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    A Gluten-Free Diet Helps Type 1 Diabetes


    Dr. Vikki Petersen D.C, C.C.N


    • Journal of Gluten Sensitivity Autumn 2012 Issue


    Image Caption: Image: CC--Allen Hazen

    Celiac.com 10/27/2017 - It has long been understood that two autoimmune diseases, celiac disease and type 1 diabetes are related. They share common genes and the incidence of celiac disease is higher among type 1 diabetics. There have been some anecdotal reports regarding children diagnosed with type 1 diabetes who were put on a gluten-free diet soon after their diagnosis and for a period of two years or more didn't require any insulin. The thought was that the gluten-free diet effectively halted the progression of the diabetes, at least for the duration of the study.


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    Studies of mice have shown that despite utilizing a genetic strain of mice that were strongly in-bred to increase the risk of type 1 diabetes, 2/3 of them did not do so when a drug was administered to prevent leaky gut. This study was performed by Dr. Alessio Fasano at the University of Maryland Celiac Research Center. Dr. Fasano is one of the world's acclaimed researchers in the area of celiac disease and gluten sensitivity.

    Leaky gut is associated with the initiation and continuation of autoimmune disease and Dr. Fasano's work with these genetically predisposed mice shed a great deal of light on the power of an undamaged gut lining to effectively forestall development of a genetic condition, in this case type 1 diabetes.

    A recent study out of Immunology, dated August 22, 2012, is titled "Dietary gluten alters the balance of proinflammatory and anti-inflammatory cytokines in T cells of BALB/c mice". The title is a mouthful but here is what the researchers out of Denmark found:

    Their initial premise was based on the idea, as I mentioned above, that dietary modifications, specifically a gluten-free diet, could reduce the risk of developing type 1 diabetes. The question they posed was, "How did this occur?"

    They discovered that wheat gluten induced the production of pro-inflammatory chemicals called cytokines that would damage the intestinal lining and immune tissues of the small intestine. More importantly, a gluten-free diet didn't just neutralize the negative effects just mentioned, but it actually caused the production of anti-inflammatory chemicals that would provide protection for the immune system and gut. So, while gluten is a known bad guy, a gluten-free diet doesn't just take the negative away, it actually induces a positive, healing response.

    Clinically we frequently see this with patients. As soon as we meet a patient with any history of autoimmune disease, we quickly test them for celiac disease and gluten sensitivity via lab tests and a 30 day elimination diet. If we discover any negative immune reaction to gluten, we begin a strict gluten-free diet.

    Happily, we often see stabilization, if not reversal, of their autoimmune disease. We support the gluten-free diet with our other protocols for normalizing gut permeability (healing a leaky gut) and strengthening the immune system. Taken together this program yields excellent results.

    If you know anyone suffering from an autoimmune disease, please show them this article. Gluten could be a component in furthering their disease and a gluten-free diet could be a positive influence in their journey to improved health.

    I hope this was helpful. Please feel free to contact me should you have any questions. And if your health is not at the level you would like, I can also offer you a free health analysis. Call us at 408-761-3900.

    Our destination clinic treats patients from across the country and internationally and we would be delighted to help you.

    To your good health.

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  • About Me

    Dr. Vikki Petersen, a Chiropractor and Certified Clinical Nutritionist is co-founder and co-director, of the renowned HealthNow Medical Center in Sunnyvale, California. Acclaimed author of a new book, "The Gluten Effect" - celebrated by leading experts as an epic leap forward in gluten sensitivity diagnosis and treatment. Dr. Vikki is acknowledged as a pioneer in advances to identify and treat gluten sensitivity. The HealthNOW Medical Center uses a multi-disciplined approach to addressing complex health problems. It combines the best of internal medicine, clinical nutrition, chiropractic and physical therapy to identify the root cause of a patient's health condition and provide patient-specific wellness solutions. Her Web site is:
    www.healthnowmedical.com

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  • Related Articles

    Jefferson Adams
    Celiac.com 02/10/2015 - A number of studies have shown a connection between celiac autoimmunity and type 1 diabetes mellitus (T1DM). Doctors recommend celiac screening for T1DM patients, but screening is not always conducted.
    Meanwhile, reports about the impact of celiac autoimmunity in T1DM have been varied. A team of researchers recently set out to determine rates of celiac autoimmunity in patients with T1DM, and to study the impact of celiac autoimmunity on nutritional parameters, glycaemic control, endocrine axes and bone health.
    The research team included A.S. Joshi, P.K. Varthakavi, N.M. Bhagwat, M.D. Chadha, AND S.S. Mittal. They are variously associated with the Department of Endocrinology of Topiwala National Medical College and BYL Nair Charitable Hospital, Mumbai Central in Maharashtra, India.
    For their study, the team conducted celiac autoimmunity screens on eighty-six consecutive patients with T1DM using immunoglobulin A (IgA) tissue transglutaminase as a marker (TTG; IgG anti-gliadin in IgA-deficient case). They compared CA positive (CA+) T1DM cases with age-matched and sex-matched CA negative (CA-) T1DM cases for anthropometry, glycaemic control (as assessed by glycated haemoglobin (HbA1c) and hypoglycaemic/hyperglycaemic episodes), endocrine (thyroid function, cortisol, growth hormone (GH) axis, gonadal axes), haematological (haemoglobin, iron profile and vitamin B12 status) and calcium metabolism parameters and bone densitometry (by dual-energy X-ray absorptiometry (DXA)).
    Consenting patients with celiac autoimmunity also underwent upper gastrointestinal (GI) endoscopy with duodenal biopsy.
    Results showed that 11 of the 86 patients, about 12.75%, screened positive for celiac autoimmunity. Of those, seven patients underwent duodenal biopsies which suggested two cases of Marsh grade III, three cases of Marsh grade II and two cases of Marsh grade I celiac disease.
    In terms of anthropometry, CA+ T1DM patients were comparable with CA- T1DM patients. Overall, CA+ patients had higher HbA1c (10.7±1.8 vs. 8.4±1.0 (93±19 vs. 68±11 mmol/mol); p
    The incidence of fractures in the past 3 years was four CA+ patients, and one CA- patient (p<0.05).
    There is an important autoimmune connection between celiac disease and T1DM. For people with T1DM, celiac disease adversely affects stature, bone health, glycaemic control and iron and B12 levels.
    The study team recommends that IgA sufficiency be established before using an IgA-based screening test for celiac autoimmunity.
    Source:
    Arab J Gastroenterol. 2014 Jun;15(2):53-7. doi: 10.1016/j.ajg.2014.04.004. Epub 2014 Jun 7.

    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.

    Jefferson Adams
    Celiac.com 02/01/2017 - More and more evidence shows a connection between gut inflammation and type 1 diabetes (T1D). A team of researchers recently set out to assess gut inflammatory profiles and microbiota in patients with T1D, and to compare them with healthy controls (CTRL) and with celiac disease patients as gut inflammatory disease controls.
    The research team included Silvia Pellegrini, Valeria Sordi, Andrea Mario Bolla, Diego Saita Roberto Ferrarese, Filippo Canducci, Massimo Clementi, Francesca Invernizzi, Alberto Mariani, Riccardo Bonfanti, Graziano Barera, Pier Alberto Testoni, Claudio Doglioni, Emanuele Bosi, and Lorenzo Piemonti. They are affiliated with the Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute in Milan, Italy.
    The team evaluated inflammatory status and microbiome composition in biopsies of the duodenal mucosa from 19 patients with T1D, 19 with celiac disease, and 16 healthy control subjects, recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. They assessed inflammation by gene expression study and immunohistochemistry and used 16S rRNA gene sequencing to analyze microbiome composition.
    Compared to CTRL and celiac disease patients, the team found an increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα and VEGFA genes in T1D patients. The immunohistochemical analysis confirmed T1D specific inflammatory status was mainly marked by increased monocyte/macrophage lineage infiltration, compared to healthy and celiac disease control tissues.
    The T1D duodenal mucosal microbiome also proved to be different from the control groups. This was mainly marked by increased Firmicutes, and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes.
    The expression of genes specific for T1D inflammation was associated with the excess of specific bacteria in duodenum. This study shows that patients with T1D show specific abnormalities in gut inflammation and microbiota.
    Greater knowledge of the complex pathogenesis of T1D will likely provide new directions for therapies targeting the gut. Look for more studies in this area in the near future, as scientists look to nail down specific treatments to prevent gut inflammation.
    Source:
    The Journal of Clinical Endocrinology & Metabolism. DOI: https://doi.org/10.1210/jc.2016-3222

    Jefferson Adams
    Celiac.com 07/05/2017 - Numerous researchers have documented a connection between celiac disease and type 1 diabetes.
    One team of researchers recently set out to examine international differences in celiac disease rates and clinical characteristics of youth with coexisting type 1 diabetes and celiac disease compared with type 1 diabetes only.
    The research team included Maria E. Craig, Nicole Prinz, Claire T. Boyle, Fiona M. Campbell, Timothy W. Jones, Sabine E. Hofer, Jill H.Simmons, Naomi Holman, Elaine Tham, Elke Fröhlich-Reiterer, Stephanie DuBose, Helen Thornton, Bruce King, David M. Maahs, Reinhard W. Holl and Justin T. Warner.
    To analyze the relationship between outcomes, including HbA1c, height-standard deviation score [sDS], overweight/obesity, and type 1 diabetes with celiac disease versus type 1 diabetes alone, adjusting for sex, age, and diabetes duration, the team created multivariable linear and logistic regression models.
    The analysis included 52,721 people under 18 years of age with a clinic visit between April 2013 and March 2014. The team used the following data sources: the Prospective Diabetes Follow-up registry (Germany/Austria); the T1D Exchange Clinic Network (T1DX) (U.S.); the National Paediatric Diabetes Audit (U.K. [England/Wales]); and the Australasian Diabetes Data Network (ADDN) (Australia).
    The researchers found biopsy-confirmed celiac disease in 1,835 young people, or 3.5%. These patients were diagnosed on average at age 8.1 years, with a range of 5.3 to 11.2 years.
    Most young people (37%) with diabetes upon celiac disease diagnosis had it for less than one year. Eighteen percent with diabetes had it for 1-2 years at celiac diagnosis, 23% had diabetes between 3 and 5 years at celiac diagnosis, while 17% had diabetes for more than 5 years at celiac diagnosis. Celiac disease rates ranged from 1.9% in the T1DX to 7.7% in the ADDN and were higher in girls than boys (4.3% vs. 2.7%, P < 0.001).
    Children with coexisting celiac disease were diagnosed with diabetes at 5.4 years on average, compared with those with type 1 diabetes only, who were diagnosed at 7.0 years of age, on average. Also, fewer children with both conditions were non-white, 15 vs. 18%.
    Height-SDS was lower in those with celiac disease (0.36 vs. 0.48) and fewer were overweight/obese (34 vs. 37%, adjusted P < 0.001), whereas average HbA1c values were comparable: 8.3 ± 1.5% (67 ± 17 mmol/mol) versus 8.4 ± 1.6% (68 ± 17 mmol/mol).
    This study clearly documented that celiac disease is not uncommon in young people with type 1 diabetes. Differences in disease rates may be due to variations in screening and diagnostic practices, and/or risk levels.
    Although the groups showed similar glycemic control, the research team encourages close monitoring of growth and nutrition in this population, due to the lower height-SDS.
    Source:
    Diabetes Care 2017 May; dc162508.  
    The researchers in this study are variously affiliated with the Children’s Hospital at Westmead, Sydney, New South Wales, Australia; University of New South Wales, Sydney, New South Wales, Australia; Charles Perkins Centre Westmead, University of Sydney, Sydney, New South Wales, Australia; Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany; German Center for Diabetes Research, Munich-Neuherberg, Germany; Jaeb Center for Health Research, Tampa, FL; Leeds Children’s Hospital, Leeds, U.K.; The University of Western Australia, Perth, Western Australia, Australia; Telethon Kids Institute, Perth, Australia; Department of Pediatrics, Medical University of Innsbruck, Innsbruck, Austria; Vanderbilt University Medical Center, Nashville, TN; Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.; Women’s and Children’s Hospital, Adelaide, South Australia, Australia; Department of Pediatrics, Medical University of Graz, Graz, Austria; St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, U.K.; John Hunter Children’s Hospital, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia; Lucile Salter Packard Children's Hospital Stanford, Stanford University Medical Center, Palo Alto, CA; and the Children's Hospital for Wales, Cardiff, U.K.

    Jefferson Adams
    Celiac.com 02/28/2018 - In an effort to discover more genes that trigger type 1 diabetes, a team of researchers recently conducted a large, prospective study of children at risk for type 1 diabetes. The end goal is to reveal more targets for treating or even preventing the disease.
    The research team included A Sharma, X Liu, D Hadley, W Hagopian, WM Chen, S Onengut-Gumuscu, C Törn, AK Steck, BI Frohnert, M Rewers, AG Ziegler, Å Lernmark, J Toppari, JP Krischer, B Akolkar, SS Rich, JX She; and TEDDY Study Group.
    The team identified six new chromosomal regions in young people who have already developed type 1 diabetes, or who have started making antibodies against their insulin-producing cells, often a step toward full-blown diabetes that requires lifelong insulin therapy. Their analysis of 5,806 individuals, which is published in the Journal of Autoimmunity, also confirms three regions already associated with one of those related conditions.
    The team observed two top autoantibodies. The first, called IAA, acts directly against insulin. The second, called GADA, acts against the enzyme glutamate decarboxylase, which regulates the insulin-producing beta cells in the pancreas. According to Dr. She, about 90 percent of patients with type 1 diabetes start with one of the autoantibodies, and many patients eventually end up with both. The second autoantibody may surface in a few days or even years later.
    They began this study with 176,586 SNPs, or single nucleotide polymorphisms. Nucleotides are basic building blocks of our genetic information. According to Sharma, the SNPs evaluated by TEDDY scientists were already linked with other autoimmune conditions like rheumatoid arthritis or celiac disease, but not type 1 diabetes.
    The researchers figured out which of these SNPs are different in TEDDY participants with type 1 diabetes versus those with Islet cell autoantibodies versus those with neither. Previous research has shown that the genes associated with IA and actual type 1 diabetes can differ. Dr. She says that even though clinicians regard Islet cell autoantibodies (IA) as a red flag for type 1 diabetes, not every child with IA goes on to develop diabetes, though multiple autoantibodies definitely increase that risk.
    The team notes that it is possible that the genes that promote IA development may differ from those that lead to full-blown disease progression.
    She says that this is the first study of gene identification for any disease to use this sort of longitudinal information. She add that this and other studies by the TEDDY research group help to clarify the search for important non-HLA genes by adding the "time to disease" perspective.
    Source:
    J Autoimmun. 2018 Jan 5. pii: S0896-8411(17)30739-4. doi: 10.1016/j.jaut.2017.12.008.  
    The researchers are variously affiliated with the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Division of Biostatistics and Data Science, Department of Population Health Sciences, Medical College of Georgia, Augusta University, Augusta, GA, US; the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA; the Division of Population Health Sciences and Education, St George's University of London, London, United Kingdom; the Pacific Northwest Research Institute, Seattle, WA, USA; the Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA; the Department of Clinical Sciences, Lund University/CRC, Malmö, Sweden; the Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, Aurora, CO, USA; the Institute of Diabetes Research, Helmholtz Zentrum München, Munich-Neuherberg, Germany; Klinikum rechts der Isar, Technische Universität München, Munich-Neuherberg, Germany; Forschergruppe Diabetes e.V., Munich-Neuherberg, Germany; the Department of Pediatrics, Turku University Hospital, Turku, Finland; the National Institutes of Diabetes and Digestive and Kidney Disorders, National Institutes of Health, Bethesda, MD, USA; and the Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.

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    Though D’Elena’s marketing seeks to capitalizes on the gluten-free trend, he knows Celiac disease is a serious health issue for some people. “[W]e’re not here to offend anybody….this is just something we're just trying to do to draw attention and do what's best for our clients," he said. 
    Still, the signs seem to be working. D'elena had fielded six offers within a few days of listing the west Phoenix home.
    "Buying can sometimes be the most stressful thing you do in your entire life so why not have some fun with it," he said. 
    What do you think? Clever? Funny?
    Read more at Arizonafamily.com.

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    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
    Our passion is to bake the very best products while bringing happiness to our customers, each other, and all those we meet!
    We are available during normal business hours at: 1-888-533-8118 EST.
    To learn more about us at: visit our site.

    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.