sensitivity: clinical relevance and recommendations for future research. Neurogastroenterol Motil. 2013 Nov;25(11):864-71. doi: 10.1111/nmo.12216. Epub 2013 Aug 12.
    4. Storms LH, Clopton JM, Wright C. Effects of gluten on schizophrenics. Arch Gen Psychiatry. 1982 Mar;39(3):323-7.
    5. Potkin SG, Weinberger D, Kleinman J, Nasrallah H, Luchins D, Bigelow L, Linnoila M, Fischer SH, Bjornsson TD, Carman J, Gillin JC, Wyatt RJ. Wheat gluten  challenge in schizophrenic patients. Am J Psychiatry. 1981 Sep;138(9):1208-11.
    6. Vlissides DN, Venulet A, Jenner FA.A double-blind gluten-free/gluten-load controlled trial in a secure ward population.Br J Psychiatry. 1986 Apr;148:447-52.
    7. Anderson LA, McMillan SA, Watson RG, Monaghan P, Gavin AT, Fox C, Murray LJ. Malignancy and mortality in a population-based cohort of patients with coeliac disease or “gluten sensitivity”. World J Gastroenterol. 2007 Jan 7;13(1):146-51.
    8. Dohan “Cereals and schizophrenia: data and hypothesis” Acta Psychiat Scand 1966; 42: 125-152
    9. Dohan et. al. “Relapsed Schizophrenics: More Rapid Improvement on a Milk-and Cereal-free Diet” Brit J Psychiat 1969; 115: 595-596
    10. Dohan et. al. “Is Schizophrenia Rare if Grain is Rare?” Biol Psychiat 1984; 19(3): 385-399
    11. Dohan “Is celiac disease a clue to pathogenesis of schizophrenia?” Mental Hyg 1969; 53: 525-529
    12. Zioudrou et. al. “Opioid peptides derived from food proteins. The exorphins” J Biol Chem 1979; 254:2446-2449
    13. Dohan FC. Genetic hypothesis of idiopathic schizophrenia: its exorphin connection. Schizophr Bull. 1988;14(4):489-94.
    14. Severance EG, Alaedini A, Yang S, Halling M, Gressitt KL, Stallings CR, Origoni AE, Vaughan C, Khushalani S, Leweke FM, Dickerson FB, Yolken RH. Gastrointestinal inflammation and associated immune activation in schizophrenia. Schizophr Res. 2012 Jun;138(1):48-53.
    15. Reichelt KL, Tveiten D, Knivsberg AM, Brønstad G.Peptides’ role in autism with emphasis on exorphins.Microb Ecol Health Dis. 2012 Aug 24;23.
    16. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A.Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.
    17. Shor DB, Barzilai O, Ram M, Izhaky D, Porat-Katz BS, Chapman J, Blank M, Anaya JM, Shoenfeld Y. Gluten sensitivity in multiple sclerosis: experimental myth or clinical truth? Ann N Y Acad Sci. 2009 Sep;1173:343-9. doi: 10.1111/j.1749-6632.2009.04620.x.
    18. Shor DB, Orbach H, Boaz M, Altman A, Anaya JM, Bizzaro N, Tincani A, Cervera R, Espinosa G, Stojanovich L, Rozman B, Bombardieri S, Vita SD, Damoiseaux J, Villalta D, Tonutti E, Tozzoli R, Barzilai O, Ram M, Blank M, Agmon-Levin N, Shoenfeld Y. Gastrointestinal-associated autoantibodies in different autoimmune diseases. Am J Clin Exp Immunol. 2012 May 25;1(1):49-55. Print 2012.
    19. Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A. Novel immune response to gluten in individuals with schizophrenia. Schizophr Res. 2010 May;118(1-3):248-55. doi: 10.1016/j.schres.2009.08.009. Epub 2009 Sep 11.
    20. Hadjivassiliou M, Grünewald RA, Davies-Jones G A B. Gluten sensitivity: a many headed hydra. Heightened responsiveness to gluten is not confined to the gut. BMJ. 1999 June 26; 318(7200): 1710–1711.
    21. Sapone A, Lammers KM, Casolaro V, Cammarota M, Giuliano MT, De Rosa M, Stefanile R, Mazzarella G, Tolone C, Russo MI, Esposito P, Ferraraccio F, Cartenì M, Riegler G, de Magistris L, Fasano A. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011 Mar 9;9:23.
    22. Sapone A, Lammers K M, Mazzarella G, Mikhailenko I, Cartenì M,  Casolaro V, Fasano A. Differential Mucosal IL-17 Expression in Two Gliadin-Induced Disorders: Gluten Sensitivity and the Autoimmune Enteropathy Celiac Disease. Int Arch Allergy Immunol. 2010 April; 152(1): 75–80. Published online 2009 November 24.
    23. https://www.celiac.com/articles/23375/1/New-Djokovic-Book-Promotes-Gluten-free-Diet/Page1.html 
    24. http://www.examiner.com/article/miami-heat-guard-ray-allen-lost-10-lbs-on-gluten-free-paleo-diet
    25. Ford RPK. The gluten syndrome: a neurological disease. Medical Hypotheses. 2009:73, 438-440
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    Guest Dr Rodney Ford

    Posted

    What an excellent commentary on this very important topic. Yes, the authors needs to be congratulated for putting this paper together. I totally agree with Dr Ron Hoggan that the authors have gone out of their way to be as conservative as possible about the value of the AGA and the proportion of the population who have gluten sensitivity. Remember that a decade ago, these gastroenterologists scoffed at the concept of gluten sensitivity - and now at last they have recognised that it is a real and common entity. In another few years they will be more confident to embrace gluten sensitivity in all of its guises.

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    Scott Adams
    Introduction
    Through his writings, we know that Hippocrates, the father of medicine, had already recognized the presence of allergic reactions in people as early as ancient times. However, the term allergy is a relatively new one, as compared to many other commonly used medical terms. In 1906, Viennese pediatrician Baron Clemens von Pirquet used the term for the first time to describe an altered response of his patients bodies. Von Pirquet believed that this altered reaction manifested itself in changes of the immune system, effected by external influences on the body, such as: food intake, the air breathed or direct skin contact. The term allergen (the substance responsible for the altered reaction) was born. At that point in time, however, von Pirquet had no means of scientifically proving that these immunological changes actually occurred in the body. It was not until the mid-1920s, that a second significant event occurred.
    Researchers found that, by injecting a minute quantity of purified allergen under the skin, certain individuals would develop a clear skin response; a welt, with or without itching and redness, could be provoked. This positive skin test for allergies would show itself most prominently in patients with hay fever, asthma, chronic rhinitis, hives and eczema. The prick test became a method of demonstrating the involvement of the immune system in allergic reactions. However, the precise biological reason for the reaction continued to remain a mystery.
    It was not until the Sixties, when an important discovery occurred which provided long-awaited scientific support for the classical allergy theory and removed any doubts about the relationship of the immune system with allergies. This breakthrough came about with the scientific discovery of immunoglobulin E (IgE) by a Japanese couple named Ishizaka.
    Classical Allergic Reaction
    The following are the chain of events which happen in allergic reactions:
    An allergen must be present in the body. This allergen is the substance which causes us to have an abnormal immunological response. Allergens tend to be protein molecules. Interestingly enough, the immune system only detects particles of a certain size as potential troublemakers and protein molecules are just the right size. In a small number of cases, the body actually responds to molecules other than proteins. These molecules, which are generally much smaller, are called haptens. By combining with protein molecules, haptens form larger complexes which can then be detected by the immune system. The allergen is detected by the B cells. These are specialized immune cells, capable of producing antibodies. Just like allergens, antibodies are protein molecules, which have the capacity to neutralize allergens. Every B cell produces its own, specific antibody, depending on the type of intruder it needs to respond to. It is easy to understand why the body must have a ready pool of millions of antibodies, in order to combat these numerous offenders. There are five main categories of antibodies (IgG, IgA, IgM, IgD and IgE) which the body releases under different circumstances (for instance to fight off various infections, etc.). In the case of allergies, the body produces the antibody immunoglobulin E (IgE), first discovered by the Ishizakas. Usually, antibodies will bind directly to the appropriate damaging substance and neutralize it. However, IgE deviates from this common path. It first attaches one of its legs to one of the bodys numerous mast cells. The other leg is used to hold on to the offending allergen. This action signals the mast cells to begin disintegrating, thereby releasing histamine. Histamine is a chemical substance responsible for a great number of complaints which may arise during allergic reactions. It causes muscle cramps and an inflammation-like process with redness and swelling of mucous membranes.
    Allergic reactions can occur under a variety of circumstances. For instance, inhaling certain substances, such as grass pollen, house dust, etc., may cause an allergic response. However, the consumption of certain foods may do the same. Allergies typically bring on complaints very rapidly upon contact with the allergen. Complaints may vary from a runny nose, sinusitis, earache or runny eyes to itching of the skin, eczema and shortness of breath.

    Intolerance
    Conventional medicine can easily diagnose and treat allergies for foods or inhalants. Here, the so-called RAST test plays a very important role, because this test can demonstrate the presence of IgE.
    However, demonstrating the presence of intolerance is more difficult. In this situation, similar to the case of classical allergies, the body responds abnormally and, in addition, the immune system does not produce IgE. It quite often takes much longer for complaints to come on, thereby masking the possible link between the offensive substance and the complaints themselves.
    These are only a few of the reasons why food intolerance is considered a fairly controversial concept in conventional medicine. Intolerance can be responsible for a wide variety of complaints which, at first glance, seem to lack a plausible explanation. Intolerance can manifest themselves as the following:
    Gastrointestinal complaints: stomach ache, irritable bowel, Crohns disease, ulcerative colitis Skin complaints: itching, eczema, hives, acne (in adults) Joint and muscle complaints: ranging from atypical pains to rheumatoid arthritis Headache and migraine Chronic fatigue Asthma, chronic rhinitis or sinusitis Pre-menstrual syndrome Hypoglycemia Depression, anxiety Sleeping disorders
    Diagnosing Intolerance
    It is impossible to accurately demonstrate intolerance through conventional testing methods.
    The Amsterdam Clinic currently uses the following test, which is very reliable.
    Another useful test is the IgG(4) antibody test. Here, the presence of IgG(4) antibodies is determined. These antibodies are the slowly occurring variety, which do not appear in the blood until 24 to 48 hours after exposure to an offending food or substance. The reliability of this test varies between 80 and 90%.
    Treatment
    Diet
    In the treatment of inhalant allergies (such as asthma, hay fever) and food allergies and intolerance, avoidance (elimination) of allergens plays an extremely important role. In the case of food sensitivities, either the cytotoxic test or IgG(4) test can help determine reactions to specific foods. Based on the test results, an elimination/rotation diet can be specifically tailored.
    Foods causing strong reactions in these tests, should (temporarily) be excluded from the diet. More moderate reactions allow for rotation of certain food items in the diet. These may be eaten once every four days. Especially during the first week(s) of the diet, withdrawal symptoms, similar to complaints stemming from the cessation of coffee, tobacco or alcohol consumption, may occur. The body seems to crave offending food items. Generally, these withdrawal symptoms disappear after a couple of weeks. Concurrently, those complaints relating to food sensitivity also diminish.
    Using this dietary approach, the reaction to food allergens may decrease in the course of time. After a three month moratorium, reintroduction of forbidden food items can be attempted, one at a time. In this way, food items still causing reactions can be isolated more easily. Often, at least part of existing intolerance completely disappear after an elimination/rotation diet.
    With the treatment for inhalant allergies, elimination is also the first step. It is obvious that patients having an allergy for cats or dogs, should avoid any contact with these pets. The situation becomes more difficult when dealing with allergies to grass or tree pollen, since total elimination is basically impossible. The same goes for house dust mite allergy. The house dust mite lives in mattresses, pillows, carpeting, drapes, upholstery, etc. Through mite-killing pesticides, special mattress and pillow covers, non-carpeted floors, etc. reasonable results can be obtained.
    Medication
    Medicines for inhalant allergies, such as antihistamines (Triludan), corticosteroids (Prednisone, Pulmicort, Becotide), cromoglycates (Lomudal, Lomusol), and airway dilating medication (Ventolin, Berotec, Atrovent) do suppress symptoms, however, they do not cure the allergy! In the realm of conventional medicine, effective medications for food allergy and intolerance do not exist at all.
    Desensitisation
    Enzyme-potentiated desensitisation (EPD) and the provocation/neutralization method are very effective treatments for food allergy/intolerance and inhalant allergy problems. These methods tackle allergy problems at the root.
    During EPD treatment, a small quantity of a food or inhalant allergen mixture is injected intradermally into the skin, in conjunction with the enzyme beta-glucuronidase. This combination causes the body to gradually adjust its exaggerated responses to food and inhalant allergens. In this way, the immune system is readjusted and reset. Initially, the injections have to be given once every two months. Gradually, however, the intervals between injections become longer and the injections can often be discontinued after a time. According to conservative estimates, at least 80% of those patients treated with EPD show considerable improvement in the course of time. Provocation/neutralization can be used both diagnostically and therapeutically. Here, separate extracts of food or inhalants, suspected as possibly offending, are injected intradermally. This causes a welt to appear in the skin. After 10 minutes, the size and nature (firmness, color, etc.) of the welt are evaluated. A positive welt will generally bring on symptoms (provocation). Depending on the size and nature of the welt, as well as, the presence of symptoms, varying concentrations are injected, until a dose is found which does not cause any welt changes or symptoms. This is the neutralizing dose. Injections with the proper neutralizing dose will bring on immediate protection against the symptoms caused by the offending food and/or inhalant. Copyright © 1996 the Amsterdam Klikiek
    For further information please contact:
    Also in THE NETHERLANDS:
    Amsterdam Kliniek
    Reigersbos 100
    1107 ES Amsterdam Z.O.
    Telephone 31 (0)20 697 53 61
    Telefax 31 (0)20 697 53 67
    Lydia S. Boeken M.D. London/Amsterdam

    Scott Adams
    The following is a March 11, 1998 post by Kemp Randolph krand@PIPELINE.COM.
    According to Dr. Hugh Sampson, Mt. Sinai Medical Center, at an AMA sponsored press briefing on Nutrition, in a list of Facts vs. Fictions, Fiction: Skin tests or blood tests can be used to diagnose food sensitivities. Fact: ...A positive test does not mean a person will react to a food...furthermore these tests do not tell whether a person has a non-IgE mediated sensitivity to food.
    He describes these tests only as useful guides and points out that diet testing is the only reliable way to identify a food allergy, preferably where the person does not know whether they have eaten the suspect food.
    Q: If I am sensitive to milk and eggs...could they damage my villi in the same way as gluten?
    A: Theres a specific note in Michael Marshs book about food allergies causing villi damage. Thats the book On Coeliac Disease, page 155. Table there shows that the Type 3 stage of intestinal response, flat destructive does occur with milk, egg, soy and chicken or fish allergies. It differs from the celiac response in that only 1 or 3 of the 5 stages of lesion connected with celiac disease occur with an allergy.
    Whats unclear from this reference and from Medline searches Ive made is whether food allergies in adults cause villi damage. All the references I found were for children. Villi destruction does occur in children with milk allergy, but this like other pediatric allergies, apparently is usually outgrown.

    Dr. Vikki Petersen D.C, C.C.N
    This article originally appeared in the Autumn 2010 edition of Celiac.com's Journal of Gluten-Sensitivity.
    Celiac.com 12/06/2010 - The hazards to health created by celiac disease and gluten sensitivity are well understood.  From nutritional deficiencies to osteoporosis, from depression to autoimmune disease, and from psoriasis to thyroid disease, there are few areas of the human body that gluten doesn’t touch in a negative way. 
    There is so much emphasis on our inadequate abilities to diagnose gluten intolerance, that when we do finally make the diagnosis I believe we are guilty of another problem—lack of adequate education to those affected patients.
    Just last month a research study was released by the American Journal of Gastroenterology, 2010 Jun; 105(6):1412-20.  The article was entitled “Mucosal recovery and mortality in adults with celiac disease after treatment with a gluten-free diet”.  The research team hailed from the Division of Gastroenterology and Hepatology at Mayo Clinic College of Medicine.
    They stated that while a positive clinical response is typically observed in most adults with celiac disease after treatment with a gluten-free diet, the rate of small intestine recovery is less certain.  Their aims were to estimate the rate of intestinal recovery after a gluten free diet in a cohort [a group of people with statistical similarities] of adults with celiac disease, and to assess the clinical implications of persistent intestinal damage after a gluten-free diet. 
    Of 381 adults with biopsy-proven celiac disease, 241 had both a diagnostic and follow-up biopsy.  Among these 241, the confirmed mucosal recovery at 2 years following diagnosis was 34% and at 5 years was 66%.  Most patients (82%) had some positive clinical response to the gluten-free diet, but it did not prove a reliable marker of intestinal recovery. 
     Poor compliance to the gluten-free diet, severe celiac disease as defined by diarrhea and weight loss, and total villous atrophy at diagnosis were strongly associated with persistent intestinal damage. 
    There was a trend toward an association between mucosal recovery and a reduced rate of all-causes of death, adjusted for gender and age. 
    The conclusions were that intestinal recovery was absent in a substantial portion of adults with celiac disease despite treatment with a gluten-free diet, and that there was an association between confirmed intestinal recovery (vs. persistent damage) and reduced mortality independent of age and gender. 
    So what can we learn from this?

    Eating gluten-free when you are sensitive will cause you to feel better.  Going on a gluten-free diet is not enough to ensure that your intestines will heal. Failing to heal your intestines puts you at increased risk for disease and death. Successfully healing your intestines reduces your incidence of death from disease.
    While you likely knew the first point, 2, 3, and 4 are perhaps less well known.  Where I see that we are failing the gluten intolerant population is in the narrow focus of eliminating gluten as the only needed treatment.  What the above research proves is that, unfortunately, for over 30% of those diagnosed simply eliminating gluten is insufficient to ensure intestinal healing. 
    If patients were educated that healing their intestine would make the difference between contracting disease or not and extending their life expectancy or not, I think they’d be more interested in ensuring that it occurs.
    I am not a researcher but my clinic sees hundreds of patients who align with the results of this study completely.  Patients come to see us who have been told that they shouldn’t consume gluten and for the most part they follow that recommendation.  They know that they feel better when they are gluten-free so that is an impetus to not cheat.  When they do cheat they know that they’ll “pay” for it but they still do so fairly regularly. 
    Why do they cheat?  Because they believe that the diarrhea, headache, bloating, etc is temporary and that when it goes away they are “fine” again.  Their thought process is not unreasonable, it’s just wrong!
    If each patient was educated that cheating created intestinal destruction that in turn put them on a fast track towards disease and early death, I believe that cheating would take on a whole new perspective.
    Patients need this education and they need it often.  Our book “The Gluten Effect” was written with this intention—our patients actually requested it.   They asked for a written reminder of why they should maintain their gluten-free lifestyle.  Later I began taping Youtube videos because other patients preferred a reminder in a video form. 
    I’m trying to say this in a few different ways because it is terribly upsetting to meet patients, as I so often do, who have been diagnosed celiac or gluten sensitive and do not follow their diet solely due to ignorance.
    After almost 25 years of clinical experience I also know that some people “hear what they want to hear” and doctors with the best of intentions cannot get through to everyone.  But I strongly believe that we could be doing a much better job at enlightenment.
    Further, we also need to educate patients about the secondary effects associated with gluten.  When the immune system of the intestine is suppressed, as is the case in the presence of gluten pathology, inhospitable and pathogenic organisms can gain entry into the intestine and remain there.  These organisms may be in the form of bacteria, parasites, amoebas or worms and if they are not identified and eradicated, complete healing of the intestines is all but impossible. 
    The good bacteria that are housed in the gut, known as the microbiome or probiotics, make up much of the intestinal immune system.  In gluten intolerant patients this important population of organisms is often insufficient due to the onslaught from gluten and pathogenic organisms.  If the population of these probiotics is not restored to a healthy, robust balance, any attempt to achieve a healthy intestine will be unsuccessful.
    Lastly, it is an interesting catch-22 that in order to digest our food we need enzymes and enzymes are made from the nutrients we digest.  This circular pattern is dramatically interrupted in the gluten intolerant patient.  Celiacs in particular suffer from very poor absorption.  It shouldn’t then come as a surprise that augmenting with proper enzymes may be critical for “priming the pump” until proper digestion of nutrients is restored.
    Unfortunately I find that few, if any, of these points are made clear to patients who are gluten intolerant.  Most believe they are doing all they need to do simply by maintaining a mostly gluten-free diet.  Nothing could be further from the truth.
    To review we need to do the following:

    Maintain a “perfect” avoidance  of gluten Test for the presence of pathogenic organisms Test for any imbalance of the probiotic organisms Evaluate the need for enzymes Evaluate for the presence of any other food sensitivities, e.g.  dairy Educate the patient until they have a full understanding of the above Test to ensure that the intestine is healed

    Dr. Rodney Ford M.D.
    Celiac.com 04/26/2017 - "The universe is made of stories, not atoms" — Muriel Rukeyser
    Helen, a woman with severe lifelong eczema/dermatitis, wrote to me a few weeks ago, saying "I have taken your advice and been strictly gluten free for five months now. The eczema inflammation is 99% gone and my skin quality has significantly improved. I do still get a bit itchy around my neck area and elbow creases, more so at night when it is warm.
    I have noticed a significant improvement in my asthma also. I still use antihistamines perhaps once or twice a week for runny nose. Does this mean I will need to be gluten free for life? Which of your books would you say would be the most relevant for someone in my position? Thank you for your assistance, regards, Helen.
    I recommended eBook: "Dermatitis Eczema: Gluten Wheat – Solving the eczema puzzle." Available at: http://www.GlutenEczema.com
    This is an excerpt from the chapter: "Children better off gluten/wheat".
    To help you get a better idea of how gluten can trigger eczema, here are narratives of some children whose eczema got better when their gluten sensitivity was recognised and treated. Most had good remission of their eczema on a gluten-free diet. Their stories told by their parents.
    To give context to the blood test values, the normal reference ranges were:
    AGA: 0–15 tTG: 0–20 Celiac disease with bad eczema
    Lily at five years old was diagnosed by me with celiac disease. Symptoms: eczema. Run down, pot tummy and slow growth. Tests: All of her blood tests were positive for celiac disease (tTG 120) and she had an abnormal intestinal biopsy which confirmed the bowel damage of celiac disease. AGA very high (115).
    Her mum said:

    "Lily has now been gluten-free for the last year. She came to see Dr. Ford to investigate her allergies. She had a blocked nose and troublesome eczema. She also had quite a pot tummy and Dr Ford said that her growth was slow (she was thin and short). Dr Ford said that she needed blood tests for gluten and celiac disease: these were both positive. So she had an endoscopy, which was abnormal, showing the villus blunting of celiac disease. Therefore, she had to go on a gluten-free diet."
    "Since she has been gluten-free over the last year, she has gotten better and better. She no longer has lots of infections, she has more energy, and interestingly, her allergies have nearly gone away. Her skin used to give her a lot of trouble – she had a lot of bad eczema. Her eczema now is very much better and she only has small amounts left in her creases. And if she has any gluten errors it flares up."
    Recovering from gluten-eczema
    Isabella, at two years old, was recovering from her eczema. I asked her mother what happens if Isabella has any gluten. Her mum said:

    "Isabella had eczema all over her body. She was on strong steroid creams. She had the positive blood tests for gluten antibodies (AGA of 66), so it was suggested I take her off the gluten. I did this."
    "I took her off gluten and it has cleared her eczema up. Now, when she does eat anything with gluten in it she gets little patches of eczema on her legs. I just can't believe it!"
    Blood all over her sheets
    Emily was three years old. She had a high anti-gliadin antibodies (AGA 48) but she did not have celiac disease (normal tTG). Her mother told me:

    "Initially her skin was really sore, dry and scratchy. She would have blood all over her sheets in the morning from scratching while she was asleep. Her poos were really sloppy and nasty."
    "But after taking gluten out of her diet her skin cleared up within days, and the itchiness of her skin settled. She was just so much happier."
    Dry skin and worsening eczema
    Breanna and Alyssa, twins aged 3 years. Symptoms: eczema and poor sleeping. Both had high AGA levels (60 & 68) and normal tTG levels (5 & 3). They did not warrant an endoscopy.
    Mum writes:

    "My twins were born at 26 weeks. During our stay in NICU they developed very dry skin, at times you felt like you wanted to peel the dry skin off. The word eczema was mentioned on more than one occasion. There is a history of eczema and asthma in our family, so at the time I tried to deny all knowledge of that word."
    Dry skin and worsening eczema
    "Eleven weeks later we took our twins home. Their skin was still dry and we were given a moisturiser to use as required. As time went on their skin didn't improve and eventually at around the age of one year they showed real signs of eczema. We started to use steroid creams: 1% Hydrocortisone to start with, then onto a much stronger steroid cream. Soon, this stronger cream was used all the time to control their eczema as the other creams were of no real help."
    "At around 2 years old, while at a playgroup session one of the mothers was talking about her daughter's eczema and how she had gone to see Dr Ford and now there were no signs of it there today. Of course my ears pricked up. I was interested to hear how her diet affected her skin and the word gluten was mentioned."
    At the time it didn't mean a lot to me. Therefore, I made an appointment and I was excited to think that we might be able to change the girls' diet and their skin condition may improve.
    They had positive gluten blood tests
    "The day arrived and we had our first visit. He talked to us about this gluten thing and that if we could avoid it then their skin might make a dramatic improvement. I was keen to try anything. Firstly, they had to have some skin prick allergy tests – it showed a reaction to wheat among a few other things. Next, the girls had a blood test confirming that they definitely had an allergy to gluten, and their iron levels were also very low. The final step was to set about changing their diet. I can honestly say that this was daunting to start with but once we got our heads around the issues, it became second nature."
    Sleeping at last!
    "One of the biggest changes we have noticed is that they are now sleeping so much better. I was constantly up and down to them all night and was getting so worn out now we can almost guarantee a full nights sleep, Yahoo!! The other major issue was the steroid cream use: we haven't used the strong steroid cream for 12 months. So for me, going gluten-free was a huge step in the right direction."
    Gluten-free gets easier
    "There are heaps of products that we can use and the staff in shops were very helpful with information and getting stock in. I have since brought a number of cook books all with sections on gluten-free that have been helpful. When baking or cooking, I now just do it the gluten-free way and everyone in our family eats it with no complaints. We have all adjusted accordingly."
    "Our thanks goes out to Dr Ford for all his help. I also send good luck to all of you who are about to embark on a gluten-free diet – the rewards will be well worth the sacrifice."
    Sharon
    Losing her hair – alopecia
    Ella, age 6 years. Symptoms: eczema, alopecia, moody, abdominal pain, multiple food allergy. AGA high (49), tTG normal (3), EMA negative, Small bowel biopsy, normal.
    Mum writes:

    "Ella is now age 6 years. At age 3 years Ella started to lose her hair. After a year of scalp treatment, by the time she turned 5 years old, all but one small patch had regrown."
    Losing her hair
    "About 4 months later a small patch of alopecia reappeared and her hair loss rapidly progressed from there. At this time her eczema, always present in a mild form, worsened and became almost impossible to control. Many forms of treatment were tried and all failed. Within the year Ella had lost all her hair and was constantly itching. Over this time Ella also complained of tummy pains and weight loss."
    Diagnosed as gluten-sensitive
    "As her father has celiac disease, we decided to get Ella checked. Her blood test was positive but the biopsy was negative for celiac disease. In discussion with the GP and some unanswered questions we eventually had an appointment with Dr Ford. After this appointment, Ella started on a strict gluten-free diet and has remained on it for the past 4 months."
    Amazing results
    "The results are amazing. Ella has stopped most of her scratching and she is far more comfortable. Ella's mood has changed and she is now a very happy little girl. Best news of all is that she has started to have a small amount of hair growth."
    "At no time, despite the variety of people seen and the fact that they were aware of family history, did anyone suggest getting Ella tested for celiac disease. It was purely parents at the end of their tether, pushing."
    Sue
    She was getting worse eczema
    Tessa, age 2 years. Symptoms: eczema, poor growth, multiple food allergy. Tests: AGA high (51), tTG normal (7), Biopsy not done.
    Mum writes:

    "Tessa was our first-born baby. She weighed a healthy 8lb and was breastfed until 6 months. I introduced solids at 5 months. Having given a bottle of expressed milk every night since she was 10 weeks, I found that she preferred this and weaned herself."
    Eczema at the time of solids
    "Tessa had eczema from the time she commenced solids, but it was manageable with mild steroid ointments. However, at six months her eczema became more distressing for her. She had her first course of antibiotics at this age."
    "We felt that we were using more and more topical steroids, oral antibiotics, and even a course of oral prednisone. None of these treatments felt satisfactory to her family. We needed a solution to prevent the problem. Not only was her skin getting worse but also she was quietly losing weight. A friend suggested visiting Dr Rodney Ford."
    Allergies to egg, dairy and peanuts
    "Our first visit involved an extensive medical history and allergy testing. Tessa was found to be allergic to egg, dairy, peanut, grass, and cats. We excluded the food allergens from her diet. But, over the next four months Tessa had a dramatic weight loss, going from the 50 percentile to falling off the Child Health nurse growth graph. She required more steroids, and antibiotics."
    Waking screaming
    "My angel baby, who had slept through the night from age 6 weeks, was now 16 months and woke every night screaming inconsolably. We were getting desperate, putting in an awful lot of work by eliminating dairy and egg with no rewards. With a new baby due to be born Tessa's exhausted parents needed answers. Back to Dr Ford we went. He suggested running some blood tests to check her gluten markers. It came back that her Anti-Gliadin Antibody was 51, suggesting that she was gluten-sensitive."
    Gluten-free as well!
    "We trailed a gluten-free, egg-free, and dairy-free diet. This was a totally overwhelming prospect for our family, as at that time we were introducing a two-week-old baby to the world! Luckily, Tessa's father, who too is an adult sufferer of eczema, was able to take all this on board and went off grocery shopping, bringing back lots of acceptable goodies. It was also at this time that I learnt of the real benefits of living in a small town."
    We had a gluten-free buddy
    "We were very fortunate that another mother of gluten-sensitive children took me by the hand grocery shopping, showing me how easy it is! Also, the church where we regularly attend made a whole week's worth of meals for the freezer which all fitted the requirements for Tessa's diet. All this really just through word of mouth!"
    At last she is better
    "We are so excited to see such an improvement. She has just been allergy tested again and we are able to introduce egg and dairy again. I had been giving small amounts of dairy already, hoping that she would have grown out of this. At one point all she would eat was cheese, so to get some calories into her that is what we fed her. Having Tessa on a gluten-free diet requires us to be organized and creative. It is especially difficult when you spontaneously decide to go out for the day: there are no guarantees that we will find appropriate food for Tessa, so usually we pack a lunch."
    Gluten-free is expensive
    "The food that is gluten-free is also usually twice the price of other foods. We have had to learn to bake, which is something I still struggle with. We have had some major disasters, especially baking cakes. Whenever it seems too difficult, and we are out of ideas, it is not too hard to find a reason to keep trying."
    Improved gluten free
    "Our little girl has significantly improved since becoming gluten-free. She has not required antibiotics or oral steroids for eczema since commencing the diet. We can now apply the topical steroid ointments as prescribed "sparingly". She no longer gets up in the morning, her pyjamas and sheets covered in blood, and forehead weeping. She can play in sandpits without fear that the sand will get into her sores, and once again they will be infected."
    "We are so lucky that something so simple as changing Tessa's diet has had such a dramatic affect on her life."
    Mum
    Think about the gluten-eczema link
    As you have been told by these families, gluten has been found to be an important trigger for eczema in these children.
    My research findings show that the majority of people over three years of age, who have ongoing and troublesome eczema, have gluten-sensitivity. When gluten is removed from their diets, they get better.
    Advice about blood testing for gluten and for information on a gluten-free diet can be found on our webpage: http://www.DrRodneyFord.com and in the previous chapters.
    This is an excerpt from Dr Rodney Ford's eBook, "Dermatitis Eczema: Gluten Wheat – Solving the eczema puzzle" Available at: http://www.GlutenEczema.com
    Written in the spirit of cooperation and knowledge sharing.

    Dr. Rodney Ford M.D.
    Celiac.com 07/27/2017 - It was five years ago when I launched the concept of "gluten is bad for us all!"
    Yes, you read that right - bad for you, bad for me, and bad for everyone else! This implies that the whole world should avoid gluten.
    This is a bold and an unrealistic statement to make. However, I thought that there was enough evidence about the harm of gluten for us to demand massive changes to everyone's diet, our farming practices and food manufacturing industry. Eventually, this could substantially improve the health of our Nations. However the practicalities of such a change would be very difficult overcome. Especially with the economic forces of Big-Pharma, Big-Agriculture and Big-Government.
    I was not alone in thinking this. Many other medical/health professionals had also reached this conclusion with the growing research evidence of gluten-related diseases. Five years ago the top 15 celiac-doctors acknowledged that gluten-related-illness was a common problem that needed much better diagnostic tests. In their landmark paper "Spectrum of gluten-related disorders: consensus on new nomenclature and classification." http://www.biomedcentral.com/1741-7015/10/13, they concluded: "all individuals, even those with a low degree of risk, are susceptible to some form of gluten reaction during their life span."
    This publication was later expanded into a book. The description of this book is: "A Clinical Guide to Gluten-Related Disorders provides primary health care providers the succinct material they need to immediately evaluate and support their patients. Gluten-related disorders have a wide presentation, and this text covers the recognition, evaluation, and multi-disciplinary approach to the management of disease. Readers will benefit from the general overview of gluten intolerance and from the common sense approach to developing treatment and dietary plans. Clinical vignettes offer clinicians real-life scenarios to help put the disease and its treatment in context for their patients."
    I predicted, that in another generation, gluten will be rejected by most reputable food processing companies. This will be a difficult concept for many people to accept because wheat products are currently the very foundation of our diet. After 10,000 years of eating gluten grains it comes as a huge shock that our staple food has been demonstrated as harmful.
    Over the last five years I continue to see children and families made very unwell by eating gluten grains. It is also likely that that gluten may not be the sole culprit, as there are other wheat proteins that are toxic to humans. However, a gluten-free diet will eliminate these other wheat proteins.
    I have just seen Caleb who is 10 years old and was referred to me three months ago because of generalised intermittent abdominal pains. These pains come and go, but trouble him on most days of the week. These pains sometimes Bring him to tears, and on occasions he has presented to the emergency department at the hospital with severe abdominal pain. The usual investigations did not show up any specific abnormality, and his scans and x-rays for all within normal limits, other than showing that he had some constipation.
    He had also been suffering from sore throats and gastric reflux has been implicated, for which he was prescribed Omeprazole.
    In addition, he was not putting on much weight.
    My concluding remarks about him were "It is possible he is gluten intolerant. This could explain all of his symptoms (abdominal pain, constipation, gastric reflux, and tiredness). His mother has irritable bowel and has previously benefited from a gluten-free diet. I recommend that Caleb go on a three month trial of a gluten-free diet. His parents will let me know of his progress in three months time."
    Well, I've just seen him again following his three-month gluten-free trial. Mum said "what a difference! He now has regular bowel motions without the need for Macrogol, he no longer has abdominal pain and his reflux has disappeared and he is no longer needing Omeprazole. In addition he is growing again. With gluten infringements he gets a sore tummy, sore throat with some reflux and constipation again."
    It has taken Caleb a while to get into the swing of things. He still will eat gluten foods if he has the opportunity! He has to pay the consequences with his symptoms. He is also growing again. I am thrilled with his progress. He needs to stay gluten-free for the long haul. He needs to be as close to gluten zero as possible. He is lucky that both of his parents have joined him on his gluten-free diet. His mother is a lot better and has lost substantial weight, his dad also feels a lot more healthy on a gluten-free diet.
    Caleb is just one of millions of children who are currently suffering from guilty related diseases, but un-diagnosed and un-recognized.
    Yes, it was five years ago when I launched the concept of "gluten is bad for us all!" I have not change my opinion. Indeed, I am more confident about what I have written about the harm that gluten has caused throughout the world. I looked the 8 following questions. I wonder what your opinion might be:
    1. Why pick on Gluten?
    10 decades of Celiac; 10 years of Gluten Syndrome; 10 months of ZERO gluten.
    2. Why is gluten so bad for us all?
    Cannot digest it; gut leaky; toxic proteins.
    3. Why are there so many sick people?
    "Nobody knows what's wrong with me." Old technology for modern disease.
    4. How much illness can be attributed to gluten?
    The catalogue of gluten-illness. Health burden of gluten.
    5. Can gluten really damaged brains and nerves and minds?
    Brain symptoms, nerve damage, mental disorders.
    6. What other illnesses might be linked to gluten?
    Auto-immune diseases.
    7. Should we really change what we eat?
    Diet - not Drugs. The alternative grains. Health-giving foods.
    8. How can we feed 7 billion people
    Is bad food better than no food?
    Dr Ford's book is available as an e-book:
    Gluten: ZERO Global (http://www.glutenZEROglobal.com)
    Gluten is bad for us all – the evidence for a gluten free planet.
    Warning: go gluten free now before it is too late.
    Written in the spirit of cooperation and knowledge sharing.

  • Recent Articles

    Jefferson Adams
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    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
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    Ingredients:
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    Cover and refrigerate for at least 1 hour. 
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    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023