• Join our community!

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

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,466
    Total Members
    3,093
    Most Online
    3sth3rcho
    Newest Member
    3sth3rcho
    Joined
  • 0

    Gluten-free Diet Prevents Diabetes (Type 1) at Same Rate as Gluten-enriched Diet


    Jefferson Adams

    Celiac.com 08/14/2007 - A study on the effects of a gluten-free diet versus a gluten-enriched diet on the incidence of diabetes in mice has yielded some surprising results that are not fully understood. The results of the study were published recently in the journal Diabetes/Metabolism Research and Reviews.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    It is well known that environmental nutrition and infections play a key role in the development of diabetes (type 1). A Czech research team made up of doctors David P. Funda, Anne Kaas, Helena Tlaskalová-Hogenová, Karsten Buschard recently set out to study the relationship between type 1 diabetes and both gluten-free and gluten enriched diets. The team tested the hypothesis that early introduction of gluten into the diet might increase diabetes incidence in mice.

    For a period of 310 days, non-obese diabetic (NOD) mice were fed one of the following diets: standard diet, a gluten-free diet, a gluten + modified Altromin diet, or a hydrolyzed-casein based Pregestimil diet. The mice were observed for signs of diabetes, including evaluation for insulitis score, and numbers of gut mucosal lymphocytes.

    Compared to mice fed the standard Altromin diet, mice fed on the gluten-free and the Pregestimil diets showd markedly lower incidence of diabetes. Incidence rates were as follows (p < 0.0001): NOD mice fed gluten-free diet (5.9%, n = 34) and Pregestimil diet (10%, n = 30) compared to mice on the standard Altromin diet (60.6%, n = 33).

    Somewhat unexpectedly, the gluten+ diet also prevented diabetes to the same degree as the gluten-free diet (p<0.0001, 5.9% n=34). Of those mice who did develop diabetes, those on the gluten-free and Pregestimil diets did so at a later time than those on a standard diet.

    Compared to control mice, non-diabetic NOD mice on the gluten-free diet and to a lesser extent also gluten+ and Pregestimil diets showed lower insulitis scores. No significant differences were found in the number of CD3+, TCR-+, and IgA+ cells in the small intestine. The researchers concluded that a gluten-enriched diet prevents diabetes in NOD mice at the same rate as a gluten-free diet.

    Diabetes/Metabolism Research and Reviews, Volume 15, Issue 5 , Pages 323 - 327

    health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
    0


    User Feedback

    Recommended Comments

    Guest Mr. H

    Posted

    This study doesn't take into account whether or not the mice in question were susceptible to celiac. I theorize, no celiac genetic markers no type 1 diabetes.

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

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

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

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

    ×   Your previous content has been restored.   Clear editor

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


  • Popular Contributors

  • Ads by Google:

  • Who's Online   6 Members, 1 Anonymous, 339 Guests (See full list)

  • Related Articles

    Scott Adams
    Diabetes Care 2002;25:1111-1122.
    Celiac.com 08/08/2002 - A recent study conducted by Dr. David B. Dunger (Addenbrookes Hospital in Cambridge) and colleagues found that children with type 1 diabetes and latent celiac disease who were put on a gluten-free diet showed significant improvement in their metabolic control and growth. The study, which was published in the July issue of Diabetes Care, looked at 11 children with type 1 diabetes and who were diagnosed with celiac disease using anti-gliadin and anti-endomysial antibodies and a biopsy for confirmation.
    The group with celiac disease had a significantly lower mean BMI standard deviation score (SDS) than that of a control group of 22 age and sex-matched children with diabetes who did not have celiac disease. The mean height SDS and C-peptide levels in the two groups were similar, while the mean HbA-1-c was lower (better) in the group with celiac disease. After one year on a gluten-free diet the group with celiac disease improved its mean BMI score to that of the control group, and its HbA-1-c score went down (improved), while the control groups HbA-1-c score increased (worsened).
    The researchers conclude that more studies are needed to support their findings that a gluten-free diet significantly improves glycemic control in children with type 1 diabetes and celiac disease.

    Scott Adams
    Clin Immunol. 2004 Apr;111(1):108-18
    According to German researchers, delaying the introduction of wheat and barley proteins could reduce the incidence of diabetes. The scientists looked at mice on diets that were modified according to protein source, and specifically looked at mice pups from female non-obese diabetic mice. Mice on lifelong wheat-free and barley-free diets (their protein source was poultry) had significantly reduced levels of diabetes (45% by age 32 weeks vs. 88% in control mice), and when they did develop diabetes, its onset was delayed. Interestingly the development of diabetes in these mice was not fully restored after adding wheat and barley proteins to their diets (58%). Further, insulin autoantibodies and insulitis scores were both reduced in the wheat and barley-free mice, and their intra-pancreatic IL-4 mRNA levels were increased. The researchers conclude: "These data support a link between dietary wheat and barley proteins and the development of autoimmune diabetes."

    Scott Adams
    Arch Dis Child 2004;89:871-876. Celiac.com 07/12/2005 – Australian researchers have determined that a gluten-free diet in children with Type 1 diabetes mellitus and celiac disease can improve both growth and diabetes control. In the study 21 children (mean age 7.5 years) with both conditions went on a gluten-free diet for 12 months, and their growth and insulin dosages were carefully measured and compared with that of two matched diabetic, non-celiac controls. The group on a gluten-free diet showed significant increases in weight and body mass index compared with the control group, although an increase in height found in the study was not found to be significant. At the time of diagnosis insulin dosages for the celiac disease group were less than that of the control group, but became similar to the controls once a gluten-free diet was started—although the increase in insulin dosage had no effect on HbA1c levels.
    The researchers conclude: “Identification and dietary treatment of celiac disease in children with diabetes improved growth and influenced diabetic control. Evaluation of the outcome of treatment of celiac disease in diabetics should include assessments of gluten intake.” Obviously all children (and everyone) with celiac disease should be on a gluten-free diet, but what is noteworthy about this study is that a connection was found between insulin levels, diabetes control, and the gluten-free diet.

    Jefferson Adams
    Celiac.com 07/14/2014 - Early life intestinal problems have previously been shown to influence diabetes rates. There is also some evidence that a gluten-free diet can lower rates of diabetes, but just how strong is the influence of gluten-free diet on the development of diabetes?
    A recent study by a group of researchers in Denmark suggests that maternal gluten-free diet greatly reduces inflammation and rates of diabetes in the offspring of certain mice. This study led the team to hypothesize that a gluten-free diet, which is known to decrease type 1 diabetes incidence, may also offer protection against diabetes when followed during the pregnancy and lactation period.
    The research team included Camilla H.F. Hansen, Åukasz Krych, Karsten Buschard, Stine B. Metzdorff, Christine Nellemann, Lars H. Hansen, Dennis S. Nielsen, Hanne Frøkiær, Søren Skov and Axel K. Hansen. They are variously affiliated with the Department of Veterinary Disease Biology of the Faculty of Health and Medical Sciences at the University of Copenhagen, the Department of Food Science, Faculty of Science, University of Copenhagen, the Department of Biology, Faculty of Science, University of Copenhagen, the Division of Toxicology and Risk Assessment of the National Food Institute at the Technical University of Denmark in Søborg, Denmark, and the Bartholin Institute in Copenhagen, Denmark.
    For their study, the team fed pregnant non-obese diabetic (NOD) mice either a gluten-free diet, or a standard diet, until all pups were weaned to standard diet. Overall, mice which experienced early life gluten-free diets had dramatically lower rates of diabetes and insulitis.
    An analysis of gut microbiota using 16S rRNA gene sequencing showed a major difference between both mothers and their offspring, marked by higher levels of Akkermansia, Proteobacteria, and TM7 in the gluten-free diet group. Gluten-free fed offspring showed increased M2 macrophage gene markers and tight junction-related genes in the gut, along with higher levels of pancreatic FoxP3 regulatory T cells.
    Gluten-free offspring also had reduced intestinal gene expression of proinflammatory cytokines. Finding more T cells in the pancreas expressing the mucosal integrin α4β7 suggests that this is due to an increase in gut-primed immune cells moving to the pancreas.
    The study shows clearly that a gluten-free diet during the fetal and early postnatal life lowers rates of diabetes. This may be due to a change in gut microbiota and a reduction in pro-inflammatory conditions in the gut and pancreas.
    Clearly, further study is needed to better understand the factors at play, and how they relate to diabetes reduction efforts.
    Source:
    American Diabetes Association. doi: 10.2337/db13-1612

  • Recent Articles

    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.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    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