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    Season of Birth May Increase Celiac Disease Risk


    Jefferson Adams

    Celiac.com 02/20/2013 - Scientific evidence indicates that the risk of developing celiac disease cannot be explained solely by genetic factors. There is some evidence to support the idea that the season in which a child is born can influence the risk for developing celiac disease. It is known that babies born in summer months are likely to be weaned and introduced to gluten during winter, when viral infections are more frequent.


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    Photo: CC--rkramer62A number of studies indicate that early viral infections can increase risk levels for celiac disease, however, earlier studies on birth season and celiac disease have been small, and their results have been contradictory.

    To better answer the question, a research team recently set out to conduct a more thorough study of the relationship between birth month and celiac disease.

    The research team included B. Lebwohl, P.H. Green, J.A. Murray, and J.F. Ludvigsson. The study was conducted through the Department of Paediatrics at Örebro University Hospital in Örebro, Sweden.

    To conduct the study, the team used biopsy reports from all 28 Swedish pathology departments to identify individuals with celiac disease, which they defined as small intestinal villous atrophy (n=29 096).

    Using the government agency Statistics Sweden the team identified 144,522 control subjects, who they matched for gender, age, calendar year and county.

    The team then used conditional logistic regression to examined the association between summer birth (March-August) and later celiac disease diagnosis (outcome measure).

    They found that 54.10% of people with celiac disease were born in the summer months compared with 52.75% of control subjects.

    So, being born in the summer is associated with a slightly higher risk of later celiac disease (OR 1.06; 95% CI 1.03 to 1.08; p).

    While summer birth was not associated with a higher rates of celiac diagnosis in later childhood (age 2-18 years: OR 1.02; 95% CI 0.97 to 1.08), it did show a slightly higher risk of developing celiac disease in adulthood (age ≥18 years: OR 1.04; 95% CI 1.01 to 1.07).

    In this study, the data show that people born during the summer months had a slightly higher risk of developing celiac disease, but that excess risk was small, and general infectious disease exposure early in life were not likely to increase that risk.

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    Guest Wanda Hinkle

    Posted

    I have not been diagnosed with celiac disease. However, I had not eaten any gluten in almost 6 months when biopsies were done. The GI doctor told me it wasn't worth it to me to eat gluten and then do biopsies. I do react strongly with only minute amounts of gluten. I had always been told I had IBS until I was 68 years old. Since then, I've read all I could find on it. This article was enlightening, but not helpful to me. I was born in November.

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    Guest sc'Que?

    Posted

    This is one of the worst articles I've seen on your site. Isn't ±3% generally considered the MARGIN OF ERROR? Am I missing something?

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    Guest Claire Spina-Kelly

    Posted

    I am born in November and I have celiac disease. So the 54% born in the summer have celiac disease and I am in the other 52.7%. I am suffering terribly and I sure hope they can find a cure.

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    Um, I don't think 1.35% is a significant enough difference to make any kind of conclusions. It seems like the Confidence Intervals would probably overlap, leaving no difference at all.

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  • Related Articles

    Jefferson Adams
    Celiac.com 06/10/2011 - Children born in the spring or summer seem to have higher rates of celiac disease, according to a study of Massachusetts children. This higher rate could be tied to certain seasonal and environmental factors, according to researchers at the Massachusetts General Hospital for Children.
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    Source:

    EurekAlert

    Jefferson Adams
    Celiac.com 10/30/2013 - Rates of celiac disease and the use of drugs to inhibit the secretion of stomach acid have both increased in recent decades. A research team recently set out to explore the association between anti-secretory medication exposure and subsequent development of celiac disease.
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    Source:
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    Jefferson Adams
    Celiac.com 08/27/2014 - Can antibiotic exposure in pregnancy increase the risk of celiac disease in children? Some researchers suspect that infant microbiota play a pathogenic role in celiac disease. The idea that antibiotic treatment in pregnancy could significantly impact the infant microbiota, and thus influence the development of celiac disease, has led many to ponder the possible connection.
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    Risk estimates remained unchanged after adjustment for breastfeeding, age at gluten introduction and infection load in the child's first year of life (HR = 1.28; 95% CI = 0.66–2.48).
    When all the data were factored, the team found no statistically significant connection between antibiotic exposure during pregnancy and celiac disease in offspring. The team suggests that this data may present an accurate picture, or it may be that they simply lack the statistical power to make a clear connection.
    Further studies are likely needed before researchers can confidently conclude that there is no connection between antibiotic exposure in pregnancy and celiac disease in offspring.
    Source:
     BMC Gastroenterol. 2014;14(75)

  • 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.
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    Jefferson Adams
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    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.
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    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). 
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    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.
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    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