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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    MEMORY/LEARNING: EATING TO LEARN: HOW GRAINS IMPACT ON OUR ABILITY TO FOCUS, COMPREHEND, REMEMBER, PREDICT, AND SURVIVE BY RON HOGGAN


    Dr. Ron Hoggan, Ed.D.


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    This article originally appeared in the Winter 2003 edition of Celiac.coms Scott-Free Newsletter.

    Evolution is an interactive process. Those of us who learn quickly and well are more likely to survive, thrive, and reproduce. Learning capacities then, are factors in the survival of our genes. Research is now revealing that cereal grains, along with other allergenic and highly glycemic foods, pose a serious threat to our sustained ability to learn. These foods have been shown to interfere at almost any stage of the learning process, impeding our attempts to focus our attention, observe, ponder, remember, understand, and apply that understanding. Grains can alter learning capacities in four specific ways: as sequelae of untreated celiac disease; through an immune sensitivity to gluten; through dietary displacement of other nutrients and; through the impact of grain on blood sugar/insulin levels.

    There are many reports of learning problems in association with untreated celiac disease. A majority of children with celiac disease display the signs and symptoms of attention deficit disorder (ADD/ADHD)1, 2 a range of learning difficulties3 and developmental delays4-6. Many of the same problems are found more frequently among those with gluten sensitivity7 a condition signaled by immune reactions against this most common element of the modern diet. Grain consumption can also cause specific nutrient deficiencies that are known to play an important role in learning. Grains can also cause problems with blood sugar/insulin levels resulting in reduced capacities for learning. Further, foods derived from grain are an important element in the current epidemic of hypoglycemia, obesity, and Type 2 diabetes8-10. Our growing understanding of the biological impact of cereal grain consumption must move educators to challenge current dietary trends.

    Part of our improved understanding comes from new testing protocols which are revealing that celiac sprue afflicts close to 1% of the general population, making it the most common life-long ailment among humans, with frequencies ranging from 0.5% to more than 5% of some populations11, 12. It is widespread and appears to occur more frequently among populations that have experienced relatively shorter periods of exposure to these grains13. The importance of this newly recognized high frequency of celiac disease becomes obvious when we examine the impact it has on learning and behavior.

    Research has identified ADHD in 66-70% of children with untreated celiac disease, which resolves on a gluten-free diet, and returns with a gluten challenge1, 2. Several investigators have connected particular patterns of reduced blood flow to specific parts of the brain in ADHD13-15. Other reports have connected untreated celiac disease with similarly abnormal blood flow patterns in the brain16. One might be able to dismiss such reports if viewed in isolation, but the increased rates of learning disabilities among celiac patients3, and the increased rates of celiac disease among those with learning disabilities leave little to the imagination17. Further, there is one report of gluten-induced aphasia (a condition characterized by the loss of speech ability) that resolved after diagnosis and institution of a gluten-free diet18. Still other investigations suggest a causal link between the partial digests of gluten (opioid peptides) and a variety of problems with learning, attention, and development.

    Gluten sensitivity, afflicting close to 15% of the general population19, 20 is an immune reaction to one or more proteins in found in grains. When a persons immune system has developed antibodies against any of these proteins, undigested and partly digested food particles have been allowed entry into the bloodstream21. The leakage of food proteins through the intestinal wall signals a failure of the protective, mucosal lining of the gastrointestinal tract, as is consistently found in untreated celiac disease. Many of the same health and learning problems that are found in celiac disease are significantly overrepresented among those with gluten sensitivity for the very good reason that many of the same proteins are being leaked into the blood of those with gluten sensitivity.

    Our cultural obeisance to grains is at odds with the remains of ancient humans. Archaeologists have long recognized that grains are a starvation food—one for which we are not well suited. Grains result in consistent signs of disease and malnourishment in every locale and epoch associated with human adoption of grain cultivation.

    Grains are a poverty food. As we increase our grain consumption, we cause deficiencies in other nutrients by overwhelming the absorptive and transport mechanisms at work in our intestines. For instance, diets dominated by grains have been shown to induce iron deficiency22—a condition that is widely recognized as causing learning disabilities23-29. This should not be surprising since iron is the carrier used to distribute oxygen throughout our bodies, including various regions of our brains. There is little room to dispute the hazards to learning posed by reductions in oxygen supply to the brain. Iron deficiency reduces available oxygen in the brain, revealing yet another dimension of gluten grains as mediators of learning difficulties.

    There is more. The impact of grain consumption on our blood sugar levels is yet another facet of its contribution to learning problems. We evolved as hunter-gatherers, eating meats, and complex carbohydrates in the form of fruits, vegetables, and seeds. Refined sugars were a rare treat wrested from bees with some difficulty. At best, it was a rare treat for our pre-historic ancestors.

    Today, with unprecedented agricultural/industrial production of refined sugars along with cultivation and milling of grain flours, these products have become very cheap and available, particularly over the last fifty years. During that time, we have added enormous quantities of grain-derived starches to the overwhelming quantities of sugar we consume. The result of this escalating dietary trend may be observed in the current epidemic rates of Type 2 diabetes, hypoglycemia, obesity, and cardiovascular disease. In the classroom, we see these trends manifest in students mood swings, behavioral disorders (fluctuating between extreme lethargy and hyperactivity), chronic depression, forgetfulness, and muddled thinking—all of which reflects the inordinate, counter-evolutionary burden placed on many homeostatic systems of the body, particularly those related to blood sugar regulation.

    The pancreas has many functions. One important activity of the pancreas is to stabilize blood sugar levels. When blood sugar is not well regulated, learning is impaired30. The pancreas secretes carefully monitored quantities of glucagon and insulin. The pancreas responds to the presence of proteins, sugar, and starch in the digestive tract by producing insulin. It produces glucagon in response to fats. The balanced presence of both of these hormones in the bloodstream is critical to learning because they regulate the transport of nutrients into cells. Too little or too much insulin can cause blood sugar levels go out of control inducing a wide range of symptoms.

    Today, when the insulin/glucagon balance goes awry, it is frequently due to insulin overproduction due to a diet dominated by sugars and starches. This overproduction is caused by chronic consumption of highly glycemic foods. The resulting elevated levels of insulin cause rapid movement of nutrients into cells, either for storage as fat, or to be burned as energy, causing increased activity levels, "hot spells", sweating, increased heart rate, etc. This energized stage requires a constant supply of sugars and starches to be maintained. Otherwise, it is soon followed by bouts of lethargy, light-headedness, tremors, and weakness, which are all signs of hypoglycemia or very low blood sugar levels.

    Despite having stored much of the blood sugars as fats, there is insufficient glucagon to facilitate its use for energy. As this condition progresses, and as blood sugar levels plummet, periods of irrational anger and/or confusion often result. These moods often result from adrenaline secreted to avoid a loss of consciousness due to low blood sugar levels. The next step in the progression, in the absence of appropriate nutritional intervention, is lapsing into a coma.

    In the short term, the answer to these fluctuations is more frequent consumption of sugars/starches. However, the long term result of such an approach is either a state of insulin resistance, where more and more insulin is required to do the same task, or a state of pancreatic insufficiency, where the pancreas is simply unable to keep pace with the demand for insulin. In either case, once this stage is reached, the individual may be diagnosed with type 2 diabetes. This disease has so increased among North Americans, particularly among children, that an autoimmune form of diabetes, previously called juvenile onset, had to be renamed to "Type 1 diabetes".

    By now, it will not surprise the reader to learn that Type 1 diabetes has also been shown to be significantly associated with gluten. Research reveals that there is considerable overlap between celiac disease and Type 1 diabetes. About 8% of celiacs also have Type 1 diabetes31-33, and 5-11% of Type 1 diabetics have celiac disease34-38. Further, Scott Frazer et al. have repeatedly shown, in animal studies, a causal, dose-dependent relationship between type 1 diabetes and gluten39-42.

    The growing reaction against gluten and other allergenic foods should not be confused with the several dietary fads of the 20th Century. The vegetarian perspective ignores the vitamin deficiencies that result from a strict vegetarian diet. The low-fat craze is another fad that has mesmerized the industrialized world for the last 30-40 years. Fortunately, this perspective has recently come under scrutiny. Despite having served as the driving force behind most physicians dietary recommendations during the last several decades, the low fat dictum is overwhelmingly being discredited by research reported in peer reviewed publications.

    Recognition and avoidance of allergenic and highly glycemic foods is a whole new trend that is based on scientific research and evidence. It reflects an improved understanding of the function of the gastrointestinal tract, the endocrine system, particularly the pancreas, and the immune system. Past dietary fads are consistently deficient in important nutrients that are necessary to our good health and survival. Further, they frequently contain substances that are harmful to us, such as the phytates that are abundantly present in whole grain foods, and interfere with absorption of many minerals.

    It is increasingly clear that grains, especially those that contain gluten, are contraindicated for human learning. The evidence is overwhelming. The mandate of eating to learn is learning to eat as our ancestors did.

    Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered here.

    References:

    1. Kozlowska, Z: (1991). Results of investigation on children with coeliakia treated many years with glutethen free diet Psychiatria Polska. 25(2),130-134.
    2. Paul, K., Todt, J., Eysold, R. (1985) [EEG Research Findings in Children with Celiac Disease According to Dietary Variations]. Zeitschrift der Klinische Medizin. 40, 707-709.
    3. Grech, P.L., Richards, J., McLaren, S., Winkelman, J.H. (2000) Psychological sequelae and quality of life in celiac disease. Journal of Pediatric Gastroenterology and Nutrition 31(3): S4
    4. Reichelt, K., Sagedal, E., Landmark, J., Sangvic, B., Eggen, O., Helge, S. (1990a). The Effect of Gluten-Free Diet on Urinary peptide Excretion and Clinical State in Schizophrenia. Journal of Orthomolecular Medicine. 5(4), 169-181.
    5. Reichelt, K., Ekrem, J., Scott, H. (1990b). Gluten, Milk Proteins and Autism: DIETARY INTERVENTION EFFECTS ON BEHAVIOR AND PEPTIDE SECRETION. Journal of Applied Nutrition. 42(1), 1-11.
    6. Reichelt, K., Knivsberg, A., Lind, G., Nodland, M. (1991). Probable etiology and Possible Treatment of Childhood Autism. Brain Dysfunction. 4, 308-319.
    7. Hoggan, R. (1997a). Absolutisms Hidden Message for Medical Scientism. Interchange. 28(2/3), 183-189.
    8. Caterson ID, Gill TP. Obesity: epidemiology and possible prevention. Best Pract Res Clin Endocrinol Metab. 2002 Dec;16(4):595-610.
    9. Hennessy AR, Walker JD.Silent hypoglycaemia at the diabetic clinic. Diabet Med. 2002 Mar;19(3):261.
    10. Kue Young T, Chateau D, Zhang M. Factor analysis of ethnic variation in the multiple metabolic (insulin resistance) syndrome in three Canadian populations.Am J Human Biol. 2002 Sep-Oct;14(5):649-58.
    11. Wahab PJ, Meijer JW, Dumitra D, Goerres MS, Mulder CJ. Coeliac disease: more than villous atrophy.Rom J Gastroenterol. 2002 Jun;11(2):121-7.
    12. Catassi C, Ratsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L. Why is coeliac disease endemic in the people of the Sahara?Lancet. 1999 Aug 21;354(9179):647-8.
    13. Langleben DD, Acton PD, Austin G, Elman I, Krikorian G, Monterosso JR, Portnoy O, Ridlehuber HW, Strauss HW. Effects of Methylphenidate Discontinuation on Cerebral Blood Flow in Prepubescent Boys with Attention Deficit Hyperactivity Disorder.J Nucl Med. 2002 Dec;43(12):1624-1629.
    14. 2: Kim BN, Lee JS, Shin MS, Cho SC, Lee DS. Regional cerebral perfusion abnormalities in attention deficit/hyperactivity disorder Statistical parametric mapping analysis. Eur Arch Psychiatry Clin Neurosci. 2002 Oct;252(5):219-25.
    15. Lou, H., Henriksen, L., Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology. 825-829.
    16. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3.
    17. Knivsberg AM. Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia.Pediatr Rehabil. 1997 Jan-Mar;1(1):25-33.
    18. 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.
    19. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. The humoral response in the pathogenesis of gluten ataxia. Neurology. 2002 Apr 23;58(8):1221-6.
    20. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness.J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Review.
    21. Husby, V., Jensenius, C., Svehag, S.(1985). Passage of Undegraded DietaryAntigen into the Blood of Healthy Adults. Scandinavian Journal of Immunology. 22, 83-92.
    22. Ma A, Chen X, Zheng M, Wang Y, Xu R, Li J. Iron status and dietary intake of Chinese pregnant women with anemia in the third trimester. Asia Pac J Clin Nutr. 2002;11(3):171-5.
    23. Kapil U, Bhavna A. Adverse effects of poor micronutrient status during childhood and adolescence. Nutr Rev. 2002 May;60(5 Pt 2):S84-90. Review.
    24. Youdim MB, Yehuda S. The neurochemical basis of cognitive deficits induced by brain iron deficiency: involvement of dopamine-opiate system. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):491-500.
    25. Otero GA, Aguirre DM, Porcayo R, Fernandez T. Psychological and electroencephalographic study in school children with iron deficiency. Int J Neurosci. 1999 Aug;99(1-4):113-21.
    26. Guesry P. The role of nutrition in brain development.
    27. Prev Med. 1998 Mar-Apr;27(2):189-94. Review.
    28. Bruner AB, Joffe A, Duggan AK, Casella JF, Brandt J. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet. 1996 Oct 12;348(9033):992-6.
    29. Soewondo S. The effect of iron deficiency and mental stimulation on Indonesian childrens cognitive performance and development. Kobe J Med Sci. 1995 Apr;41(1-2):1-17.
    30. McCarthy AM, Lindgren S, Mengeling MA, Tsalikian E, Engvall JC. Effects of diabetes on learning in children. Pediatrics. 2002 Jan;109(1):E9.
    31. Bertini M, Sbarbati A, Valletta E, Pinelli L, Tato L. Incomplete gastric metaplasia in children with insulin-dependent diabetes mellitus and celiac disease. An ultrastructural study.BMC Clin Pathol. 2001;1(1):2.
    32. Schuppan D, Hahn EG. Celiac disease and its link to type 1 diabetes mellitus.J Pediatr Endocrinol Metab. 2001;14 Suppl 1:597-605.
    33. Holmes GK. Coeliac disease and Type 1 diabetes mellitus - the case for screening.Diabet Med. 2001 Mar;18(3):169-77. x
    34. Saukkonen T, Vaisanen S, Akerblom HK, Savilahti E. Coeliac disease in children and adolescents with type 1 diabetes: a study of growth, glycaemic control, and experiences of families.Acta Paediatr. 2002;91(3):297-302.
    35. Spiekerkoetter U, Seissler J, Wendel U. General Screening for Celiac Disease is Advisable in Children with Type 1 Diabetes.Horm Metab Res. 2002 Apr;34(4):192-5.
    36. Barera G, Bonfanti R, Viscardi M, Bazzigaluppi E, Calori G, Meschi F, Bianchi C, Chiumello G. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospective longitudinal study.Pediatrics. 2002 May;109(5):833-8.
    37. Hansen D, Bennedbaek FN, Hansen LK, Hoier-Madsen M, Hegedu LS, Jacobsen BB, Husby S. High prevalence of coeliac disease in Danish children with type I diabetes mellitus.Acta Paediatr. 2001 Nov;90(11):1238-43.
    38. Aktay AN, Lee PC, Kumar V, Parton E, Wyatt DT, Werlin SL. The prevalence and clinical characteristics of celiac disease in juvenile diabetes in Wisconsin.J Pediatr Gastroenterol Nutr. 2001 Oct;33(4):462-5.
    39. MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW. A type 1 diabetes-related protein from wheat (triticum aestivum): cDNA clone of a wheat storage globulin, Glb1, linked to islet damage.J Biol Chem. 2002 Oct 29.
    40. Scott FW, Rowsell P, Wang GS, Burghardt K, Kolb H, Flohe S. Oral exposure to diabetes-promoting food or immunomodulators in neonates alters gut cytokines and diabetes.Diabetes. 2002 Jan;51(1):73-8.
    41. Scott FW, Cloutier HE, Kleemann R, Woerz-Pagenstert U, Rowsell P, Modler HW, Kolb H. Potential mechanisms by which certain foods promote or inhibit the development of spontaneous diabetes in BB rats: dose, timing, early effect on islet area, and switch in infiltrate from Th1 to Th2 cells.Diabetes. 1997 Apr;46(4):589-98.
    42. Scott FW. Food-induced type 1 diabetes in the BB rat.Diabetes Metab Rev. 1996 Dec;12(4):341-59.
    • Of Relevant interest:
      Gormanous M, Hunt A, Pope J, Gerald B. Lack of knowledge of diabetes among Arkansas public elementary teachers: implications for dietitians. J Am Diet Assoc. 2002 Aug;102(8):1136-8.

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    Would be excellent except references are not numbered as per footnotes, so difficult to ascribe journals to article statements.

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    BMJ 2004;328:438-439 (21 February) Celiac.com 02/27/2004 – The following report is interesting, but I believe that serological studies done on those with schizophrenia would be a far better way to conduct such a study. Also, the use of such a small control group cannot accurately predict the actual incidence of schizophrenia in those with celiac disease. –Scott Adams
    According to a Danish study published in the British Medical Journal, people with celiac disease may have an increased risk of developing schizophrenia. Previous studies have also suggested an association between these two disorders. The study identified 7,997 people over age 15 who were admitted to a Danish psychiatric unit for the first time between 1981 and 1998 and were diagnosed with schizophrenia. The researchers selected 25 random controls and matched their year of birth and sex, and identified any history of celiac disease, ulcerative colitis or Crohns disease in both groups, and in their parents. A "moderately strong risk relation between coeliac disease and schizophrenia" was discovered in the data, and the researchers stress that these findings only reflect a small proportion of cases, as both disorders are rare. The prevalence of celiac disease among schizophrenics was 1.5 cases per 1,000 compared to 0.5 cases per 1,000 in the larger control group, which means that there is a three times greater risk of schizophrenia in those with celiac disease. Interestingly Crohns disease and ulcerative colitis were not associated with an increased risk of schizophrenia.
    According to Dr. Eaton: More research is needed to understand the link between celiac disease and schizophrenia. The most important question is whether treatment for celiac disease, in the form of a gluten-free diet, would benefit the small proportion of individuals with schizophrenia who are genetically prone to celiac disease but have not been diagnosed with it."

    Jefferson Adams
    Celiac.com 07/13/2009 - Doctors are recommending that kids with mental and behavioral disorders, and with low cholesterol be tested for celiac disease.
    This, after findings from a recent study suggest that low plasma cholesterol levels might have a role in the development and pathogenesis of certain behavioral disorders such as schizophrenia, depression, and obsessional neurosis in people with celiac disease.
    It is well documented that children with celiac disease face higher rates of certain behavioral disorders such as schizophrenia, depression, and obsessional neurosis. Still, not much is known about the development and pathogenesis of celiac-related mental and behavioral disorders.
    A team of researchers made up of Italians Luca Mascitelli, M.D., Francesca Pezzetta, M.D., and American Mark R. Goldstein, M.D. set out to investigate the matter.
    A large scale study of patients aged 6–16 years showed that most people with celiac disease harbored illness of low-grade intensity that was often associated with "decreased psychophysical well-being."
    Furthermore, a recent study found that adolescents with celiac disease face higher rates of depressive and disruptive behavioral disorders, especially before adopting a gluten-free diet. 2 For some, psychiatric symptoms appear to improve after the patients started a gluten-free diet.
    Interestingly, children with malabsorption and steatorrhea due to celiac disease often have lower concentrations of blood cholesterol. Moreover, people with celiac disease, but who show no signs of overt cholesterol malabsorption, often show low levels of blood cholesterol, while normal to high cholesterol levels have been shown effective in ruling out celiac disease.
    Add to that the fact that low cholesterol has been tied to other mental disorders. In particular, a national sample of non-institutionalized, non-African American children of school-age found a statistically significant association between low cholesterol and aggressive behavior.
    Low cholesterol has also been tied to the onset of conduct disorder during childhood among male criminals. Therefore, they recommend that screening for celiac disease be considered in children and adolescents with mental disorders and low cholesterol.
    Psychosomatics 50:300-301, May-June


    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Winter 2010 edition of Journal of Gluten Sensitivity.
    Celiac.com 10/06/2010 - Do you know where LSD comes from? It is made from gluten grains.  In 1938 Albert Hofmann, a Swiss chemist, discovered LSD, having refined it from a mold that grows on grains.  However, it was not until 1943 that he discovered its psycho-active properties.  In his own words Hofmann states: “I synthesized the diethylamide of Iysergic acid with the intention of obtaining an analeptic.” The expectation of such a drug was based on its source—ergot—which grows on gluten grains and causes ergotism, also known as ergotoxicosis, ergot poisoning, holy fire, and Saint Anthony’s Fire. 
    This poisonous mold has long been known to infect gluten grains.  It was to prevent the development of these molds that the Romans invented central heating systems.  They stored their grains on the lowest floor of residences and other buildings that were centrally heated and well ventilated.  Their fears of ergot were based on the powerful and bizarre symptoms that developed in people who ate grains that had become moldy with ergot.  Some afflicted individuals began to hallucinate, often becoming so mentally disturbed that they injured or killed themselves.  Others experienced loss of blood circulation to their extremities which became gangrenous.  Their digits and limbs sometimes fell off before these people died.  Some experienced a combination of these two sets of symptoms.  Animals sometimes display similar symptoms after consuming moldy grains. 
    Familiar with the vaso-constricting nature of ergot, Dr. Hofmann was trying to develop a stimulant drug that, in combination with another drug refined from ergot, could be used to halt hemorrhaging following childbirth.  Hofmann experienced an accidental dosing of LSD.  Here are some of his comments from his laboratory notes:

    Last Friday, April 16, 1943, I was forced to stop my work in the laboratory in the middle of the afternoon and to go home, as I was seized by a peculiar restlessness associated with a sensation of mild dizziness.  On arriving home, I lay down and sank into a kind of drunkenness which was not unpleasant and which was characterized by extreme activity of imagination.  As I lay in a dazed condition with my eyes closed (I experienced daylight as disagreeably bright) there surged upon me an uninterrupted stream of fantastic images of extraordinary plasticity and vividness and accompanied by an intense, kaleidoscope-like play of colors.  This condition gradually passed off after about two hours. From http://www.psychedelic-library.org/hofmann.htm. Several days later Dr. Hofmann intentionally ingested 250 µg of LSD which he hypothesized would be a threshold dose.  Here is what he said about his second ingestion:
    April 19, 1943: Preparation of an 0.5% aqueous solution of d-lysergic acid diethylamide tartrate. 4:20 P.M.: 0.5 cc (0.25 mg LSD) ingested orally.  The solution is tasteless. 4:50 P.M.: no trace of any effect.  5:00 P.M.: slight dizziness, unrest, difficulty in concentration, visual disturbances, marked desire to laugh... At this point the laboratory notes are discontinued: The last words were written only with great difficulty.  I asked my laboratory assistant to accompany me home as I believed that I should have a repetition of the disturbance of the previous Friday.  While we were cycling home, however, it became clear that the symptoms were much stronger than the first time.  I had great difficulty in speaking coherently, my field of vision swayed before me, and objects appeared distorted like images in curved mirrors.  I had the impression of being unable to move from the spot, although my assistant told me afterwards that we had cycled at a good pace.  http://www.psychedelic-library.org/hofmann.htm The difficulty Hofmann experienced with speaking coherently is reminiscent of a 1988 case report from Massachusetts General Hospital in which a patient was admitted for investigation of bowel complaints.  While in the hospital he became unable to speak coherently.  Eventually diagnosed with celiac disease, he was placed on a gluten free diet.  After several months on the diet, his speech was fully returned.  But I’m getting ahead of myself.  We were talking about Hofmann’s discovery.  LSD arrived in the USA in 1948 and was used to gain a better understanding of the schizophrenic experience:

    In psychiatry, the use of LSD by students was an accepted practice; it was viewed as a teaching tool in an attempt to enable the psychiatrist to subjectively understand schizophrenia.  http://en.wikipedia.org/wiki/History_of_LSD These students who tried LSD apparently failed to consider that the connection between the symptoms of LSD ingestion and schizophrenia might be due to a common source—psycho-active peptides from gluten grains.  About a decade after LSD had crossed the Atlantic, and from a very different research perspective, Dr. Curtis Dohan began investigating the possibility that gluten grains might be a factor in schizophrenia.  He had found that people with celiac disease and those with schizophrenia both excrete increased quantities of specific groups of indoles in their urine.  Some such indoles are known to be psychoactive and some psychoactive alkaloids also contain such indoles. 
    Having learned about this connection between celiac disease and schizophrenia, Dr. Dohan then undertook a study in which he examined hospital admission rates for schizophrenia both during periods of plenty and during World War II grain shortages.  He found that there was, indeed, a reduction in admissions during grain shortages, which normalized when ample grains became available again. 
    Dohan’s next step, along with several colleagues, was to design and conduct a single-blind cross-over study of schizophrenic patients in a locked ward.  They found that symptoms of schizophrenia abated on a gluten-free, dairy-free diet.  These same patients relapsed on re-introduction of these foods.  These data were published in The British Journal of Psychiatry in 1969.  Dohan’s findings were replicated and published in the January1976 issue of Science by Man Mohan Singh and Stanley Kay.
    Three years later, Christine Zioudrou and her colleagues demonstrated the presence of psychoactive peptides in the incomplete digests of gluten grains, including some with morphine-like properties, which they named “exorphins”.  Subsequent research by Fukudome and Yoshikawa has shown that there are five separate sequences from gluten grains that have psycho-active properties.  They named these exorphins A4, A5, B4, B5, and C. 
    At some point in this process, Dohan may have learned about the pseudo-hallucinations sometimes reported in celiac patients.  The primary difference between the schizophrenic’s hallucinations and those associated with celiac disease is that the celiac patient can exercise conscious control to stop them.  The schizophrenic appears unable to do this. 
    As he continued to accumulate more such data, Dohan went on to publish 16 more papers and letters over the next twenty years demonstrating an impressive body of evidence to support his suspicion that psychoactive peptides from gluten and possibly dairy proteins had a powerful impact on many cases of schizophrenia.  Yet, to an even greater extent than today, most people simply could not believe that such supposedly healthful foods as gluten grains and dairy products could be causing illness.  It was probably this paradigm that helped lead to subsequent publications and a period of dormancy in this area of research. 
    Several reports of very small numbers of schizophrenic patients, chronic patients, which Dohan had specifically identified as unlikely to respond to the diet, showed no benefit from a gluten-free diet.  Other studies were improved through double-blinding but weakened by extremely limited dietary control, permitting visitors to bring food to patients participating in that study, essentially abrogating the value of the entire study.  Some researchers ignored Dohan’s assertions that celiac disease could serve as a model for studying schizophrenia.  They chose, instead, to produce data that discredited the possibility that schizophrenia is identical to celiac disease by showing that most schizophrenic patients do not show signs of malabsorption.  Other work, conducted in the same vein, showed that celiac antibodies are not found in most schizophrenic patients. 
    Despite all the powerful evidence compiled by Dohan and others, this wave of studies and letters discredited Dohan’s work by contradicting notions that Dohan had never voiced.  For instance, he never expressed the notion that schizophrenia was celiac disease.  He simply asserted that there were compelling similarities and a small but significant overlap between schizophrenia and celiac disease, suggesting the need to explore gluten as a possible contributing factor in schizophrenia.  Considerable data support that notion but Dohan’s vigorous and persistent pursuit of this important discovery was soon depicted as a personal quest.  For instance, in a private email with one of Dohan’s contemporaries, Dohan was repeatedly called “unscientific.” Yet, fifteen years later, this same researcher has since participated in a published study that supports Dohan’s hypothesis. 
    Fortunately for all of us, the last dozen years have seen a resurgence of interest in the gluten hypothesis regarding schizophrenia, beginning with a case report by De Santis et al.  They described a patient with schizophrenia and a SPECT scan showing abnormal blood flow patterns in the brain typical of schizophrenia.  This patient developed symptoms of celiac disease and was placed on a gluten free diet.  Not only did this patient’s celiac symptoms disappear, her/his symptoms of schizophrenia disappeared and blood flow patterns in her brain normalized.  The gluten-free diet was the only plausible explanation for these changes.  
    A list of reports suggest important reasons to investigate the impact of gluten on our brains.  For instance, Dr. Knivsburg reported the discovery of two cases of celiac disease and one of milk protein sensitivity among 15 dyslexic children.  That is a huge increased incidence over the general population.  Similarly, Dr. Kozlowska found that almost 70% of celiac children have ADHD that normalizes on a gluten-free diet.  The Massachusetts General Hospital case study mentioned earlier reported celiac-associated aphasia that resolved on a gluten free diet.  Dr. Hu and colleagues report a laundry list of cognitive impairments in association with celiac disease including amnesia, acalculia, confusion, and personality changes.  Many of these disabilities wax and wane according to the gluten content of the diet. 
    However, the notion of gluten-driven cognitive deficits, including learning disabilities, and behavioral abnormalities in association with non-celiac gluten sensitivity, has only recently gotten some research attention.  For instance, Alexandra Blair of The TimesOnline in the United Kingdom reported on an informal study conducted at a small school for dyslexic children in Northumberland.  They got some startlingly positive improvements in students’ performance after placing them on a gluten free diet.  Dr. Marios Hadjivassiliou et al.  at the Royal Hallamshire Hospital in Sheffield, U.K.  have repeatedly reported that a majority of patients with neurological disease of unknown origin are also gluten sensitive while only about one third of these patients have celiac disease. 
    Kalaydjian et al.  reviewed the medical literature to about 2005 and called for large, controlled studies of the connection between gluten and schizophrenia because it is clear that some schizophrenic patients benefit enormously from a gluten free diet.  Similarly, earlier this year, Kraft et al.  reported on a schizophrenic patient who was diagnosed at seventeen years of age.  Fifty three years later, at her doctor’s suggestion, she undertook a ketogenic diet to lose weight.  Not only did she lose weight, she also lost all signs and symptoms of schizophrenia. 
    As 2009 comes to a close, two more publications have made this year into something of a turning point for this research.  Cascella et al.  state that “Our results confirm the existence of a subgroup of patients with antibody characteristics associated with the presence of a specific immune response to gluten.”
    Similarly, Samaroo et al.  report that their findings “….  indicate that the anti-gliadin immune response in schizophrenia has a different antigenic specificity from that in celiac disease…” they go on to assert that the genetic HLA markers for celiac disease were not found in the schizophrenic patients they studied. 
    At the most basic level, we know that gluten causes increased intestinal permeability among a wide range of genetically susceptible individuals.  We also know that substances from moldy grains will cause schizophrenic symptoms in any of us.  It is not a great leap to suggest that, in the context of gluten-induced increased intestinal permeability, similarities in hallucinations, altered brain perfusion, and a range of cognitive deficits found in schizophrenia, celiac disease, and gluten sensitivity might all be rooted in the commonest food in our diets from which hallucinogenic drugs can be produced. 
    Institutional nutrition and food programs for the needy and/or homeless include large proportions of inexpensive gluten-laden foods.  Such diets, often provided charitably for those at the lowest socio-economic strata, are at least self-defeating.  Further, such foods are often consumed at this economic level despite visible molds growing on them.  I have heard stories of homeless persons scavenging through dumpsters located at or near bakeries.  There can be little doubt that such eating practices perpetuate the very psychiatric conditions that have reduced many of these people to a state of homelessness. 


    Jefferson Adams
    Celiac.com 02/13/2013 - A team of researchers wanted to determine whether levels of immunoglobulin G (IgG) were associated with a later diagnosis of a non-affective psychotic disorder.
    The researchers included H. Karlsson, Å. Blomström, S. Wicks, S. Yang, R.H. Yolken, and C. Dalman. They are affiliated with the Department of Neuroscience at the Karolinska Institute in Stockholm, Sweden.
    To accomplish their goal, the team analyzed archival dried blood spots taken from newborns in Sweden between 1975 and 1985 with verified register-based diagnoses of non-affective psychoses made between 1987 and 2003 and comparison subjects matched on sex, date of birth, birth hospital, and municipality.
    The team reviewed samples from a total of 211 case subjects and 553 comparison subjects who agreed to take part in the study. They pulled data for factors associated with maternal status, pregnancy, and delivery from the Swedish Medical Birth Register.
    They used enzyme-linked immunosorbent assay to analyze the results for levels of IgG directed at gliadin (a component of gluten) and casein (a milk protein) in eluates from dried blood spots. They then calculated odds ratios for levels of IgG directed at gliadin or casein for non-affective psychosis.
    Comparison subjects associated with non-affective psychosis showed levels of anti-gliadin IgG (but not anti-casein IgG) above the 90th percentile of levels observed (odds ratio=1.7, 95% CI=1.1-2.8).
    This connections was not affected by differences in maternal age, immigrant status, or mode of delivery. They also found that gestational age at birth, ponderal index, and birth weight were not associated with maternal levels of anti-gliadin IgG.
    From their study, they concluded that high levels of anti-gliadin IgG in the maternal circulation are associated with an elevated risk for the development of a non-affective psychosis in offspring.
    They point out that more research is needed to identify the mechanisms underlying this association in order to develop preventive strategies.
    Source:
    Am J Psychiatry. 2012 Jun;169(6):625-32. doi: 10.1176/appi.ajp.2012.11081197.

  • Recent Articles

    Jefferson Adams
    Celiac.com 04/20/2018 - A digital media company and a label data company are teaming up to help major manufacturers target, reach and convert their desired shoppers based on dietary needs, such as gluten-free diet. The deal could bring synergy in emerging markets such as the gluten-free and allergen-free markets, which represent major growth sectors in the global food industry. 
    Under the deal, personalized digital media company Catalina will be joining forces with Label Insight. Catalina uses consumer purchases data to target shoppers on a personal base, while Label Insight works with major companies like Kellogg, Betty Crocker, and Pepsi to provide insight on food label data to government, retailers, manufacturers and app developers.
    "Brands with very specific product benefits, gluten-free for example, require precise targeting to efficiently reach and convert their desired shoppers,” says Todd Morris, President of Catalina's Go-to-Market organization, adding that “Catalina offers the only purchase-based targeting solution with this capability.” 
    Label Insight’s clients include food and beverage giants such as Unilever, Ben & Jerry's, Lipton and Hellman’s. Label Insight technology has helped the Food and Drug Administration (FDA) build the sector’s very first scientifically accurate database of food ingredients, health attributes and claims.
    Morris says the joint partnership will allow Catalina to “enhance our dataset and further increase our ability to target shoppers who are currently buying - or have shown intent to buy - in these emerging categories,” including gluten-free, allergen-free, and other free-from foods.
    The deal will likely make for easier, more precise targeting of goods to consumers, and thus provide benefits for manufacturers and retailers looking to better serve their retail food customers, especially in specialty areas like gluten-free and allergen-free foods.
    Source:
    fdfworld.com

    Jefferson Adams
    Celiac.com 04/19/2018 - Previous genome and linkage studies indicate the existence of a new disease triggering mechanism that involves amino acid metabolism and nutrient sensing signaling pathways. In an effort to determine if amino acids might play a role in the development of celiac disease, a team of researchers recently set out to investigate if plasma amino acid levels differed among children with celiac disease compared with a control group.
     
    The research team included Åsa Torinsson Naluai, Ladan Saadat Vafa, Audur H. Gudjonsdottir, Henrik Arnell, Lars Browaldh, and Daniel Agardh. They are variously affiliated with the Institute of Biomedicine, Department of Microbiology & Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; the Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; the Department of Pediatric Gastroenterology, Hepatology and Nutrition, Karolinska University Hospital and Division of Pediatrics, CLINTEC, Karolinska Institute, Stockholm, Sweden; the Department of Clinical Science and Education, Karolinska Institute, Sodersjukhuset, Stockholm, Sweden; the Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden; the Diabetes & Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; and with the Nathan S Kline Institute in the U.S.A.
    First, the team used liquid chromatography-tandem mass spectrometry (LC/MS) to analyze amino acid levels in fasting plasma samples from 141 children with celiac disease and 129 non-celiac disease controls. They then crafted a general linear model using age and experimental effects as covariates to compare amino acid levels between children with celiac disease and non-celiac control subjects.
    Compared with the control group, seven out of twenty-three children with celiac disease showed elevated levels of the the following amino acids: tryptophan; taurine; glutamic acid; proline; ornithine; alanine; and methionine.
    The significance of the individual amino acids do not survive multiple correction, however, multivariate analyses of the amino acid profile showed significantly altered amino acid levels in children with celiac disease overall and after correction for age, sex and experimental effects.
    This study shows that amino acids can influence inflammation and may play a role in the development of celiac disease.
    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
    If you’ve flown anywhere lately, you may have seen them. People flying with their designated “emotional support” animals. We’re not talking genuine service animals, like seeing eye dogs, or hearing ear dogs, or even the Belgian Malinois that alerts its owner when there is gluten in food that may trigger her celiac disease.
    Now, to be honest, some of those animals in question do perform a genuine service for those who need emotional support dogs, like veterans with PTSD.
    However, many of these animals are not service animals at all. Many of these animals perform no actual service to their owners, and are nothing more than thinly disguised pets. Many lack proper training, and some have caused serious problems for the airlines and for other passengers.
    Now the major airlines are taking note and introducing stringent requirements for service animals.
    Delta was the first to strike. As reported by the New York Times on January 19: “Effective March 1, Delta, the second largest US airline by passenger traffic, said it will require passengers seeking to fly with pets to present additional documents outlining the passenger’s need for the animal and proof of its training and vaccinations, 48 hours prior to the flight.… This comes in response to what the carrier said was a 150 percent increase in service and support animals — pets, often dogs, that accompany people with disabilities — carried onboard since 2015.… Delta said that it flies some 700 service animals a day. Among them, customers have attempted to fly with comfort turkeys, gliding possums, snakes, spiders, and other unusual pets.”
    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
    So, to the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service and emotional support animals.
    Source:
    cnbc.com

    admin
    WHAT IS CELIAC DISEASE?
    Celiac disease is an autoimmune condition that affects around 1% of the population. People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems.
    Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases.
    Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. 
    CLASSIC CELIAC DISEASE SYMPTOMS
    Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others.
    LESS OBVIOUS SYMPTOMS
    Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important.
    NO SYMPTOMS
    Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. 

    CELIAC DISEASE VS. GLUTEN INTOLERANCE
    Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? 
    CELIAC DISEASE VS. NON-CELIAC GLUTEN SENSITIVITY (NCGS)
    Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there.

    There are four main differences between celiac disease and non-celiac gluten sensitivity:
    No Hereditary Link in NCGS
    Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders
    Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers
    People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy
    Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)?
    IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS.

    To add more confusion, many cases of IBS are, in fact, celiac disease in disguise.

    That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. 
    Crohn’s Disease and celiac disease share many common symptoms, though causes are different.  In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis.  
    Crohn’s treatment consists of changes to diet and possible surgery.  Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection.
    Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS
    Diagnosis of celiac disease can be difficult. 

    Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. 
    But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. 
    Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult.  Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis.
    TESTING
    There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis.
    Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products.

    BIOPSY
    Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide.

    WHY A GLUTEN-FREE DIET?
    Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. 
    A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years.
    For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease.
    WHAT ABOUT ENZYMES, VACCINES, ETC.?
    There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease.
    There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes.

    Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. 

    For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement.

    ASSOCIATED DISEASES
    The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions:
    Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include:
    Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers:
    Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES:
    Celiac Disease Center, Columbia University
    Gluten Intolerance Group
    National Institutes of Health
    U.S. National Library of Medicine
    Mayo Clinic
    University of Chicago Celiac Disease Center

    Jefferson Adams
    Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease.
    A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat.
    Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease.
    As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results.
    Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease.
    It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet.
    Read more at Digitaltrends.com , and at Newscientist.com