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    Stranded Without Her Mom


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Autumn 2012 Issue


    Image Caption: Image: CC--ap220859

    Celiac.com 09/15/2017 - In Pennsylvania, there is a six-year-old little girl (we'll call her Amy) who has not been allowed to see her mother (we'll call her Cindy) since June 21st because Amy's dad takes issue with a diet that excludes gluten and other allergenic foods. You might think that this is due to a dispute arising out of the dissolution of a marriage, but that is not the case. However, I'm getting ahead of myself. I need to start describing this situation as it began about six years ago, when her father was arrested for public drunkenness, resisting arrest, and creating a public disturbance, when Amy was less than a year old. Dad (we'll call him Steve) struggled with unemployment and part-time employment as a truck driver, falling further and further into arrears on his child support payments. Cindy had primary custody, and every second weekend, Steve took care of Amy.


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    Conflicts between Cindy and Steve quickly arose over the dietary restrictions mentioned above. Cindy wanted Amy to be healthy and she thought she could achieve that goal by allowing her to eat only wholesome foods, excluding cow's milk, gluten, soy, tree nuts, and refined sugar. She made these choices partly because she observed better behavior in Amy when she excluded these foods, partly because she observed gastrointestinal symptoms, including abdominal bloating, when Amy ate these foods, and partly because Amy tested positive for IgE antibodies against tree nuts, and other testing, conducted after Amy was on a diet that had already excluded these foods, showed mildly positive results for gluten, cow milk, and soy. Who can say how strongly Amy would react to these foods if she were eating them on a daily basis?

    However, Steve apparently does not believe in such diets or testing. He refused to cooperate with the prescribed dietary restrictions despite a court ordering him to do so. This court order had been in place for four years, yet when he testified in court, asserting that he had been following the diet for Amy, he could not even say what gluten is, or what foods contain gluten.

    Not surprisingly, despite the court's provision of visitation rights for Cindy, Steve has found one excuse after another to refuse Cindy access to their daughter, since gaining full custody based on a deeply flawed claim that Cindy has Munchausen's syndrome by proxy (MSBP). My comments, of course, only represent one side of the story. However, most of us who follow a gluten free diet have, at some point, had to deal with similarly resistant attitudes, although they are not usually taken to such extremes.

    After years of support payment delinquency and non-compliance with court orders, Steve showed up in court on June 21st, with legal counsel, a psychiatrist's report asserting that Cindy has MSBP, and claiming that he has a full-time job and is therefore able to support Amy, despite long standing arrears on his child support payments to Cindy. Where did all this money come from to pay for these expensive representatives and expert reports? And how is it that Steve overlooked bringing his child support payments up to date before paying these other expenses? Further, Steve is demanding child support payments when he has yet to pay up his own arrears.

    The court took away her daughter based on a flimsy report that accused Cindy of Munchausen's Syndrome by Proxy. At that time, Cindy was not allowed to defend herself or speak on her own behalf. She was not even allowed to read the report that accused her of MSBP! The judge has also sealed the record so Cindy cannot get a copy of it! It appears that she doesn't have a right to face her accuser.

    One of Steve's experts ignored the fact that Amy was only getting gluten on every second weekend, at the time she was tested, and asserted that Amy's mildly positive test results for food sensitivities to gluten, soy, and cow's milk were somehow meaningless. (This may also be rooted in the currently contested value of IgG food allergy testing, which would fill another article.) The psychiatrist asserted that Cindy's dietary restrictions for Amy indicate that Cindy has Munchausen's syndrome by proxy and that Cindy is therefore abusing Amy with this diet. The most insane part of this whole scenario is that any of the many Paleodiet advocates, including S. Boyd Eaton, M.D., professor Loren Cordain, Ph.D., professor Melvin Konner, M.D., Ph.D., and professor Staffan Lindeberg, M.D., Ph.D. would endorse this diet as almost universally healthful. Many low carbohydrate advocates, such as professor Stephen Phinney, M.D., Ph.D., professor Jeff Volek Ph.D., R.D., and professor Jay Wortman, M.D., would similarly approve this diet as providing a much more healthful start for this child than the conventional American diet that most American children her age are eating. Some of these Paleodiet and low carbohydrate experts have raised their own children on similar diets because of the health benefits such eating habits confer. Do they have Munchausen's syndrome by proxy too?

    Let's take a look at this diet, one element at a time. Cindy wants her daughter to avoid refined sugar. Not only is it unhealthy, Cindy believes that Amy's behavior deteriorates when consuming refined sugar, and the work of all of the above scientists supports Cindy's concerns. One research group, Fiorito et al, showed that sweetened beverage consumption at age five predicts lifelong elevated sugar consumption, and both current and future adiposity (1). With obesity looming as one of the greatest health challenges facing Americans today, it is little wonder that Cindy is concerned.

    Relatedly, the Center for Science in the Public Interest (CSPI) quotes Marion Nestle, chair of the Department of Nutrition and Food Studies at New York University, as saying, "Because sugary foods often replace more healthful foods, diets high in sugar are almost certainly contributing to osteoporosis, cancer, and heart disease" (2). Similarly, Mohammad Akhter, the executive director of the American Public Health Association stated that "Health officials must take prudent action to stem the dilution of the American diet with sugar's empty calories" (2). The CSPI offered these and other statements from a number of health experts and organizations in their petition asking the U.S. government's Food and Drug Administration (FDA) to require labeling that would specify the sugar content of beverages and processed foods. They also want the FDA to provide guidelines that will recommend a limit on daily consumption of refined sugars, just as they do with vitamins. There can be little doubt that refined sugar is an important and pervasive health threat to Americans. Certainly the reduction or exclusion of refined sugars provides no basis for legitimate criticism of Cindy's exclusion of this harmful food substance from Amy's diet.

    Cindy also wants Amy to avoid soy. Some evidence suggests that chronic ingestion of soy-derived genestein induces chromosomal imbalances in epithelial cells of human breast tissues, thereby increasing one's risk of developing breast cancer later in life (3). Further, soy, as with many other legumes, contain high concentrations of several types of anti-nutrients. Soy protein isolate, a very common processed food additive, has the highest saponin content of all legumes, at 10,600 mg/kg (4). These saponins can damage and penetrate the membranes of almost all human cell lines. This is the means by which they penetrate the intestinal mucosal barrier, enter the circulation, and damage red blood cells, inhibiting their capacity to carry oxygen (4). Soy is also very high in phytate content. Phytates bind to iron, calcium, zinc, and magnesium, forming a bond that cannot be broken by human digestive processes or enzymes. The net result is that when soy is consumed, much of the important trace minerals from other foods consumed at the same time are wasted in one's fecal matter rather than being absorbed through the gut enterocytes (5).

    The impact of soy-derived phytates alone may not be sufficient to induce deficiency in the context of a mineral-rich diet. However, children often experience trace mineral deficiencies during growth spurts, and soy consumption would serve to accentuate these deficiency states (5). Similarly, the approximately 20% of the protease inhibitors in soy that survive cooking (assuming that all soy is cooked prior to consumption) incite the pancreas to increase production and excretion of protease enzymes, particularly trypsin. This particular protease induces increased intestinal permeability. Soybean lectin also increases intestinal permeability. Both combine to cause a leaky gut and an increased risk of developing additional food sensitivities. Also, soy isoflavones impair iron metabolism (4). Clearly, there is no good reason to question Cindy's dietary choices for Amy based on her exclusion of soy.

    Cindy also wants to protect her daughter from the health hazards of cow's milk, which is both a very common allergen and has long been reported to induce iron deficiency in infants and young children (5). This latter may be the result of the high levels of bio-available calcium in milk. Calcium competes for the absorptive mechanisms that also moves, zinc, magnesium, and iron into our circulation (5). Zinc is critical to healthy function of the innate immune system. Magnesium serves in a wide range of processes that aid the healthy development of a child's body. And iron is critical to a child's intellectual development and wellbeing (5).

    Milk has also been implicated in causing or raising insulin resistance, acne, and a host of hormonal abnormalities. Some evidence suggests that these problems are caused by the hormones in cow's milk and their impact on our hormonal receptors and our own hormonal production (4). These harmful hormones from cow milk include bovine insulin, insulin-like growth factor 1, and estrogen, all of which have been shown to impact on human health (4). Further, soy and dairy proteins are both numbered among the eight most allergenic foods in the U.S. food supply, along with tree nuts and wheat (4). Cow milk allergy alone is estimated to afflict "from 2 to 3 percent of children between the ages of one and three" (4). Milk has also been implicated in some cases of asthma. Others argue that the health benefits of dairy consumption outweigh the detriments. However, "a 2007 meta analysis from the Harvard School of Public Health reported that high calcium intake had no therapeutic effect on hip fractures in 170,000 women and 68,000 men" (4) p. 102.

    Now let's look at gluten. Most research regarding the impact of a gluten free diet has only examined its impact on children with celiac disease, who almost universally benefit in learning and behavior from gluten avoidance. However, a gluten free diet has also been shown, in the context of a test group of 533 children, to improve school readiness among 100% of children with celiac disease, 86% of those with non-celiac gluten sensitivity (as measured by IgG and/or IgA antibodies against gliadin) and among at least 43% of gluten insensitive patients who attended a pediatric gastroenterology practice in New Zealand, between 2001 and 2005 (6). Others have reported, in the absence of celiac disease, significant reductions in the number and severity of learning disabilities following a six months trial of a gluten free diet (7). Still others are now reporting that non-celiac gluten sensitivity is an important clinical condition (8) and that this newly recognized clinical condition may be accompanied by consequences as dire as those found in untreated celiac disease (9). Long standing evidence, and considerable new research combine to support dietary exclusion of gluten for from 12% to 40%+ of the U.S. Population (10, 11).

    We are forced to wonder exactly which facet of the diet Cindy is trying to keep Amy on could suggest a condition of Munchausen's syndrome by proxy? This is a condition that is defined by the fabrication of symptoms or symptoms induced by the caregiver. I can understand someone who is not well versed in recent nutritional research claiming that this is a harsh and restrictive diet. However, the health benefits such a diet confers are far greater than the inconvenience it imposes. It is a completely benign diet that only offers benefit to the child. And, after repeated demonstrations that he has little regard for court orders that do not suit him, Steve now has custody of this young child, and he is blocking her mother and Amy from spending time together. That behavior alone says a great deal about just how concerned he is about the welfare of this child.

    The MSBP diagnosis is largely based on Steve's claims that he never saw any symptoms related to the foods to which Cindy believes Amy is allergic/sensitive when Amy was with him. However, in the short term it is quite likely that she did not display any signs or symptoms, especially for those symptoms caused by the opioids in gluten and dairy (12). Cindy would be dealing with the withdrawal symptoms in the first week or so after Amy returned home from a weekend with her dad, but not while being fed those opioid-containing foods (13, 14, 15).

    I understand that MSBP mothers can cause their children a great deal of harm. I also understand that such a diet would be a huge undertaking for someone like Steve, who doesn't believe in such things. However, for those of us who have experienced the miraculous improvements that come with the kind of healthy diet that Cindy is insisting on for Amy, this harmless diet only offers improved health and development. To suggest MSBP on the basis of this diet reflects a gross level of ignorance on a dietary level. It also says a great deal about the current state of Medicine and the field of Psychiatry that a practitioner could construe such a diet as suggestive of any mental illness, unless independent thinking is now a diagnostic characteristic of one of the maladies defined in the Diagnostic and Statistical Manual of Mental Disorders IV (DSM IV).

    Sources:

    1. Fiorito LM, Marini M, Francis LA,Smiciklas-Wright H,Birch LL. Beverage intake of girls at age 5 y predicts adiposity and weight status in childhood and adolescence1,2,3 Am J Clin Nutr. 2009 October; 90(4): 935–942. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2744622/ 
    2. http://www.cspinet.org/new/sugar.html
    3. Kim YM, Yang S, Xu W, Li S, Yang X. Continuous in vitro exposure to low-dose genistein induces genomic instability in breast epithelial cells. Cancer Genet Cytogenet. 2008 Oct 15;186(2):78-84. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590788/
    4. Cordain L, The Paleo Answer. Wiley & Sons. Hoboken, NJ, 2012 p. 72 -147
    5. Hoggan R, The Iron Edge . Waterside Works. Calgary, Canada. 2008.
    6. Ford R, Hoggan R, Fung T, Marini A. School readiness paper - unpublished data
    7. Blair A, Wheat-free diet gives food for thought: A school claims dyslexic children show astonishing improvements with special meals The Times, June 12, 2004 http://www.timesonline.co.uk/tol/news/uk/article444290.ece
    8. Carroccio A, Mansueto P, Iacono G, Soresi M, D'Alcamo A, Cavataio F, Brusca I, Florena AM, Ambrosiano G, Seidita A, Pirrone G, Rini GB. Non-Celiac Wheat Sensitivity Diagnosed by Double-Blind Placebo-Controlled Challenge: Exploring a New Clinical Entity. Am J Gastroenterol. 2012 Jul 24.
    9. Anderson LA, McMillan SA, Watson RG, Monaghan P, Gavin AT, Fox C, Murray LJ. Malignancy and mortality in a population-based cohort of patients with coeliac disease or "gluten sensitivity". World J Gastroenterol. 2007 Jan 7;13(1):146-51.
    10. Braly J, Hoggan R, Dangerous Grains. Penguin/Avery, NY. 2002
    11. Davis W, Wheat Belly. Rodale, NY. 2011
    12. Fanciulli G, Dettori A, Demontis MP, Tomasi PA, Anania V, Delitala G. Gluten exorphin B5 stimulates prolactin secretion through opioid receptors located outside the blood-brain barrier. Life Sci. 2005 Feb 25;76(15):1713-9. Epub 2004 Dec 20.
    13. Yoshikawa M, Takahashi M, Yang S. Delta opioid peptides derived from plant proteins. Curr Pharm Des. 2003;9(16):1325-30.
    14. Horváth K, Gráf L, Walcz E, Bodánszky H, Schuler D. Naloxone antagonises effect of alpha-gliadin on leucocyte migration in patients with coeliac disease. Lancet. 1985 Jul 27;2(8448):184-5.
    15. Schick R, Schusdziarra V. Physiological, pathophysiological and pharmacological aspects of exogenous and endogenous opiates. Clin Physiol Biochem. 1985;3(1):43-60.
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    Guest AWOL cast iron stomach

    Posted

    Ouch and a somewhere in this a little girl is dealing with much psychological stress this situation is causing her in addition to the potential allergens/sensitivities. Hmmm maybe food sensitivities run on Dad's side and they are also affecting his behavior and mood as well. What a mess. Sad, sad, mess for all involved. So based on the article am I to believe Cindy was diagnosed with MSBP without actually sitting down with the physician herself for assessment but indirect assessment ? Wow

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    Guest Cristina

    Posted

    I think this article says less about food allergy concerns than it does about the animosity between grown adult(s) during divorce. Many marriages end poorly and those involved take it out on the children to punish those on the opposite side. It's sad that this little girl is not able to see her mother. I also question how it is possible that the mother was diagnosed with MSBP without her permission or an examination by a psychiatrist? Whatever the facts of the case, it sounds like this little girl would be a pawn no matter what the circumstances. The father just latched onto the dietary restrictions as a way to have his day in court.

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    "Cindy was not allowed to defend herself". This statement is not plausible. Even in situations where the court system is totally corrupt, which definitely happens, people are allowed to defend themselves. Any competent lawyer can assure that this happens, and I do not believe that she was denied the right to a lawyer. Obviously, the diet described in the article is a healthy diet to follow and Cindy and Amy were screwed by the system, no doubt due at least partly to unscrupulous judges and lawyers. But, making such ridiculous claims makes the whole story suspect. In any case, I am not sure the point of the article. It would seem that the only constructive purpose would be to try to reverse the legal decisions so that Amy would eat a healthy diet and see her mother like children are supposed to do. But, the identities are not revealed in the article, so this worthy purpose cannot be achieved.

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    Guest Frances L. Garcia, MD

    Posted

    This is a very sad situation for the child. Probably a "good old boys" situation in which Judges and doctors allow their own personal beliefs about the proper behavior and standing of women to determine outcomes. How can Cindy not be allowed to defend herself? Where is the harm done to the child? How can a court give the father custody when he has proven time and time again that he is not trustworthy? If in doubt that Munchhausen is at work, give the child a proper shelter that is neither parent. I was diagnosed with Celiac Disease about 20 years ago. After a life time suffering from severe eczema, asthma, malabsorption, vitamin K deficiency with nosebleeds, fatigue, migraine, etc. I am leading a healthy life without gluten, and soy. My celiac disease was diagnosed via a biopsy, by the way. Any exposure to gluten makes me very ill within 4 houirs of ingestion. I avoid it like the plague it is.

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    Parents lamented that most social events involving family, friends, or organizations revolved around food.  Many extended family members don’t understand  celiac disease and the necessity of eating and living gluten free.  Attending family events was viewed as very stressful, leading to discord and arguments between parents.  Parents reported the complexity of invitations to birthday parties, especially those at pizza and fast food eateries.  Friends didn’t know how to accommodate or were fearful of making a child sick and some friendships ended.  One mother noted that it was “very lonely at first” and another stated that “disease scares people away.”  While almost all families in the study experienced these challenges at some level, others remarked at how fortunate they were to have family and friends who go out of their way to accommodate.  There are grandmothers who do gluten free baking, friends who order gluten free pizza and cake for birthday parties, and neighbors who keep gluten free snacks on hand for play dates.  
    Celiac disease was reported to bring significant changes to travel plans and destinations as well as the frequency of taking trips.  “Food issues are huge,” spontaneity is gone, and stress levels are high.  Some families don’t travel because “all the effort went into where we can eat,” while others make all travel choices based on where they can eat.  Many mothers discussed “horrible” experiences traveling and huge coolers of food that were packed.  One parent stated, “When we leave the house for a trip it’s like treading water.  I’m nervous until we get to a destination where we can eat. I try to make sure they’re full before we get in the car.”  Another indicated that “it’s more trouble than it’s worth.”  Still other families continue to travel frequently.  They plan carefully, choose accommodations with kitchens, and use gluten free apps to find restaurant options.  Some even travel world-wide to places like Australia, Trinidad, China, India, and Peru, without incident.
    Religious affiliation is also a life change affected by  celiac disease.  Church pot luck dinners and youth group snacks were mentioned as problematic, but receiving communion was the biggest challenge.  While some churches allow gluten free communion wafers, others do not.  Many parents wrestled with what decision they would make when their child was ready for first communion and some families reported that they left the church because of these issues. One family spent considerable time examining their allegiance to the Catholic faith knowing their son would not be able to fully participate.  After much soul searching the parents decided they were very devout and made the decision to follow all aspects of the church’s teachings, including forgoing birth control.  Baby number seven is on the way!
    The life changes resulting from  celiac disease affected the mothers in this study more than the fathers.  Mothers typically do more of the meal planning and preparation, grocery shopping, and child care, making them more vulnerable to the affects of gluten free eating on the family.  Mothers reported stress, depression, anger, guilt, and anxiety after their children were diagnosed.  One mother stated that she “went into mourning for months” and another reported that she was “overwhelmed” even though she is a nutritionist.  Several mothers cried during their phone interviews.  
    An unexpected life change that resulted from a child’s  celiac disease diagnosis came in the form of career changes.  Several mothers transformed or altered their careers after their children started eating gluten free.  One mother dropped her work time to twelve hours a week in order to have more time to grocery shop and cook, while another mother added part-time work to pay for gluten free food and a therapist for her son.  Two mothers entered college and became nutritionists, one opened a gluten free bakery, and one quit her job to do gluten free awareness.
    Conclusions and Recommendations for Parents
    Celiac disease brings significant life changes and challenges to children and families. Almost all the children in this study did eat gluten free, both at home and at school.  However, most children pack their lunches and only a small percentage of children have a 504 plan or IEP.   celiac disease does have an impact on children’s academic performances and experiences, especially for those children who have extreme sensitivity to gluten.  In addition, eating gluten free brings profound social challenges and life changes for children and families and the potential for mental health concerns.  Mothers, in particular, are significantly impacted by their child’s diagnosis and some experience stress, anxiety, and depression.  
    There are a number of things you as a parent can do to alleviate challenges brought on by  celiac disease and improve the quality of life for your children, yourselves, and your families.  Schools are not fully informed about  celiac disease and many children have educational, social, and dietary needs that are not being met in school settings.  The legal implications for schools who do not meet the requirements of Section 504 of the Rehabilitation Act of 1973 are many.  Become informed about Section 504 and the Individuals with Disabilities Education Act (IDEA) and request advocacy assistance when needed.  It will be important for you to learn how to advocate for your child’s safety, security, and school success.  The National Foundation for  celiac Awareness (NFCA) is a nonprofit organization that can assist by providing excellent online resources and advocacy support.  Request that accommodations, including those related to learning, academic performance, behavior, and mental health, be written into a 504 plan that is specific to your child’s needs.  Your 504 planning meeting should include all school personnel who interact with your child, including the principal, guidance counselor, nurse, classroom teachers, food service director, and cafeteria workers.  You may find yourself in the role of trainer or informant during this meeting, as many of these individuals may not have heard of  celiac disease.  Do your homework and be prepared with handouts and website addresses that cover topics such as  celiac awareness, symptoms, the risks of cross contamination, and foods to avoid. (See Appendix)
    If your child is interested in eating school lunch, request gluten free lunches that are commensurate with lunches served to typical children.   Ask for training for cafeteria staff so they can prepare a separate kitchen area with dedicated cooking utensils, appoint a staff member and alternate who will be in charge of preparing your child’s lunch, and fully understand the effects of cross contamination.  If your child chooses to pack a lunch ask for microwave access so food can be warmed at school.  Finally, request that the school store a three-day supply of gluten free food for your child in the event of an extended lockdown.  
    Your child’s safety must extend from the cafeteria into the classroom.  You can decide how you wish to share your child’s  celiac disease with the class.  Any information shared must be age appropriate.  In the elementary grades visit the classroom to talk about  celiac disease so children are well informed.  If possible, bring in a gluten free snack to share.  This is especially important if your child is being teased.  (Just be sure that the gluten free snack is especially tasty!), Children’s books are available that you can read to the class as a way to begin discussion, although most are written at a primary grade level (See Appendix).  Although some parents want to keep their child’s health issues private, sharing is critical in the case of  celiac disease because there are many things classmates can do to help keep your child safe.
    Request that gluten free classroom materials be available for your child (crayons, glue, a Play Doh substitute, cooking ingredients) and in the case of younger children, for the entire class.  The risk of contamination is great if children with  celiac disease are in a room with airborne flour or if they touch materials that have gluten and then put their hands in their mouth.  In addition, your child should never miss out on educational opportunities such as field trips, school related camps, road trip sporting events, and cooking and art projects as result of their gluten free needs.  These types of accommodations can be written into a 504 plan so you can be assured of equal educational experiences.
    Ensure that your child does not miss out on social experiences such as girl or boy scouts, church groups, birthday parties, sleepovers, and family events because they need to eat gluten free.  These experiences play a critical role in any child’s social development.  If possible, allow your child to attend such events independently, especially as he/she gets older, so he/she is able to make a successful transition to living independently.  Call in advance to see what food will be served and, if possible, replicate with gluten free versions.  Try to reassure adults who are worried that children with  celiac disease will get sick at social events that children must learn to live in a world with gluten and avoid exposure.
    Become involved in  celiac support groups with your child to ease the burden of adjusting to a new diagnosis and dealing with the day to day challenges of gluten free living.  R.O.C.K. (Raising Our  celiac Kids) has chapters in approximately 38 states and the District of Columbia and organizations such as the National Foundation for  celiac Awareness, the  celiac disease Foundation, the Gluten Intolerance Group, and the  celiac Sprue Association also provide services and support. (See Appendix)
    Consider eating more naturally gluten free foods (lean meat, fruits, vegetables, eggs, yogurt, and whole grains like quinoa) at home to reduce food costs and improve health. There is nothing innately healthy about eating products made with rice flour, tapioca flour, and potato starch.  They are low in fiber and high in calories and carbohydrates.  Anyone who says they are going on a gluten free diet to lose weight but eats gluten free pasta and pizza will be very disappointed.  
    Finally, analyze your attitude about your children’s  celiac disease and their need to eat gluten free for life.  If you are frustrated, angry, or depressed about their diagnosis they will experience those same feelings.  In this study, it was very apparent that children who demonstrated sadness, anger, or mental health symptoms were often modeling the mind-set of their parents.  In contrast, those parents who had positive attitudes about the  celiac diagnosis (e.g. my children are healthier now and growing more, there are plenty of gluten free alternatives, etc.) had children who exhibited that same upbeat outlook.
    Appendix of Resources and Children’s Literature:
    National Foundation for  celiac Awareness, Available at http://www. celiaccentral.org/About-NFCA/19/ Celiac Sprue Association, Available at http://www.csa celiacs.info/index.jsp Celiac Disease Foundation, Available at http://www.celiac.org/ Gluten Intolerance Group, Available at http://www.gluten.net/ Raising Our   celiac Kids (R.O.C.K.), Available at https://www.celiac.com/articles/563/1/ROCK-Raising-Our- celiac-Kids---National- celiac-Disease-Support-Group/Page1.html Gluten-Free Kids: Raising Happy, Healthy Children with  celiac disease, Autism, and Other Conditions by Danna Korn Incredible Edible Gluten-Free Food for Kids: 150 Family-Tested Recipes by Sheri Sanderson Bagels, Buddy, and Me: A Story about Gluten Intolerance and  celiac disease by Melanie Krumrey The  celiac Kid by Stephanie Skolmoski Cilie Yack is Under Attack: A Story About a Boy with  celiac disease by Caryn Talty Adam’s Glute Free Surprise: Helping Others Understand Gluten Free by Debbie Simpson No More Cupcakes & Tummy Aches by Jax Peters Lowell Mommy, What is  celiac disease: A Look at the Sunny Side of Being a Gluten-Free Kid by Katie   Chalmers Eating Gluten-Free with Emily: A Story for Children with  celiac disease by Bonnie J. Kruszka

    Kay A. Chick, Ed.D.
    Celiac.com 11/15/2016 - Do you know someone who has lived with celiac disease for over eighty years? Someone who lived on nothing but mashed bananas for a year? Someone who continued to eat gluten for over 30 years because doctors didn't know how to treat a celiac diagnosis? Someone who experienced serious physical, emotional, and family challenges as a result? Well, I met such an individual at the International Celiac Symposium in Chicago in the fall of 2013. Clara (a pseudonym) attended my poster session, The Educational, Social, and Family Challenges of Children with Celiac Disease: What Parents Should Know. As she stood before my poster with tears in her eyes she began to say, "This is me. This is me." Through a brief conversation then, and several lengthy telephone interviews that followed, she shared her incredible story with me and gave me permission to share it with you.
    Clara was born in 1933 on a citrus ranch in California and was the youngest of five children. She was very sick as a baby with what her family thought was a "terrible case of the flu." She lost muscle tone, had wrinkly skin, and some mornings she didn't move or even open her eyelids without the help of her mother. She looked malnourished and had a distended stomach. When she was two, her parents took her to Dr. Victor E. Stork, but he was not sure what the problem might be. A few weeks later, the doctor attended a conference where he described Clara's symptoms. He learned of another child with similar symptoms who had been diagnosed with celiac disease and fed nothing but mashed bananas. After Dr. Stork informed Clara's parents, Clara's father purchased a big hook and drove to the Long Beach docks to buy bananas. He hung bunches of bananas on their back porch to ripen and she was fed nothing but mashed bananas for over a year. What started as half a teaspoon at a time quickly grew until she was eating many bananas each day. This part of Clara's story greatly intrigued me, as I had just read the research of Sidney Haas. In the 1920s Hass successfully treated eight children who were "anorexic" from celiac disease with the banana diet while untreated children did not survive (Guandalini, 2007).
    Growing up, Clara was a happy child but had no appetite and didn't enjoy food. She was very small for her age and, at times, was made to stay at the dinner table until she ate everything on her plate. Clara's mother, a practical nurse, thought she might be allergic to fat. The family kept a quarter of a beef in a freezer locker 25 miles away and her mother scraped the fat off the beef before giving it to Clara. She was also made to finish her breakfast, typically oatmeal, toast, and orange juice, before going to school in the morning. Clara routinely had vomiting and diarrhea each morning, and didn't understand why this didn't happen to other children. She missed school often because she had abdominal discomfort and was weak. Clara hid in the girls' restroom during recess and physical education so she wouldn't have to participate. Since she was unsuccessful at athletics she found it easier to sit on a toilet with her feet pulled up so no one would see her.
    Clara continued to miss a great deal of school but was required to do her school work at home. During second grade she worked ahead, completing both second and third grade work. Consequently, she was allowed to skip third grade, which only accentuated her small size. When she entered high school people thought she was in third or fourth grade. After entering puberty at age 14 she finally acquired an appetite and began to grow much taller. At this point in her life, Clara decided that she would never be sick again. She graduated from high school in 1950, after acting in dramatic productions, serving as president of the Girls' League, and planning the ten year class reunion.
    Clara married at age twenty, between her junior and senior years in college. She had few symptoms during this time and was hired as a kindergarten teacher. Her husband was drafted and she taught in several different places on the west coast while he was in the service. During this time, Clara had a baby girl followed by two miscarriages. Three weeks after the birth of their second child Clara became very ill and lost her hair. They had no insurance and she lost a dramatic amount of weight. She weighed only 80 pounds and her husband had to carry her from the bed to the couch. The vomiting and diarrhea got worse and her mother had to take care of her babies. She was on heavy doses of medication and her doctors thought her gastrointestinal problems "were all in her head."
    Clara's speech became "jumbled" and she was not making sense. Her doctor sent her to a psychiatrist who placed her in a "sanitarium." She was hospitalized for several months where she felt very isolated and alone. Her relatives weren't told where she was and her father would not allow her mother to visit her. At the sanitarium Clara received shock treatments every three days, ten in all. Her sister offered her son's college fund to pay the sanitarium bill so that Clara would be allowed to leave.
    When Clara returned home she found she had lost much of her memory. She didn't remember how to hold a knife and her daughter, who was three, taught her how to tie her shoes. She was on sedatives and slept much of the time. She does not know how she took care of her children during this time. Clara and her husband had little money, so she took in ironing and taught preschool. It took them twelve years to pay off the hospital bills.
    It was fifteen years after this experience, and two babies later, that Clara finally got treatment for her celiac disease. She was hospitalized at UCLA Medical Center for a month while more tests and an intestinal biopsy were completed. It was 1972, and she was now 39 years old. The gastroenterologist finally confirmed the diagnosis of celiac disease and told her that she would never be able to eat pie, bread, or cake ever again. Clara was so thrilled that it was "just food" that would make a difference and not cancer. The doctor told her that there was no reason why she was still alive. Within two months she was noticing a difference and had gained weight. Clara was able to go back to teaching part-time and started teaching full-time in 1981.
    After her celiac diagnosis Clara did her best to avoid grains completely. One doctor told her to eat wheat germ, a product she clearly was correct in avoiding. In the 1970s she tried to make bread with rice, but her attempts were very unsuccessful. Clara started a support group in 1984 which was part of the Celiac Sprue Association. Little by little the group started receiving information on eating gluten-free, as many of these foods were readily available in Europe. By 1988 there were some gluten-free foods available in California. Clara experimented with cooking and breads and tested recipes for Carol Fenster's cookbooks. Her household today is totally gluten-free, with the exception of a loaf of bread for her husband. She and her husband traveled extensively after their retirement, visiting every state except Hawaii, along with the Caribbean and Australia.
    As far as lessons learned, Clara believes that people should listen to each other. She says, "If a person says, I feel horrible, someone should listen. The medical profession didn't listen to me. They said it was all in my head. If they had listened I could have been helped." It is unfortunate that her doctors didn't listen, as Clara could have been diagnosed much sooner. Willem-Karel Dicke first published an article on the importance of a gluten-free diet for the treatment of celiac disease in 1941 (Berge-Henegouwen & Mulder, 1993).
    Since my own celiac diagnosis came within two months of the onset of symptoms, I marvel at how someone could live for 39 years while still eating gluten. I think about the lessons to be learned from Clara's story. I consider the advancements that have been made in the diagnosis and treatment of celiac disease and the ease with which I'm able to eat gluten-free. And I send a reminder of the importance of early detection and the physical and emotional consequences that individuals like Clara face when a celiac diagnosis is delayed.
    References:
    Guandalini, S. (2007). A brief history of celiac disease. Impact, 7, (3), 1-2. Van Berge-Henegouwen, G. P., & Mulder, C.J. (1993). Pioneer in the gluten-free diet: Willem-Karel Dicke 1905-1962, over 50 year of gluten-free diet. Gut, 34, 1473-1475.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 01/24/2017 - Diabetes is a condition in which blood glucose rises high enough to cause: damage to blood vessel walls, neurological injury, vision loss, and a host of other maladies. Most currently recognized cases of diabetes fall into one of two categories which are identified as type 1 and type 2 diabetes. While these two types of diabetes share many symptoms, the underlying causes are, in most cases, quite distinct, although there is also some overlap which will be explored shortly. There are also cases of gestational diabetes and some researchers are now suggesting that type 3 diabetes may be yet another entity that causes accelerating cell death in the brain, resulting dementia (1) but these latter two types of this condition are not included in the current discussion.
    All but one of these forms of diabetes involves cellular resistance to the action of insulin, although there is some gray area between type 1 and type 2 diabetes. Type 1 diabetes is the result of an autoimmune attack on a specific group of pancreatic cells called islets of Langerhans. These are the cells that produce insulin, a hormone that moves glucose out of the bloodstream and into various cells. About 14% of type 2 diabetics are also thought to experience a late-onset, slowly developing damage to pancreatic islet cells, which results in reduced insulin production in combination with their insulin resistance(2). This may be caused by autoimmunity, similar to type 1 diabetes, or it may be damage induced by other factors. Nonetheless, while type 2 diabetes can often be controlled either during weight loss or by reduced carbohydrate consumption alone, type 1 diabetes is not typically viewed as a condition that can be remedied by a change in eating habits. Yet there are some hints in the literature suggesting that dietary interventions may be therapeutically useful, especially if begun early enough in the disease process.
    Researchers Amanda MacFarlane and Fraser Scott report that there are several environmental factors, including specific foods, as well as viral, bacterial, and chemical agents that have been hypothesized to incite an autoimmune attack on the islet cells (2). They also report that about half of the animals that develop type 1 diabetes are mounting an immune response to wheat, which may also be involved in the attack on the insulin producing cells of the pancreas by either or both of two pathways they outline (2, 3). These hypothesized biological processes are identified as molecular mimicry or bystander activation and cell death. While these authors favor bystander activation, either or both of these pathways may lead to an autoimmune attack on pancreatic islet cells. Regardless of the specific biological route, type 1 diabetes can be induced in a significant portion of genetically susceptible rats and mice, simply by feeding them a diet dominated by wheat gluten. Further, the severity of their disease varies directly with the proportion of wheat gluten in the diet (2). These investigators go on to say that "These similarities between coeliac disease in humans and diabetes in BB rats, NOD mice and type 1 diabetic patients are consistent with the idea that wheat is involved in diabetes pathogenesis, possibly by inducing a subclinical, gut inflammation in many individuals that develop this form of diabetes" (2).
    They go on to report that: "Our data suggest that dietary modulation has effects at two (or more) levels:
    At the target cells before classic insulitis, changing the growth pattern of insulin-producing cells, enhancing islet mass and changing metabolism and insulin reserves . Dampening an ongoing inflammatory condition in the gut." (2)
    Scott's work (4, 5) along with investigations conducted by several groups of his colleagues (6-10) indicate that significant numbers of diabetes patients show immune reactions to the prolamins which are storage proteins in wheat, rye, and barley. Further, investigators have long understood that there is significant overlap between celiac disease and type 1 diabetes, with estimates ranging between 5% and 12% in each disease group (2, 11). MacFarlane and Scott point out that 33% to 40% of patients with type 1 diabetes show transglutaminase autoantibodies which are similar to those found in celiac patients but usually at lower levels (2).
    Low concordance rates in monozygotic (identical) twins also suggest that environmental factors play a large role in causing type 1 diabetes (2). Again, the most compelling evidence indicates that dietary consumption of wheat gluten and similar prolamins is an important factor in the autoimmune attack that destroys the pancreatic capacity to produce insulin, in genetically susceptible individuals.
    Indirect support for this perspective is offered by animal research published in July of 2011. It shows that gamma-Aminobutryic acid (GABA) supplements not only inhibit the autoimmune attack on islet cells, GABA also incites regeneration of insulin producing cells (12). GABA is a non-toxic substance that is produced by the beta cells of the pancreas (13). It plays an inhibitory role throughout the nervous system which may be significant when taken in conjunction with Rodney Ford's identification of gluten as the agent which, directly and indirectly, induces neurological damage in those with celiac disease and those with non-celiac gluten sensitivity. One pathway Ford identifies is gluten-induced neuronal excitation leading to cellular self-destruction. In light of Ford's hypothesis, the inhibitory role of GABA on neuronal tissues, both at and near synapses, offers an inviting new window for envisioning the process that incites, and therefore may reverse, type 1 diabetes.
    Clearly there is considerable cause to suspect gluten grain consumption as an important factor in the onset and perpetuation of many cases of type 1 diabetes. While genetically coded HLA markers predispose to the disease, and a number of other environmental factors may play a role in its pathogenesis, prolamins from wheat and its close relatives are clearly a frequent and important contributor to this life-long condition in which exogenous insulin (injection with hypodermic needles) is necessary for maintaining optimal health (12) while living with this malady. However, given the insights offered by the above, the following case history may offer insights that might otherwise incite only scepticism. MacFarlane and Scott suggest the following: "One approach to achieving this [prevention] is to understand and modify the environmental factors that induce disease or equip those at risk with better means of avoiding or handling these agents"(2).
    Case Study:
    On January 18, 2008, three year old K and her anxious mother were taken to a hospital emergency department in Gilbert, AZ, where the attending physician concluded that the child had experienced a febrile seizure of about 5 minutes' duration. At examination, she had a 102.5 degree temperature. In addition to fevers, K complained of abdominal pain and showed abdominal bloating. During this examination of K, she vomited. Laboratory tests showed elevated glucose (133 mg/dl) and an elevated white blood cell count (19,000). Tylenol was used to bring K's temperature down and she was discharged with instructions for the parents to administer more Tylenol as needed, and to follow up with her regular health care provider within two days.
    By February 29, K experienced more fevers, ranging between 101 and 104, intermittently over 24 hours. Every four hours, when the effects of the previous dose of Tylenol wore off, the fever would, again, spike to 103-104. K was taken to see her regular physician the following day and urinalysis revealed ketone bodies. K and her parents were then sent to the emergency department of Banner Children's Hospital.
    At the hospital, testing showed elevated urinary ketone bodies in the Large category, and blood showed elevated glucose at 193 mg/dL. Type 1 diabetes was diagnosed and K was admitted to hospital where she stayed for four days. Her condition was stabilized with ½ unit of Novalog and 4 units of Lantus. Meanwhile parents were educated about type 1 diabetes, insulin measurement and injection. They were taught to inject 1 unit of insulin for every 20 grams of carbohydrates consumed (20:1 ratio). K's parents repeatedly wondered, in the presence of the diagnosing endocrinologist, just how much insulin K was producing and how many carbohydrates a thirty pound child needed to be healthy? *
    K's father has a history of joint pain when consuming gluten grains. K was still experiencing abdominal bloating and because of the overlap between type 1 diabetes and celiac disease (2) serum IgA antibody tests were undertaken and both transglutaminase and gliadin antibody tests were negative. However, the parents observed that variations in the types of food K ate seemed to have a greater impact on blood glucose than a specific food's putative sugar content.
    In keeping with their observations that different foods, despite their equal sugar content, produced different blood glucose results, the father's history of joint pain when eating gluten, K's abdominal bloating, and the widely documented connection between gluten grains and type 1 diabetes, these foods and several others were eliminated from her diet.
    K's parents were quickly able to adjust the insulin therapy to a 40:1 ratio while K typically maintained a blood glucose range of between 80 and 95 mg/dl, which is well within the reference range for a healthy, non-diabetic person. In fact, this is a far narrower range than is prescribed by the American Diabetes Association which is 70-120 mg/dl for diabetic patients. K's family continued to target and achieve the 80-95 mg/dl range.
    After a few months of lower than normal blood sugars, still on insulin therapy, with the carbohydrate ratio now 40/1, the parents sought permission from the endocrinologist to take K off insulin completely, on the condition that her blood sugar continued within the normal range of 85-95 mg/dl. This was monitored on a daily basis. The first 24 hours were a success and another day was granted.
    After six months of following a strict and intense food therapy diet for K, the family started reintroducing foods. Some foods were reintroduced without a rise in blood sugar. She was also able to eat a larger amount of carbohydrate each meal with the same blood sugar control. Clearly, the pancreas was producing increasing quantities of insulin.
    On August 21, 2008, six months into this intensive and individualized food therapy, the patient's blood test results indicated a regeneration of the pancreas and a complete reversal of her type 1 diabetes. Her A1C was 4.8, well within the normal range for a non-diabetic person.
    Today, more than three years later, the patient is still insulin free and is using food therapy alone to maintain healthy and normal glucose control. Signs of pancreatic inflammation were also absent. Each of these findings echo MacFarlane and Scott on the issue of dietary intervention in animal studies.
    The intensive food therapy has now been replaced with a maintenance program. The variety of foods the patient can eat is vast. However, grain and casein continue to be avoided. It appears that, in this case, these foods may have contributed to K's Type 1 diabetes. It may also be that the underlying cause of the fever K experienced early in this process was a factor in the onset of her type 1diabetes, and the transient nature of this fever, and its cause, may be at the root of her recovery from this ailment. Nonetheless, given the many converging research findings indicting grains and dairy proteins, along with K's suggestive signs and symptoms, and her father's reactions to gluten, continued avoidance of these foods seems a more likely explanation.
    Thoughtful readers may also wonder just how much insulin K was producing, at the time of her diagnosis, and just how many carbohydrates a thirty pound child needs to be healthy? It may be that GABA supplements and other chemical miracles will be unnecessary for large numbers of children who suffer from type 1 diabetes. Perhaps early diagnosis and permanent dietary adjustments will be what is needed to facilitate complete recovery for many, perhaps most, children afflicted by this insidious condition. Perhaps this case history will provide the necessary impetus to encourage undertaking controlled studies of dietary factors early in the disease process of type 1 diabetes.
    * While there are no carbohydrates that are essential to good health, there are essential amino acids and essential fats.
    Sources:
    de la Monte SM, Wands JR. Alzheimer's disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol. 2008 Nov;2(6):1101-13. http://www.medicine.uottawa.ca/Students/MD/BlockOrientation/assets/documents/e_inf_week05.pdf http://www.elements4health.com/type-1-diabetes-patients-have-immune-response-to-wheat-proteins.html Scott FW, Sarwar G, Cloutier HE. Diabetogenicity of various protein sources in the diet of the diabetes-prone BB rat. Adv Exp Med Biol 1988; 246: 277–85. Scott F. Dietary initiators and modifiers of BB rat diabetes. In:Shafrir E, Renold AE, eds. Frontiers in Diabetes Research:Lessons from Animal Diabetes. London: Libbey, 1988: 34–9. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr 1993; 69: 597–607. Funda DP, Kaas A, Bock T, Tlaskalova-Hogenov H, Buschard K. Gluten-free diet prevents diabetes in NOD mice. Diabetes Metab Res Rev 1999; 15: 323–7. Bao F, Yu L, Babu S et al. One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies. J Autoimmun 1999; 13:143–8. Lampasona V, Bonfanti R, Bazzigaluppi E et al. Antibodies to tissue transglutaminase C in type I diabetes. Diabetologia 1999; 42: 1195–8. Pocecco M, Ventura A. Coeliac disease and insulin-dependent diabetes mellitus: a causal association? Acta Paediatr 1995; 84: 1432–3. Hansen D, Brock-Jacobsen B, Lund E, Bjørn C, Hansen LP, Nielsen C, Fenger C, Lillevang ST, Husby S. Clinical Benefit of a Gluten-Free Diet in Type 1 Diabetic Children With Screening-Detected Celiac Disease A population-based screening study with 2 years' follow-up Diabetes Care 29:2452-2456, 2006 Soltani N, Qiu H, Aleksic M, Glinka Y, Zhao F, Liu R, Li Y, Zhang N, Chakrabarti R, Ng T, Jin T, Zhang H, Lu WY, Feng ZP, Prud'homme GJ, Wang Q. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes.Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11692-7. Epub 2011 Jun 27. Bouzane B, Postmedia News June 28, 2011 Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/30/2017 - Dear attending physician:
    If you are reading this it is because your patient either expects you to refuse or you have refused to test them for celiac disease. You may believe, in keeping with prior training, that this patient does not display the signs or symptoms associated with celiac disease. However, the symptom complex of celiac disease has recently undergone dramatic changes, beginning with the understanding that celiac disease is a systemic, rather than an intestinal ailment. World renowned researchers have weighed in on this issue, with peer reviewed reports that repeatedly establish the protean manifestations of celiac disease. They defy prior algorithms for symptom assessment toward diagnosing celiac disease. In the past, undiagnosed celiac patients were often identified as asymptomatic because their symptoms were simply not diarrhea, abdominal bloating, and muscle wasting. However, the Celiac Disease Center at the University of Chicago lists more than 300 presenting symptoms of celiac disease (1). The same group also offers a list of symptoms that demonstrate the wide range of apparently unrelated symptoms that can indicate celiac disease, only the first two of which represent these classical symptoms (2).
    Recurring abdominal bloating and pain Chronic or recurrent diarrhea Constipation Nausea or emesis Liver and biliary tract disorders (increased serum transaminases, primary sclerosing cholangitis) Weight loss Pale, foul-smelling stool Iron-deficiency anemia unresponsive to iron therapy Fatigue Failure to thrive or short stature Delayed puberty Arthralgia Tingling numbness in the legs Pale sores inside the mouth Dermatitis herpetiformis Abnormal dentition (tooth discoloration, loss of enamel) Unexplained infertility or recurrent miscarriage Osteopenia or osteoporosis Peripheral neuropathy Psychiatric disorders (anxiety or depression) Please remember that any one or more of the above symptoms and/or ailments may indicate untreated celiac disease, so testing for celiac disease is an important, inexpensive step toward assisting a patient to resolve these troubling, sometimes debilitating, symptoms.
    Overweight and obesity may also indicate underlying celiac disease. Today's affluence and accompanying food surpluses permit people who are not absorbing nutrients efficiently to eat enough to more than compensate for otherwise calorically deficient diets. Thus, only a minority of celiac disease cases present with classical symptoms in most of the first world. In fact, some reports indicate that overweight patients with celiac disease are as common as those who are underweight ( 3, 4, 5). This is why researchers have long employed the iceberg metaphor to describe the mass of people with celiac disease. The vast majority these people with celiac disease remain undiagnosed (6). Until sensitive and specific serological screening tools became available, very few cases were diagnosed and celiac disease was erroneously considered rare.
    In addition to alleviating quite a lot of human suffering, early detection offers some rather large economies for the health care system, as many of the more serious ailments that often befall those with untreated celiac disease may be averted through these inexpensive serological tests and subsequent prescription of a strict gluten free diet.
    Prior to the therapeutic use of a gluten free diet, mortality was reported at 36% among 73 children with celiac disease (7). Admittedly, it is likely that these were the more serious cases and perhaps some cases of misdiagnosis. However, even as recently as 1989, adult celiac patients experienced almost double the early mortality rate seen in the general population (8), so an early diagnosis and treatment of celiac disease is not just helpful in mitigating current symptoms, it is a powerful form of preventive medicine that is coincidental to the appropriate diagnosis and treatment of celiac disease.
    Let me expand on that last comment a little further. Chronic depression (9), ADHD (10), neurological (11) and neuromuscular disorders(12) treatment-resistant iron deficiency (13, 14), impaired lung function (15, 16) a variety of lymphomas including B cell and T cell (17, 18, 19) and adenocarcinomas (20, 21) dental enamel defects (22, 23) autoimmune thyroid disease (24, 25 ) autoimmunity in general (26) type 1 diabetes (27, 28) kidney disease (29) liver disease (30, 31) skin disease (32, 33) seizure disorders (34) gait disorders (35) obesity (36) fatigue (37) anxiety (38) infertility (39) osteoporosis (40) learning disorders (41, 42) aphasia (43) and many more such sequels to untreated celiac disease (44) impose an enormous economic burden on our health system and education system. This burden weighs on most levels of government, private insurance companies, families, and individuals. Much of this unnecessary cost is ultimately passed along to taxpayers and/or are incorporated into insurance premiums. We all pay.
    And the human costs are even greater. Attention deficits and learning disabilities impose life-long inhibitions on success and are corrosive to self esteem. Depression robs us of individual, economic and social achievements, as well as denying us the day-to-day pleasures of life. Similarly, anxiety and infertility are socially isolating and heartbreaking, each in their own ways. Neurological and seizure disorders, including gait disorders, can inhibit our mobility and/or our safe function in this increasingly complex and fast-paced society. Impaired lung function can prohibit or interfere with normal, desirable activities ranging from pleasant walks, sports, and even having sex. Lymphomas and adenocarcinomas can have rapidly fatal consequences. The individual and familial consequences are often devastating. Type 1 diabetes tethers us to insulin injections and requires that we maintain a careful balance between carbohydrate intake and insulin injections. The challenges of this diet dwarfs the inconvenience of a gluten free diet, and a late celiac diagnosis may require that some people comply with both sets of dietary constraints. Skin disease can also exact an enormous social toll, and this is ignores the discomfort and embarrassment of constant itching and scratching, as well as the pain associated with the most common skin diseases connected to celiac disease. Similarly, obesity is not only socially excluding, it poses its own sets of health hazards and life shortening penalties. As osteoporosis becomes more and more common, we can see that society's increasing nutritional dependence on gluten grains may well have set the stage for this degenerative condition, often requiring painful and expensive joint replacement surgeries as our bones gradually crumble and shrink. The dramatic loss of our ability to produce intelligible speech, called aphasia, is by no means the least of this list. The horrific nightmare of being unable to speak to others and have them understand us has been the lived experience of at least one individual. His speech slowly returned after his celiac diagnosis and some time on a gluten free diet. Too many of us are not so lucky.
    Many of us see ourselves, and our symptoms, in the many posts, blog comments, listservs and websites that discuss celiac disease. Yet outdated medial training can create barriers to patients seeking testing. However, given the above, peer reviewed data and expert opinions, it is difficult to imagine any reasonable argument for refusing to test a patient who requests serological testing for celiac disease. The cost is minimal and the potential benefits to those who are diagnosed, and our society, are enormous.
    Current data suggest a prevalence of celiac disease in the general population at somewhere around 1%, based on serological testing for selective antibodies. However, newly emerging data suggest that a portion of the population that is at least six or seven times the size of the group with celiac disease mounts an innate immune response to gluten grains. The careful characterization of one pathway for activating intestinal inflammation by non-gluten components of these grains, leaves open the possibility of "gliadin-dependent signaling pathways that still remain to be characterized" (45).
    Other forms of non-celiac gluten sensitivity, as signaled by IgG class antibodies against gliadin, are seen in 10% to 12% of the general population. Whether these segments of the population with non-celiac gluten sensitivity overlap or are distinct has yet to be determined, so it remains unclear whether they form 10% of our population, or as much as 19% of our culture. Finally, based on a new book by the world renowned pediatric gastroenterologist and allergist, Dr. Rodney Ford, titled Gluten: Zero Global, there is considerable evidence to suggest that, with their many other anti-nutrient, addictive, allergenic, and blood-glucose altering features, gluten grains are a questionable macronutrient food source for humans (46).
    Thus, testing for non-celiac gluten sensitivity, may offer many of the benefits that testing for celiac disease offers. Your patient and I are asking that you heed the above data from your professional literature and the first dictum of your profession, by 'first doing no harm', and ordering testing for celiac disease and non-celiac gluten sensitivity.
    Sincerely,
    Dr. Ron Hoggan, Ed. D.
    Sources:
    1. http://www.cureceliacdisease.org/wp-content/uploads/2011/09/CDCFactSheets10_SymptomList.pdf
    2. http://www.cureceliacdisease.org/medical-professionals/guide/symptoms
    3. Dickey W, Kearney N. Overweight in celiac disease: prevalence, clinical characteristics, and effect of a gluten-free diet. Am J Gastroenterol. 2006 Oct;101(10):2356-9
    4. Tucker E, Rostami K, Prabhakaran S, Al Dulaimi D. Patients with coeliac disease are increasingly overweight or obese on presentation. J Gastrointestin Liver Dis. 2012 Mar;21(1):11-5
    5. Cheng J, Brar PS, Lee AR, Green PH. Body mass index in celiac disease: beneficial effect of a gluten-free diet. J Clin Gastroenterol. 2010 Apr;44(4):267-71.
    6. Katz KD, Rashtak S, Lahr BD, Melton LJ 3rd, Krause PK, Maggi K, Talley NJ, Murray JA. Screening for celiac disease in a North American population: sequential serology and gastrointestinal symptoms. Am J Gastroenterol. 2011 Jul;106(7):1333-9. doi: 10.1038/ajg.2011.21. Epub 2011 Mar 1.
    7. Hardwick C. 1989, as described in Holmes GKT. Non-malignant complications of coeliac disease. Acta Paediatr Suppl. 412: 68-75. 1996.
    8. Logan RF, Rifkind EA, Turner ID, Ferguson A. Mortality in celiac disease. Gastroenterology. 1989 Aug;97(2):265-71.
    9. Zipser RD, Farid M, Baisch D, Patel B, Patel D. Physician awareness of celiac disease: a need for further education. J Gen Intern Med. 2005 Jul;20(7):644-6.
    10. ADHD (10),Niederhofer H. Association of attention-deficit/hyperactivity disorder and celiac disease: a brief report. Prim Care Companion CNS Disord. 2011;13(3).
    11. neurological and neuromuscular disorders (11, 12,) Currie S, Hadjivassiliou M, Clark MJ, Sanders DS,
    12. Wilkinson ID, Griffiths PD, Hoggard N. Should we be 'nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-1221.
    13. Hadjivassiliou M, Chattopadhyay AK, Davies-Jones GA, Gibson A, Grünewald RA, Lobo AJ. Neuromuscular disorder as a presenting feature of coeliac disease. J Neurol Neurosurg Psychiatry. 1997 Dec;63(6):770-5.
    14. Fayed SB, Aref MI, Fathy HM, Abd El Dayem SM, Emara NA, Maklof A, Shafik A.
    Prevalence of celiac disease, Helicobacter pylori and gastroesophageal reflux in patients with refractory iron deficiency anemia. J Trop Pediatr. 2008 Feb;54(1):43-53.
    15. Cekın AH, Cekın Y, Sezer C. Celiac disease prevalence in patients with iron deficiency anemia. Turk J Gastroenterol. 2012 Oct;23(5):490-5.
    16. Robertson DA, Taylor N, Sidhu H, Britten A, Smith CL, Holdstock G. Pulmonary permeability in coeliac disease and inflammatory bowel disease. Digestion. 1989;42(2):98-103.
    17. Edwards C, Williams A, Asquith P. Bronchopulmonary disease in coeliac patients. J Clin Pathol. 1985 Apr;38(4):361-7.
    18. Bautista-Quach MA, Ake celiac disease, Chen M, Wang J. Gastrointestinal lymphomas: Morphology, immunophenotype and molecular features. J Gastrointest Oncol. 2012 Sep;3(3):209-25.
    19. Leslie LA, Lebwohl B, Neugut AI, Gregory Mears J, Bhagat G, Green PH. Incidence of lymphoproliferative disorders in patients with celiac disease. Am J Hematol. 2012 Aug;87(8):754-9.
    20. Elfström P, Granath F, Ekström Smedby K, Montgomery SM, Askling J, Ekbom A, Ludvigsson JF. Risk of lymphoproliferative malignancy in relation to small intestinal histopathology among patients with celiac disease. J Natl Cancer Inst.2011 Mar 2;103(5):436-44.
    21. Benhammane H, El M'rabet FZ, Idrissi Serhouchni K, El Yousfi M, Charif I, Toughray I, Mellas N, Riffi Amarti A, Maazaz K, Ibrahimi SA, El Mesbahi O. Small bowel adenocarcinoma complicating coeliac disease: a report of three cases and the literature review. Case Rep Oncol Med. 2012;2012:935183.
    22. Vecchio R, Marchese S, Gangemi P, Alongi G, Ferla F, Spataro C, Intagliata E. Laparoscopic treatment of mucinous adenocarcinoma of jejunum associated with celiac disease. Case report. G Chir. 2012 Apr;33(4):126-8.
    23. El-Hodhod MA, El-Agouza IA, Abdel-Al H, Kabil NS, Bayomi KA. Screening for celiac disease in children with dental enamel defects. ISRN Pediatr. 2012;2012:763783.
    24. Erriu M, Sanna S, Nucaro A, Orrù G, Garau V, Montaldo C. HLA-DQB1 Haplotypes and their Relation to Oral Signs Linked to Celiac Disease Diagnosis. Open Dent J. 2011;5:174-8.
    25. Cats EA, Bertens AS, Veldink JH, van den Berg LH, van der Pol WL. Associated autoimmune diseases in patients with multifocal motor neuropathy and their family members. J Neurol. 2012 Jun;259(6):1137-41.
    26. Bardella MT, Elli L, De Matteis S, Floriani I, Torri V, Piodi L. Autoimmune disorders in patients affected by celiac sprue and inflammatory bowel disease. Ann Med. 2009;41(2):139-43
    27. Nass FR, Kotze LM, Nisihara RM, de Messias-Reason IT, Utiyama SR. Autoantibodies in relatives of celiac disease patients: a follow-up of 6-10 years. Arq Gastroenterol. 2012 Jul-Sep;49(3):199-203.
    28. Saadah OI, Al-Agha AE, Al Nahdi HM, Bokhary RY, Bin Talib YY, Al-Mughales JA, Al Bokhari SM. Prevalence of celiac disease in children with type 1 diabetes mellitus screened by anti-tissue transglutaminase antibody from Western Saudi Arabia. Saudi Med J. 2012 May;33(5):541-6.
    29. Van den Driessche A, Eenkhoorn V, Van Gaal L, De Block C. Type 1 diabetes and autoimmune polyglandular syndrome: a clinical review. Neth J Med. 2009 Dec;67(11):376-87.
    30. Welander A, Prütz KG, Fored M, Ludvigsson JF. Increased risk of end-stage renal disease in individuals with coeliac disease. Gut. 2012 Jan;61(1):64-8.
    31. Drastich P, Honsová E, Lodererová A, Jarešová M, Pekáriková A, Hoffmanová I, TuÄková L, Tlaskalová-Hogenová H, SpiÄák J, Sánchez D. Celiac disease markers in patients with liver diseases: A single center large scale screening study. World J Gastroenterol. 2012 Nov 21;18(43):6255-62.
    32. Massironi S, Rossi RE, Fraquelli M, Bardella MT, Elli L, Maggioni M, Della Valle S, Spampatti MP, Colombo M, Conte D. Transient elastography in patients with celiac disease: a noninvasive method to detect liver involvement associated with celiac disease. Scand J Gastroenterol. 2012 Jun;47(6):640-8
    33. Caproni M, Bonciolini V, D'Errico A, Antiga E, Fabbri P. Celiac disease and dermatologic manifestations: many skin clue to unfold gluten-sensitive enteropathy. Gastroenterol Res Pract. 2012;2012:952753.
    34. Criado PR, Criado RF, Aoki V, Belda W Jr, Halpern I, Landman G, Vasconcellos C. Dermatitis herpetiformis: relevance of the physical examination to diagnosis suspicion. Can Fam Physician. 2012 Aug;58(8):843-7.
    35. Maniar VP, Yadav SS, Gokhale YA. Intractable seizures and metabolic bone disease secondary to celiac disease. J Assoc Physicians India. 2010 Aug;58:512-5.
    36. Hadjivassiliou M, Grünewald R, Sharrack B, Sanders D, Lobo A, Williamson C, Woodroofe N, Wood N, Davies-Jones A. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain. 2003 Mar;126(Pt3):685-91.
    37. Balamtekin N, Demir H, Baysoy G, Uslu N, Yüce A. Obesity in adolescents with celiac disease: two adolescents and two different presentations. Turk J Pediatr. 2011 May-Jun;53(3):314-6.
    38. Greenfield JR, Samaras K. Evaluation of pituitary function in the fatigued patient: a review of 59 cases. Eur J Endocrinol. 2006 Jan;154(1):147-57
    39. Smith DF, Gerdes LU. Meta-analysis on anxiety and depression in adult celiac disease. Acta Psychiatr Scand. 2012 Mar;125(3):189-93.
    40. Choi JM, Lebwohl B, Wang J, Lee SK, Murray JA, Sauer MV, Green PH. Increased prevalence of celiac disease in patients with unexplained infertility in the United States. J Reprod Med. 2011 May-Jun;56(5-6):199-203.
    41. Rastogi A, Bhadada SK, Bhansali A, Kochhar R, Santosh R. Celiac disease: A missed cause of metabolic bone disease. Indian J Endocrinol Metab. 2012 Sep;16(5):780-5
    42. 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.
    43. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6.
    44. 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.
    45. Norström F, Sandström O, Lindholm L, Ivarsson A. A gluten-free diet effectively reduces symptoms and health care consumption in a Swedish celiac disease population. BMC Gastroenterol. 2012 Sep 17;12:125
    46. Junker Y, Zeissig S, Kim SJ, Barisani D, Wieser H, Leffler DA, Zevallos V, Libermann TA, Dillon S, Freitag TL, Kelly CP, Schuppan D. Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4. J Exp Med. 2012 Dec 17;209(13):2395-408
    47. Ford R. Gluten: Zero Global. YfoodX Ltd. Christchurch, New Zealand. 2012.

    Eleanore Dara
    Celiac.com 09/22/2017 - Misdiagnosed my sophomore/ junior year of High School, 3 years ago, with celiac disease, I became obsessed with the science of this ailment and how it was supposedly affecting me. I was shocked by how little is known about this autoimmune disease and the many gaps in research done on it. One such gap is that of cross-contamination in the household, where it is likely to have a daily impact on those following gluten-free diets. Because of this, I decided to help fill this gap in scientific knowledge with a manageable project based on cross-contamination in the home, asking whether one can share common kitchen cookware that is used with gluten containing foods, or if people, to help maintain a gluten-free diet, need designated ones for their food preparation.
    Either way that this research played out would be beneficial to the gluten-free community. For example, some families with members on gluten-free diets will spend a lot of money to buy all new ‘gluten-free' designated cookware and utensils to help minimize cross-contamination. Part of the relevancy of this project is economical, as designated cookware can be very costly. Despite the cost, other factors affect the value of this research, including the impracticality of having a double set of kitchen appliances, which would be very bulky and impractical for those with limited space. Another factor that influences the significance of this project is beyond one's home; celiac disease brings a lot of social stress. By assuring there is limited or no cross-contamination from common kitchen appliances after customary washing, these individuals would be able to have some confidence when eating at friends' or families' homes. On the other end, if this research shows that there is cross-contamination with shared supplies it will highlight the need for dedicated ones to maintain a strict gluten-free diet. Just because a gluten-free recipe is used, a given dish may not be genuinely gluten free if there is contamination from cookware.
    Hazards and Concerns
    To fully understand the hazards of gluten contamination, a few things must first be established: What is gluten? Who is it harmful to? How and to what extent must it be avoided? How does cross-contamination occur?
    What is Gluten?
    The United States Food and Drug Association (FDA) have been trying to define "gluten" for years. The current proposed definition is, "the proteins that naturally occur in a ‘prohibited grain' that may cause adverse health effects in persons with celiac disease."(1) These prohibited grains are any species belonging to triticum, hordeum and secale or more commonly called respectively: wheat, barley, and rye, though other prohibited grains exist as hybrids of any of the three.(2) That being said, not all proteins in these three types of grains are toxic to those with celiac disease as there are two parts to glutens: prolamins, the immunotoxic ones, and glutenins, the safe ones.(3) The prolamins in the three main prohibited grains, wheat, barley, and rye, are gliadin, hordein, and secalin.(4)
    Who Does Gluten Harm?
    Gluten is toxic to certain individuals with celiac disease, an autoimmune disease that also goes by the names of: coeliac disease, celiac sprue, nontropical sprue, and gluten-sensitive enteropathy.(5) A Thomson Healthcare Company study estimated that up to 1.5 Million Americans, or one in 133 people, have celiac disease, though other individuals avoid gluten as well, such as those with gluten intolerance, or other ailments where a gluten-free diet is believed to lessen their symptoms.(6) This strict abstention from gluten is because celiac disease cannot be cured, or mediated with medication as yet. The only way to help those affected is by following this strict diet.
    How and to What Extent Must it be Avoided?
    Foods that contain wheat, rye, and barley, or any hybrid of these grains contain gluten. Gluten is a very common protein in foods, whether from bread, or as an additive to provide a thicker texture, such as in soups. This versatility makes processed foods, in the eyes of those on gluten-free (gluten-free) diets, something to be wary of. Because of this caution, companies want their products to be certified gluten-free, which according to the FDA calls for
    Despite current unknowns regarding contamination, a strict gluten-free diet must exclude all foods that contain gluten and minimize cross-contamination. This means from eating out, to staying in, gluten must be avoided. Topical products where gluten is added, such as in some lotions or body washes, should also be avoided. Despite the widespread use of gluten there are gluten-free grains and foods, such as beans, rice, millet, corn, amaranth, and soy.
    How Does Cross-contamination Occur?
    Cross-contamination is a term usually directed toward accidental spread of bacteria due to not cooking food, washing hands or materials. However, in this article it refers to the accidental transfer or content of gluten, the protein that is toxic to those with celiac disease.
    In my personal experience and research on celiac forums, when a member of a family goes gluten-free the family will most likely continue eating a regular diet. In addition, as the average time it takes to be diagnosed from the first onset of symptoms is 10 years in the United States, these families have kitchen supplies that they have been using with gluten.(8) With little public knowledge about celiac disease and going gluten-free, people tend to overlook cross-contamination. Theoretically, in the simple act of making a sandwich with gluten-free bread there are many different ways for it to become contaminated. For example, from a shared jar of peanut butter or jelly with crumbs accidentally getting into it and then dipped out onto the gluten-free bread, or crumbs on the surface it's prepared on sticking to the gluten-free bread.
    Research Investigation
    The investigation of common kitchen appliances that are frequently exposed to gluten and cleaned by customary sanitation techniques calls for the conduction of an enzyme linked immunoassay (ELISA) test when using them to prepare gluten-free food. Various well used kitchen appliances, wood and plastic cutting boards, cast iron skillets, both seasoned and unseasoned, Teflon and aluminum pans, and ceramic and glass bowls were contaminated with gluten, using whole wheat flour slurry, and then washed by their standard cleaning technique, either scrubbing with hot soapy water, or wiping with a paper towel and water.
    Afterward a certified gluten-free substance, in this case millet flour, was added and let sit to allow adherence of any gluten remaining on the ‘cleaned' surface. Figure 1 illustrates the extraction solutions that were made from the samples and injected into the Microwell plates with the anti-body coating and the various washes of the ELISA test.
    Then, the gliadin, if present, bound to the walls of the wells due to its antibody coating and the wells were washed to eliminate remaining parts in the well. Next, the enzyme Horseradish Peroxidase, or HRP enzyme, adheres post-injection to any gliadin present as an amplifier and is again washed to remove extra parts. Lastly, a 3,3', 5,5'-Tetramethylbenzidine, or TMB substrate was added which turns blue in the presence of a peroxidase, in this case the adhered HRP enzyme, which can only be there if there was gliadin to attach to. This color after a acid stop solution, which turns it yellow, is added is then assessed using a Microwell plate reader for its absorbency which, when compared with a standards curve made from known samples, by the company, will be used to determine the gluten content, in parts per million, of all the samples individually.
    Results
    Intuition may lead one to think that well developed standard cleaning techniques for most appliances, and the difficulty in transferring proteins to a gluten-free medium from a surface that has been cleaned, will make gluten cross-contamination unlikely. However, due to factors such as porosity and oiliness, some surfaces may harbor gluten. Typically, far less rigorous cleaning techniques are used on the seasoned cast iron skillet and it is very porous and oily so the gluten proteins have a better chance of binding to it and then transferring to a gluten free medium. Given the test results of the ELISA test, this is mostly true. Despite the logic being the same, and it being the intuitive most likely candidate for cross-contamination a different appliance with the same sanitation technique proved to exceed the gluten parts per million limit where as the cast iron did not.
    The only absorbency ratings from the samples that interpolated to be greater than the 20 ppm of gluten allowance were two extractions from the Teflon pan. All other ratings, including two other Teflon pan extractions, were below the limit.
    Conclusion
    Ninety-four percent of the sample extractions showed less than the 20 parts per million of gluten which is the threshold for something to be declared gluten-free. Teflon had half of its extractions above the limit, as such Teflon should be deemed cross-contaminated. However, the Teflon's other extraction samples had well below 20ppm. This could have been due to the sample's gluten free sample being rather large and thus only part of it could have gotten contaminated (positive cross-contamination) and other parts not (negative cross-contamination). All others samples were classified as gluten-free due to being below the 20ppm allowance.
    In conclusion, the values of gluten cross-contamination, in ppm, were too small to hinder the integrity of the gluten-free medium in all but Teflon. Thus, to the extent of the experiment done, having tested only eight different kitchen appliances, with only two different sanitation techniques, common kitchen appliances that are frequently exposed to gluten, can be cleaned by customary methods and used to prepare gluten-free food with the exception of Teflon appliances.
    This research project could be extended by more trials. For example, eight types of common kitchen appliance were used, but only one appliance was used to represent each type. More trials could be done within each type, using different brands, variations in extent of wear, etc. In addition, the only type of contaminant used was whole-wheat slurry. Other forms of contaminant should be tested as well, to show the universality of the cross-contamination, or lack thereof. This should include different gluten-containing substances, as well as some dry and some wet.
    Unfortunately, this research question will have exceptions as the extent of washing and wear on an appliance is a more subjective issue. This means that even if it is found on a larger scale that certain appliances have been found to be safe for producing gluten-free foods, it should still be avoided when possible for those with celiac disease as if not washed properly; it could go beyond the 20ppm allowance and be immunotoxic to these individuals.
    Vested interest is always a concern with research, and thus it must be pointed out that no company or university holds any interest in this project and no help was given financially or academically, only that The University of Detroit Mercy allowed me to use their lab for the duration of the experiment and Microwell plate reader. In addition, both sides of the results would prove beneficial, so the data were not interpreted with a bias toward any desired result.
    Eleanore Dara is a "rising scientist" and is an incoming biochemistry student on a Research Track Major at the University of Scranton in Pensnsylvania.
    References:
    "Questions and Answers on the Gluten-Free Labeling Proposed Rule." U S Food and Drug Administration. N.p., 23 Jan. 2007. Web. 31 Jan. 2011.  https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm  Ibid. Amaya-González, et al. "Amperometric Quantification of Gluten in Food Samples Using an ELISA Competitive Assay and Flow Injection Analysis." Electoanaylsis 23.1 (2010): 108+. Wiley Online Library. Web. 8 Mar. 2011. "What Is Gliadin? What Is Its Role In Gluten Sensitivity?." Gluten Free Around The World, Traditional Foods Make Eating an Adventure. N.p., n.d. Web. 25 Mar. 2012. http://www.gluten-free-around-the-world.com/gliadin.html  Snyder, Cara et al. "Celiac Disease Coeliac Disease, Celiac Sprue, Nontropical Sprue, Gluten-Sensitive Enteropathy." The National Center for Biotechnology Information. N.p., 3 June 2008. Web. 31 Jan. 2011. Cerrato, Paul L. "Gluten Intolerance: more common than thought. (Complementary Therapies Update)." RN 66.8 (2003): 23. General One File. Web. 28 Mar. 2011. "Questions and Answers on the Gluten-Free Labeling Proposed Rule." U S Food and Drug Administration. N.p., 23 Jan. 2007. Web. 31 Jan. 2011.   https://www.fda.gov/Food/GuidanceRegulation/GuidanceDocumentsRegulatoryInformation/Allergens/ucm362880.htm  Adams, Scott. "USA - Average Time to Diagnosis = 10 Years - Celiac.com." Celiac Disease & Gluten-free Diet Information at Celiac.com. Scott Adams, 26 July 1996. Web. 16 Feb. 2012. http://www.celiac.com/articles/48/1/USA---Average-Time-to-Diagnosis--10-Years/Page1.html.

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    Jefferson Adams
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    Serve is a bowl with tortilla chips and guacamole.

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

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

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.