Jump to content

Important Information

This site places cookies on your device (Cookie settings). Continued use is acceptance of our Terms of Use, and Privacy Policy.

  • Sign Up
  • Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Member Statistics

    84,982
    Total Members
    4,125
    Most Online
    NicoleD9686
    Newest Member
    NicoleD9686
    Joined
  • 0

    The Celiac Disease Confusion


    Rivkah Roth D.O., D.N.M.
    The Celiac Disease Confusion
    Image Caption: Photo: CC--Joelk75

    Celiac.com 08/28/2012 - What's In A Name and When Does Celiac Predisposition Become A Disease?

    No doubt that global awareness about celiac disease and its possible involvement in a myriad of other (mostly autoimmune response related) conditions is growing. Growing, unfortunately, is confusion about terminologies and medical implications.


    Photo: CC--Joelk75The “Common” Understanding

    "Celiac disease" has become a generic blanket term not unlike how "Kleenex" today signifies no more than a box of tissue paper of any brand. So, in the public mind, "celiac disease" today stands for everything connected to a reaction to gluten.[1]

    Such an approach is highly imprecise and misses

    1. the need for distinction between non-celiac and/or celiac gluten sensitivity and
    2. the fact that a predisposition does not necessarily constitute disease.


    The 2012 Internationally Accepted Definition

    In an attempt to bring some clarity to the medical community, the world’s leading celiac minds earlier in 2012 met for an international convention in Oslo, Norway.[2]  During that convention, and after considering many of the most commonly used terms, they recognized

    …the presence of genetic, predisposing patterns…

    and called for a

    …distinction between "celiac disease" versus "gluten-related disorders"…
    [3]

    Let us be clear: This terminology refers solely to the underlying toxic effect of gluten rather than the possibly resulting disorders that may be based on other, additional triggers as well.


    Genotyping Tells Non-Celiac from Celiac Gluten Sensitivity

    Along with ever mounting genotype-related research, detailed HLA-DQ2/DQ8 human leukocyte antigen genotyping[4] today allows us to distinguish between predispositions to non-celiac and/or celiac gluten sensitivity (NCCGS) predisposition.

    Increasingly, research results link gluten issues to a considerable list of specific conditions and, therefore, allow for and promote a “natural” approach (i.e. gluten free diet and lifestyle) to resolve a complex panel of non-obvious signs and symptoms.

    Accordingly, "Celiac" is not (yet) a disease but a metabolic predisposition, i.e. the body’s inability to digest certain grain proteins, prolamines, etc.—much like a gasoline fueled car will sputter and eventually corrode on diesel fuel.


    Predisposition vs. Disease

    A genetic predisposition to celiac only becomes a disease (e.g. celiac disease or one of the non-celiac gluten sensitivity enabled conditions)[5] if the body’s inability to digest gluten and certain other grain proteins is ignored at the expense of the immune system.[6]

    In other words, an individual genetic predisposition to celiac only develops into full blown disease if that particular individual does not adhere to a gluten-free diet and lifestyle.

    An European Union et al commissioned research paper concluded:

    The environment clearly plays a crucial role in the development of celiac disease:
    No gluten, no disease!….

    …Because gluten is present in relatively large amounts in a variety of common food products, the daily gluten intake in a Western diet is high. In combination, we see that every HLA-DQ2– and/or -DQ8–positive individual is exposed to a large repertoire of immunogenic and abundant gluten peptides, and this may be an important factor determining disease development. There is, at present, no evidence linking additional environmental factors to celiac disease.
    [7]


    Big Business: Catering to a Gluten Free Diet

    The facts are everywhere and are illustrated further by these research abstract numbers posted on PubMed:

    • 18,565 on “celiac disease” (607 alone in 2012 – Jan. to Jly.)
    • 9,689 on “gluten” (385 in 2012 – Jan. to Jly.)
    • 3,447 on “glutenfree” (192 in 2012 – Jan. to Jly.)

    In addition, 38,878 abstracts deal with wheat research, whereof 1,862 in 2011, and 1,384 in 2012 to date (Jan. to Jly.).

    Clearly: $6.1bn spent 2011 on gluten-free foods in the USA—and a 30% growth from 2006 to 2010 in Canada to $2.64bn—indicate “Big Business” complete with the risk of missed, omitted, and mis-information for the goal of promoting greater consumption of gluten-free processed foods.

     

    The Challenge

    Our present naming confusion, therefore, may end up fuelling potential manipulation and mismanagement of the patient and consumer from the part of medical, pharmaceutical, supplement, and food industries.

    Even the above mentioned latest attempt at coordinating nomenclature and distinction between non-celiac and/or celiac gluten sensitivity brings with it several major flaws and challenges:

    • It may take years for new naming conventions to become accepted throughout the international medical and dietary community.
    • Recognizing a term such as "gluten-related disorders" or “non-celiac gluten sensitivity” calls for a total revamping of our medical and diagnostic systems in order for the large number (so far about 160) of autoimmune and other disorders to be recognized as gluten-related.  

    In addition, future questions will arise as research identifies and confirms more genetic links:

    • Already, clinic practice shows that some of the "celiac" patients, previously diagnosed by positive intestinal biopsy[8] and serological findings now, on genotyping[9], turn out to carry "non-celiac" and not “celiac” gluten sensitivity alleles.

    Where does this leave such individuals on the traditionally used "celiac disease" versus "gluten-related disorder" specter?

    Clearly, despite good intention for a more precise naming distinction, it appears that additional work is needed in order to entrench new medical terminology and disease pictures.

     

    Conclusion

    Until then, whenever one of my patients receives a positive HLA gene test, I will adhere for clarity’s sake to the terms of “non-celiac” and/or “celiac gluten sensitivity” (NCCGS).

    This terminology refers solely to the underlying toxic effect of gluten and prevents a wrong implication of predisposition=disease diagnosis. Instead, “non-celiac and/or celiac gluten sensitivity” will simply point to the inherited underlying predisposition to specific additional triggers and complications if exposed to gluten.

    Most importantly, I will make sure to instill in my patients that disease is not the inevitable outcome of their genetic predisposition, and that a 100% gluten-free diet and lifestyle allows for avoidance, control, and perhaps even reversal of a complex web of interrelated autoimmune-based conditions and disorders, both for non-celiac and for celiac gluten sensitivity related disorders.



    [1] http://www.ncbi.nlm.nih.gov/pubmed/22351716  Ann Intern Med. 2012 Feb 21;156(4):309-11. Nonceliac gluten sensitivity: sense or sensibility?

    [2] http://www.ncbi.nlm.nih.gov/pubmed/22345659  Gut. 2012 Feb 16. [Epub ahead of print] The Oslo definitions for coeliac disease and related terms.

    [3] http://www.ncbi.nlm.nih.gov/pubmed/19940509  Int Arch Allergy Immunol. 2010;152(1):75-80. Epub 2009 Nov 24. Differential mucosal IL-17 expression in two gliadin-induced disorders: gluten sensitivity and the autoimmune enteropathy celiac disease.

    [4] http://www.ncbi.nlm.nih.gov/pubmed/22123644  Curr Opin Gastroenterol. 2012 Mar;28(2):104-12.  Advances in coeliac disease.

    [5] See future articles posted in these pages...  

    [6] http://www.ncbi.nlm.nih.gov/pubmed/21787225  Int Rev Immunol. 2011 Aug;30(4):197-206.  Important lessons derived from animal models of celiac disease.

    [7] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC209453/?tool=pmcentrez  J Clin Invest. 2001 November 1; 108(9): 1261–1266. doi:  10.1172/JCI14344  PMCID: PMC209453  Interplay between genetics and the environment in the development of celiac disease: perspectives for a healthy life.

    [8] http://www.ncbi.nlm.nih.gov/pubmed/22742547  Arch Pathol Lab Med. 2012 Jul;136(7):735-45.  An update on celiac disease histopathology and the road ahead.

    [9] http://www.ncbi.nlm.nih.gov/pubmed/21593645  J Pediatr Gastroenterol Nutr. 2011 Jun;52(6):729-33.  HLA-DQ genotyping combined with serological markers for the diagnosis of celiac disease: is intestinal biopsy still mandatory?


    0


    User Feedback

    Recommended Comments

    Guest laura puckett

    Posted

    I am glad to see that a "non celiac sensitive" possible diagnosis is considered. I was diagnosed with this in Italy but not accepted in U.S.A. Incidentally, my symptoms have almost disappeared and I gained 30# ( I was only 70# and kept losing). Also, many of my family were tested: my daughter, brother and first cousin have been diagnosed with celiac disease!

    Share this comment


    Link to comment
    Share on other sites
    Guest Denise

    Posted

    The focus must be on gluten syndrome! Please investigate the brilliant and progressive work of Dr. Rodney Ford from New Zealand. After my 13 year old son tested negatively for celiac disease, his pediatrician actually told him to continue eating gluten until his villa were totally destroyed and therefore, he'd pass the celiac disease test. We pursued gene testing and found he has the gene for celiac disease... so thank god my son had the common sense to never eat gluten again. ALL his symptoms completely disappeared. Proactive prevention is the key to optimal health, safety and well being!

    Share this comment


    Link to comment
    Share on other sites
    Guest Shirley Braden

    Posted

    Thanks for the discussion. I, for one, would like the see the definition of gluten issues expanded. Maybe the term will be another one like gluten syndrome, and there will be levels and one will be celiac disease. I think one vital piece of information is missing from your article though. 2 -3% of "gold standard," biopsy-proven celiacs do not have celiac genes. I personally know several individuals diagnosed with celiac disease who do no have the genes (or ones identified to date anyway). With experts saying that there are at least 3 million with celiac in the U.S. (stat from University of Chicago Celiac Disease Center), 2-3% is still a fairly large number. And if you are one of those folks who was told you did not have celiac disease because of lack of genes and no further testing was done, this fact may be critical to a diagnosis and your health.

    Share this comment


    Link to comment
    Share on other sites
    Guest Dan Marvin

    Posted

    I suffer from both celiac disease and Crohn's disease and after reading the article, it almost seemd to imply that a 100% gluten-free diet might result in my Crohn's going away (160 auto immune related to gluten sensitivity), or at least into remission. If that is true, I would be very excited!

    Share this comment


    Link to comment
    Share on other sites

    To Dan - if you have Crohn's then you may want to look into the Specific Carbohydrate Diet. This was developed specifically for those with Crohn's. It is gluten-free, but it has further restrictions. Other similar diets are GAPS and the Paleo diet. All these diets focus on real food and avoiding inflammatory foods. Sometimes it takes more than just removing gluten to get to optimal health.

    Share this comment


    Link to comment
    Share on other sites
    Guest Priscilla

    Posted

    The focus must be on gluten syndrome! Please investigate the brilliant and progressive work of Dr. Rodney Ford from New Zealand. After my 13 year old son tested negatively for celiac disease, his pediatrician actually told him to continue eating gluten until his villa were totally destroyed and therefore, he'd pass the celiac disease test. We pursued gene testing and found he has the gene for celiac disease... so thank god my son had the common sense to never eat gluten again. ALL his symptoms completely disappeared. Proactive prevention is the key to optimal health, safety and well being!

    What were his symptoms?

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • About Me

    Semi-retired natural health professional, lecturer and published author with doctorates in osteopathy, natural medicine, acupuncture and traditional Chinese medicine. Practiced and taught in Canada, Switzerland and Israel, and specializes in non-celiac and celiac gluten sensitivity, early diabetes risk recognition and avoidance, fibromyalgia and other autoimmune conditions. My site is: www.rivkahroth.com

  • Related Articles

    Dr. Scot Lewey
    This article appeared in the Summer 2006 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 08/31/2006 - All of us have patterns of proteins on the surface of our white blood cells. These proteins are known as human leukocyte antigens (HLA), one of which is DQ. Celiac disease and non-celiac gluten sensitivity (NCGS), and several autoimmune conditions occur more frequently with certain HLA DQ types. DQ gene testing is performed by analyzing cells from a blood sample or from a Q-tip swab of the mouth. HLA types have a naming system that can be confusing even to scientists and physicians but here is my explanation of the testing, the results, and what they may mean to you and your family.
    Each of us has two copies of HLA DQ. Because there are 9 serotypes of DQ we are all DQx/DQx where x is a number between 1 & 9. For example, I am DQ2/DQ7. I received the DQ2 from one of my parents and the DQ7 from the other. Because we get one DQ type from each of our parents and give one to each of our children it is easy to to see how the DQ genes pass through a family. This is important because two DQ types, DQ2 and DQ8, are estimated to be present in over 98% of all people who have celiac disease, the most severe form of gluten sensitivity.
    Rarely, true celiac disease or dermatitis herpetiformis, the skin disease equivalent of celiac, have been reported to occur in people who do not have DQ2 and/or DQ8. However, according to unpublished data from Dr. Ken Fine of Enterolab, the other six types, except DQ4, are associated with risk for elevated stool antibodies to gliadin, the toxic fraction of gluten, and/or tissue transglutaminase (tTG) an enzyme. Both of these antibodies are usually elevated in the blood of individuals with celiac disease though they may be normal in the blood of individuals who are gluten sensitive and have a normal small intestine biopsy but respond favorably to a gluten-free diet.
    Fine has publicly reported that elevated stool antibodies to gliadin and/or tTG have been detected in all of the untreated celiacs tested in his lab and 60% of non-celiacs who have symptoms consistent with gluten sensitivity but in none of the controls tested including cow manure. Follow up surveys of those individuals with elevated stool antibodies who initiated a gluten-free diet compared with those with elevated antibodies who did not reportedly showed significantly improved quality of life and improved symptoms in the gluten-free group.
    He also reported DQ2 and DQ8 positive individuals have had, as a rule, the highest elevations of stool gliadin antibody followed by those who are DQ7 positive. Only those who are doubly positive for DQ4 have not been found to have significantly elevated antibodies to indicated gluten sensitivity. This is consistent with the differences in prevalence rates of celiac disease seen in various parts of the world since DQ4 is not generally found in Caucasians of Northern European ancestry where celiac incidence is highest but in those from Asia or Southern Africa where there is a very low incidence of celiac disease and gluten intolerance.
    DQ2 & DQ8, the two major types present in 90-99% of people who have celiac disease, are present in approximately 35-45% of people in the U.S., especially those of Caucasian race of Northern European ancestry, with highest risk of celiac disease but the prevalence in U.S. of celiac disease is 1%. Though a prevalence of 1 in 100 is very common and much higher than had been believed for years, only a fraction of the genetically at risk are confirmed to have celiac disease by abnormal blood tests and small intestine biopsies. However, the number of people who report a positive response to gluten-free diet is much higher.
    The stool antibody tests results would support this and the concept of a spectrum of gluten sensitivity that is much broader and in need of better diagnostic definitions. I am an example of someone who is DQ2/DQ7 who has normal blood tests for celiac disease but abnormal stool antibody tests and symptoms that responded to gluten-free diet. The strict criteria for diagnosing celiac disease, which is abnormal blood tests and a characteristic small intestine biopsy showing classic damage from gluten, is much narrower than what is being seen clinically.
    It is becoming obvious to many of us who have personal and professional medical experience with gluten intolerance and celiac disease that the problem of gluten sensitivity is much greater and extends beyond the high risk celiac genes DQ2 and DQ8. Traditionally it is reported and believed by many that if you are DQ2 and DQ8 negative you are unlikely to have celiac disease or ever develop it, though this cannot be said with 100% certainty especially since there are documented cases of celiac disease and the skin equivalent of celiac disease, known as dermatitis herpetiformis (DH) in individuals who are DQ2 and DQ8 negative.
    Therefore, knowing your DQ specific serotype pattern may be helpful for several reasons. For example, if you have more than one copy of DQ2 or DQ8, you carry two of the major genes. For example, if you are DQ2/DQ2, DQ2/DQ8, or DQ8/DQ8, a term Scott Adams of www.celiac.com has dubbed a "super celiac" you may be at much higher risk for celiac disease and have more severe gluten sensitivity. Certainly if you are DQ2 and/or DQ8 positive you are at increased risk for celiac disease. After a single copy of DQ2 or DQ8, it appears that DQ7/DQ7 might be next highest risk. Dr. Fine has also noted some other associations of the DQ patterns with microscopic or collagenous colitis, neurologic manifestations of gluten sensitivity and dermatitis herpetiformis, which has been one of the gluten sensitive conditions noted to be, at times, occurring in DQ2, DQ8 negative individuals.
    Why some people get celiac Disease or become gluten sensitive is not well understood but certain factors are believed to include onset of puberty, pregnancy, stress, trauma or injury, surgery, viral or bacterial infections including those of the gut, medication induced gut injury or toxicity e.g. non-steroidal anti-inflammatory medications such as aspirin, ibuprofen, etc., immune suppression or autoimmune diseases especially since several of those factors are associated with onset or unmasking of gluten sensitivity in someone who is at risk or not manifesting any recognizable symptoms. There is also well known group of individuals who are termed "latent" celiacs. They are at high risk because they have close relatives who have celiac disease with whom they share one or more of the celiac genes DQ2 and/or DQ8 though they usually have few or no symptoms but sometimes have abnormal blood tests and/or biopsies indicating possible or definite celiac disease. Others have negative blood tests and normal biopsies but symptoms that respond to a gluten-free diet.
    The severity of the sensitivity to gluten appears to be related to the DQ type, family history (highest risk is in the non affected identical twin of a celiac), pre-existing intestinal injury, degree of exposure to gluten (how frequent and large a gluten load an individual is exposed to), and immune status. Once initiated, gluten sensitivity tends to be life long. True celiac disease requires life-long complete gluten avoidance to reduce the increased risk of serious complications of undiagnosed and untreated celiac such as severe malabsorption, cancers, especially of the GI tract and lymphoma, other autoimmune diseases and premature death due to these complications.
    Again, DQ testing can be done with cells from blood or by a swab of the inside of the mouth but not all labs test for or report the full DQ typing but only the presence or absence of DQ2 and DQ8. The lab that performs DQ testing is usually determined by an individual insurance company on the basis of contracts with specific commercial labs. However, if your insurance contracts with Quest Labs or the Laboratory at Bonfils (Denver, CO) full DQ can be done if ordered and authorized by the insurance company.
    For those willing to pay out of pocket, Bonfils performs full DQ testing for Enterolab (www.enterolab.com) on a sample obtained by a Q tip swab of the mouth. Since it is painless and non-invasive it is well tolerated especially by young children. Also because the testing can be ordered without a physician and the sample obtained in their home using a kit obtained from Enterolab it is convenient. The kit is returned by overnight delivery by to Enterolab who forwards the test onto Bonfils. The cost is $149 for the genetic testing alone and has to be paid for in advance by credit card or money order and is generally not reimbursed by insurance.
    Enterolab also provides the stool testing for gliadin and tissue transglutaminase antibodies to determine if gluten sensitivity is evident. The gliadin antibody alone is $99 or the full panel includes genetic typing, stool testing for gluten and cows milk protein antibodies, and a test for evidence of malabsorption is $349.
    Again, the advantages of full DQ testing is determining if someone has more than one copy of DQ2 or DQ8 or carry both and therefore have a higher risk for celiac disease or more severe gluten intolerance. If you are DQ2 or DQ8 negative then your risk of celiac disease is low, though not non-existent. If you are not DQ4/DQ4 then you do have risk for gluten sensitivity. If you determine all DQ types within enough family members you can piece together a very accurate history of the origin of celiac and gluten sensitivity within a family and make some very accurate predictions of risk to other family members.
    Though the lay public and many clinicians are finding the genetic tests helpful, many, including most physicians, do not understand the genetics of gluten sensitivity. We are awaiting Dr. Fines published data on the significance of stool antibody tests and their association to the other DQ types as his lab is the only lab offering the stool antibody tests in the U.S. Other celiac researchers in U.S. have failed to reproduce his assay but scattered reports in the literature are appearing including a recent article in the British Medical Journal indicating stool antibody testing is feasible, non-invasive, and using their protocol, highly specific but not sensitive for celiac disease in children. (Editors note: When present, these antibodies indicate celiac disease. However, they are not present in many cases of celiac disease.)
    In the meantime, many patients are faced with the uncertainty and added cost of full DQ testing and stool testing due to the failure of traditional blood tests, small bowel biopsies, and the presence or absence of DQ2 and DQ8 to diagnose or exclude gluten sensitivity. Physicians unfamiliar with this testing are increasingly presented with the results and confused or skeptical pending published reports. The medical community continues to lack a consensus regarding the definitions of non-celiac gluten sensitivity and what tests justify recommendations for gluten-free diet. It is clear that gluten sensitivity, by any criteria, is much more common than ever thought and a hidden epidemic exists.
    Dr. Scot Lewey is a physician who is specialty trained and board certified in the field of gastroenterology (diseases of the digestive system) who practices his specialty in Colorado. He is the physician advisor to the local celiac Sprue support group and is a published author and researcher who is developing a web based educational program for people suffering from food intolerances, www.thefooddoc.com
    Article Source: EzineArticles.com

    Dr. Ron Hoggan, Ed.D.
    This article appeared in the Autumn 2008 edition of Celiac.com's Scott-Free Newsletter.
    Celiac.com 01/14/2009 - Gluten sensitivity and celiac disease have long been seen as a gut disease. Unfortunately, this has resulted in a variety of erroneous medical perceptions, leading to limited and distorted perspectives on the impact of gluten on human health. After a battle of more than 50 years, celiac disease is now widely recognized both in and out of the medical profession, as common and treatable only with a gluten-free diet. (This is largely thanks to the proactive efforts of a few researchers and many support group members over the last two or three decades.) Recognition of the importance of a gluten-free diet in dermatitis herpetiformis has still not reached the same level. Some dermatologists continue to prescribe Dapsone, often deriding or even failing to apprise their patients of the gluten-free diet as an alternative therapy. This is especially important for reducing the risks of certain cancers, yet many stubbornly refuse to even suggest this therapeutic alternative. Neurologists, psychiatrists, and psychologists, despite compelling evidence of the nefarious impact of gluten in a wide range of neurological and psychiatric diseases, typically continue to ignore these data in favor of pharmacological interventions. (Unlike pharmaceutical manufacturers, gluten-free food suppliers do not wine and dine physicians.)   These chemical treatments involve a cacophony of attendant side effects and lengthy periods of experimentation to find the “correct” dosage that ultimately fails to fully relieve the patients’ symptoms or arrest the progression of the disease, while usually reducing patients to a more manageable, though limited state of consciousness.  From epilepsy to cerebellar ataxia, to peripheral neuropathy, to schizophrenia, to bi-polar disorder, to attention deficit disorders, to learning disabilities, to depressive illness, the treatment of choice is pharmacological rather than dietary.    
    Similarly, we have large, vocal, and politically active groups that loudly decry the consumption of a variety of foods, from meat, to fish, to various plant families, with little or no evidence to support such interdictions. Others tout one or more food additives or consumption practices as great and wonderful substances/practices that will cure all ailments and guarantee a long and productive life. These strange recommendations range from consumption of watermelon seed extract, to acai berries, a variety of fasting procedures prescribing one or two foods during the “fasting” period, food combining, juicing, egg white omelets, wheat grass, low fat diets and even colon cleanses that involve putting coffee up your rectum. Again, there is little solid evidence to support these practices yet they appear to develop quite a following.   
    I’m not suggesting that most mainstream medical professionals support these cleansing and dietary fads. However, much of the medical profession’s resistance to their own professional literature in which solid evidence indicts gluten as a cause of disease, while embracing questionable pharmaceutical solutions, is closely akin to the superstitious practices and outrageous claims that litter the Internet and the popular media. The evidence is clear and compelling. Neurological, psychiatric, and autoimmune diseases are often mitigated by gluten restriction. Yet we continue to hear about pharmacological interventions that offer less relief and little long-term hope of remission.    
    The widely published pediatric allergist and gastroenterologist, Rodney Ford, has argued a compelling case for his theory that gluten induced neurological damage is where the gluten syndrome and celiac disease begin, in his recent book titled “Full of It”. It is a theory that makes sense of otherwise puzzling individual variations in the course of gluten-induced disease.   It also explains the high frequency of gluten antibodies found by M. Hadjivassiliou and his group, in patients with neurological diseases of unknown origin (57%) while only a quarter of that percentage had celiac disease.
    Dohan and Grassberger, followed by Singh and Kay, clearly established a therapeutic role for a gluten-free, dairy-free diet in schizophrenia. Subsequent publication of several deeply flawed, poorly designed, and sloppily conducted studies have allowed for the common rationalization required for ignoring the solid, earlier findings mentioned above. This denial continues despite the recent publication, by Anthony De Santis and his group, of SPECT findings in a schizophrenic patient whose blood flow patterns in the brain, and behavior returned to “normal” following institution of a gluten-free diet.  
    Similar work with autistic subjects, conducted by Kalle Reichelt, Paul Shattock, and a host of others, has shown that gluten-free, dairy-free diets offer real promise for symptom reduction in this very challenging sub-population. Similarly, some amazing reversals of learning disabilities, through gluten-free diets, have been reported at Nunnykirk School in the United Kingdom. Further, about two thirds of untreated celiac children show signs and symptoms of attention deficit disorders.  These children have long been reported to normalize within one year of beginning a gluten free diet (see: http://members.shaw.ca/oldsite/My_Master%27s_thesis.htm).   
    Despite all of this contrary evidence, most allopathic practitioners continue to insist that gluten is a healthful food and they continue to recommend its daily consumption. They may be willing to concede gluten’s role in celiac disease and even in dermatitis herpetiformis, but they continue to ignore all of the other reported findings in association with the broad spectrum of diseases in which gluten sensitivity or celiac disease is grossly overrepresented. They continue to ignore or deny the potential value of a gluten free diet in the face of compelling evidence. Most of these same medical practitioners and investigators would be deeply offended by my suggestion that they are little different from those advocating coffee enemas or juicing. Yet their beliefs are not based on the evidence presented in their professional literature. In my dictionary, acting on irrational beliefs is called ‘superstition’. It is the superstitious resistance to solid evidence that is most frustrating when dealing with ignorance – whether the impetus is to push coffee enemas into your rectum or ingest yet another chemical compound from a prosperous pharmaceutical manufacturer despite evidence that a gluten-free diet might produce results that are more desirable to the patient.


  • Popular Contributors

×