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    Celiac Disease, Irritable Bowel Syndrome, and Gluten Sensitivity


    Jefferson Adams

    Celiac.com 10/09/2009 - The causes and mechanisms that fuel the development of gastrointestinal symptoms, along with the individual perceptions of those symptoms are varied and, in many cases, not well understood.


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    A team of researchers recently set out to explore the clinical and experimental evidence regarding the possible association between gluten sensitivity, celiac disease, irritable bowel syndrome, and the development of gastrointestinal symptoms.

    The research team was made up of Elena F. Verdu, MD, PhD, David Armstrong, MA, MB, BChir, and Joseph A. Murray, MD. The team's hypothesis is that, even in the absence of fully developed celiac disease, gluten exposure can trigger symptoms that mirror FBD.

    To test that hypothesis, the team set out to see how many people with gluten sensitivity are likely to suffer from symptoms similar to functional bowel disorder (FBD).

    The team proposes model for the exploring and assessing factors influencing the development of gastrointestinal symptoms and dysfunction by gluten in FBD and organic disease.

    They elaborate on their hypothesis that gluten sensitivity and post-infectious irritable bowel syndrome (IBS) represent two triggers that can explain at least part of the wide range of IBS symptoms and dysfunction. Better understanding this relationship offers researchers a better understanding of the role of mucosal responses to luminal factors in FBDs.

    The team proposes that the animal model of gluten sensitivity in human leukocyte antigen (HLA)- DQ8 mice
    permits exploration of mucosal pathophysiological changes that develop before the onset of advanced inflammation in gluten sensitive individuals.

    A clearer picture of the means by which gluten triggers symptoms in sensitive individuals will help to shed light on the interactions between host genotype, diet, and intestinal microbiota in triggering gluten sensitivity.

    The goal of the review is to shed light on the connections between celiac disease, IBS, and gluten sensitivity, as well as to emphasize several important facts.

    First, 'gluten sensitivity' is marked by one or more various immunological, morphological, or symptomatic problems that may also be common to celiac disease and IBS.

    Second, gluten sensitivity and classic celiac disease may have common roots, but people with gluten sensitivity do not meet the clinical threshold for celiac disease.

    Third, while gluten sensitivity and IBS may share common symptomatology, gluten sensitivity by definition is not IBS.

    Successful treatments for IBS have are few, due to the lack of pharmacological targets and even a conceptualized framework for the basic pathogenetic mechanisms.

    In some patients with symptoms of post-infectious IBS, doctors have been able to associate the role of subtle persistent inflammation in as a likely trigger for gut immune responses.

    They conclude that recent clinical evidence supports the view of gluten sensitivity as the likely cause of gastrointestinal symptoms that would otherwise point to of IBS.

    This information dovetails with other recent information regarding the prevalence of gluten sensitivity. The idea that gluten sensitivity is far more widespread than believed , and that gluten sensitivity lies at the heart of numerous gastrointestinal and other systemic disorders is rapidly gaining support from data, and drawing new believers within the scientific community.

    Source:
    Am J Gastroenterol 19 May 2009; doi: 10.1038/ajg.2009.188

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    For a person suffering from celiac and Chron's disease this article was well written and very enlightening.

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  • Related Articles

    Jefferson Adams
    Celiac.com 05/06/2008 - In the majority of people with celiac disease,strict adherence to a gluten-free diet can result in a quality of lifethat is on par with non-celiacs. Still a small percentage of celiacsseem to suffer from persistent gastrological discomfort in the form ofirritable bowel or irritable-bowel-like symptoms. Very few studies havebeen done on persistent gastrological problems in adults with celiacdisease. Those that have been done rely upon univariate statisticalanalysis in clinical samples at the secondary or tertiary care leveland fail to assess the potential influence of non-celiac diseasespecific factors, which are considered to be a risk factor of irritablebowel syndrome (IBS), such as mental disorders, or gender.
    Ateam of researchers made up of doctors Winfried Hauser, Frauke Musial,Wolfgang Caspary, Jurgen Stein, and Andreas Stallmach set out todetermine rates of irritable bowel syndrome, irritable bowelsyndrome-related symptoms, and consecutive health care-seeking behaviorand their influence upon health-related quality of life (HRQL) and anyconceivable bio-psychosocial factors influencing adult patients withceliac disease. The research team made a medical and socio-demographicsurvey of 1000 adult celiac patients from the German Celiac Society bypost. The medical portion of the survey included bowel history. Theteam also had patients fill out a Short Form Health Survey (SFHS),along with the Hospital Anxiety and Depression Scale.
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    A totalof 446 patients indicated that they had biopsy-proven celiac disease. Of these 446patients, 18 were excluded because they indicated adherence to agluten-free diet for less than 1 year. Sixteen patients were tossed outbecause they reported a major non-adherence to the gluten-free diet. Thus,the study group was confined to 412 patients with self-reportedbiopsy-proven celiac disease who were on a strict gluten-free diet for at least one year. The survey showed that out of these 412 patients that met the criteria, 96 patients, or just over 23% metmodified Rome I criteria for Irritable Bowel Syndrome. Of those 96patients, 76 patients, or nearly 80%, made an effort to get help, bothmedical and non-medical, as a result of the bowel symptoms (we’ll callthe patients who sought help "irritable bowel syndrome patients").
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    Limited studies indicate that gender differencesin visceral perception, cardio-autonomic responses, gastrointestinalmotility, and brain activation patterns to visceral stimuli are afactor in irritable bowel syndrome. Gender differences in psychosocialfactors have not been fully studied.
    The results of this studyalso support the need for further investigation to determine exactly whatfactors contribute to the bio-psychosocial model of what is called’celiac irritable bowel syndrome.’
    Future psycho-physiologicalstudies in patients with celiac disease and irritable bowel syndromeshould look to determine if psychological discomfort can prolongmucosal inflammation, reduce visceral pain thresholds, or disturb gutmotility.
    In the event that the right psychotherapeutictreatment for irritable bowel syndrome-like symptoms and/or mentaldisorder serve to improve reduced HRQOL in adult patients with celiacdisease and irritable bowel syndrome-like symptoms, it might benecessary to take a second look at interventional practices.
    So,in a nutshell, this all means that things like mental health, gender,and other non-clinical factors might play a role in irritable bowelsyndrome-like symptoms in people with celiac disease, and that furtherstudy is needed to sort out all of the possibilities and determine ifthere might be better ways to treat celiac disease that will reduce oreliminate irritable bowel syndrome-like symptoms.
    Psychosomatic Medicine 69:370 –376 (2007)


    Diana Gitig Ph.D.
    Celiac.com 05/18/2011 - Irritable Bowel Syndrome (IBS) is based on a clinical description only; there are no pathophysiological pathways definitively associated with it. It is characterized as gastrointestinal symptoms with no discernable cause. A diagnosis of IBS depends on recurrent abdominal pain or discomfort for at least three days per month in the last three months, with the onset of the discomfort either associated with a change in frequency or appearance of stool or alleviated by defecation. A number of different mechanisms have been suggested as potential causes of IBS. These range from psychological origins, to increased visceral hyperalgesia (sensitivity to pain), to the low grade gut inflammation and altered gastrointestinal permeability and motility observed in IBS patients. Complicating matters is that most patients exhibit only a subset of symptoms. Since gluten has been demonstrated to negatively affect even people without celiac disease by an unknown mechanism (see Study Shows Gluten Intolerance Without Celiac Disease), and the underlying causes of IBS remain unclear, Dr. Elena Verdu wondered if gluten might contribute to IBS.
    Like those with IBS, patients with gluten sensitivity lack the antibodies against tissue transglutaminase that are the hallmark of celiac disease but nonetheless suffer immune mediated inflammation in their gut. Interestingly, when IBS patients without celiac eliminated gluten from their diet, 68% of them reported more severe pain, bloating, and tiredness upon gluten rechallenge. But how – by what mechanism? No changes were detected in intestinal permeability or fecal lactoferrin, a marker of intestinal inflammation. However, it is possible that these phenomena persisted, just at below the level of detection.
    Based on these data, and other evidence that is rapidly accruing suggesting that gluten can negatively affect those without celiac disease, Dr. Verdu suggests that IBS patients might be screened for anti-gliadin antibodies even if they lack antibodies against tissue transglutaminase. These nonspecific antibodies can indicate an immunological response to gluten, and thus their presence could used to determine if their symptoms might be alleviated by adherence to a gluten free diet. She makes sure to point out, though, that this is probably not the case for all IBS patients.
    Source:

    Am J Gastroenterol 2011; 106:516–518

    Jefferson Adams
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    Source:
    Arthritis Res Ther. 2013 Nov 27;15(6):R201.

    Jefferson Adams
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    Source:
    Inflamm Bowel Dis. 2015 Apr;21(4):847-53. doi: 10.1097/MIB.0000000000000335.

  • Recent Articles

    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:
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    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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    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
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    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).
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    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.
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    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.