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Found 4 results

  1. Celiac.com 05/11/2016 - You just got out of your daughter's doctor's appointment and have been told: "It is confirmed, she has celiac disease." What do you do? Tell everyone else in the family they must follow a gluten-free diet? What do you do when you have a merged family of celiacs and non-celiacs? My mother went through this very thing. With being celiac herself, she well informed herself via the internet as to what did and didn't have gluten in it. Both my oldest brother and I were eventually diagnosed celiac. This left my other brother and my father being the only two non-celiacs. It can be difficult to wrap your head around just how important maintaining a gluten-free diet is for a celiac when you aren't celiac yourself. So yes, sharing your toaster with both gluten and gluten-free bread can make a celiac ill. Having wheat flour in your kitchen can cross-contaminate, be ingested by a celiac resulting in an adverse reaction in either the celiac child or adult. Keeping gluten away from a celiac is extremely important. Removing those croutons from the top of that salad does not suddenly make it "safe" for any celiac. I am celiac and my husband is not. My 1 year old, Brixton, hasn't eaten any gluten to date. He will also have to be tested when he gets a little older as celiac disease is genetic. How do I maintain a gluten-free household that is both healthy for me and satisfying for my husband? Easy! Get two toasters, seriously! An extra pot just for those special nights my husband wants real good ol' gluten loaded fettuccini. I buy premade boxed treats and snacks that have gluten in them so he doesn't feel "deprived" and so I also don't have to make him cookies and treats with gluten in them. I can say my husband really has taken to gluten-free baked items. I make gluten-free waffles and pancakes every weekend and he drools over them. Not to mention the delicious gluten-free cookie dough I make! Yum! He also knows that when we go out to a restaurant, anything is game for him. He goes to town on the fresh bread, pasta, etc. that the restaurants have. We do however try to maintain a healthy diet from day to day, therefore we primarily eat protein, vegetables, fruit and good (healthy) fats. For those days we want a little something extra, we always have boxed gluten snacks for him and some delicious gluten-free flours for me to whip up something tasty for my whole family. The most important thing to remember is that a gluten-free diet isn't just a diet someone with celiac disease "can" follow if they want. It is a necessary diet and lifestyle they MUST follow for their health and wellbeing. Consider it their "medication" for the disease. With that in mind it may make the celiac and non-celiac families live in harmony.
  2. 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
  3. Celiac.com 08/06/2009 - A study by a team of Spanish researchers puts the world on notice that gluten may trigger adverse reactions in both celiacs and non-celiacs alike. The research team was made up of E. Arranz, D. Bernardo, L. Fernandez-Salazar, J. A. Garrote and their colleague S. Riestra, all doctors based in Spain. According to the current medical wisdom, innate immunity to gluten plays a critical role in the development of celiac disease (celiac disease). This innate immune response is caused by a reaction to the ‘toxic’ gluten peptides that is mediated by interleukin (IL) 15, like the 19-mer through a DQ2-independent mechanism, and which causes epithelial stress and triggers the intraepithelial lymphocytes to turn into natural killer (NK)-like cells, which then causes enterocyte apoptosis and a compromised permeability of the cells lining of the gut…and, violà, celiac disease! It is by breaching this lining that immuno-dominant peptides, such as the 33-mer peptide, come into contact with the lamina propria, which triggers adaptive immunity. The innate specific response in celiac disease has been pretty well documented, but until recently, no one had described any differential factors between people with celiac disease and those without. Since the toxic 19-mer triggers its damaging effects through a DQ2-independent mechanism, doctors wondered whether the innate immune response was common in both people with and without celiac disease, and whether the adaptive response is emblematic only of susceptible people with celiac disease. A team of researchers recently set out to determine just that, beginning with biopsies from at least three patients with celiac disease who were observing a gluten-free diet and three patients who are free of celiac disease. The research team consisted of D. Bernardo, L. Fernandez-Salazar, J. A. Garrote and their colleague S. Riestra, all based in Spain. The team applied crude gliadin, the gliadin synthetic 19-mer and deaminated 33-mer peptides to the biopsy tissue after discarding the presence of lipopolysaccharide. They did this at concentrations of 100 mg/ml for 3 hours to mimic what are considered the standard timing and concentration in the digestive tract after a routine meal. The research team then washed the specimens and cultured them for 21 hours in new clean culture medium to assess whether an innate stimulus is reflected by an adaptive response. Here’s some technical jargon: Each sample cultured in basal medium served as an internal control. Innate immune mediators IL15 and nitrites were measured by western blot in the biopsy protein extract along with a Griess reagent system in the 3 h supernatants respectively. mRNA levels of adaptive immunity mediators like signal transducers and activators of transcription (STAT) 1, STAT3, tumour necrosis factor a, interferon (IFN) c, IL23 (p19), IL27 (p28) and IL12 (p35) were determined by real-time polymerase chain reaction using b actine levels as house-keeping. Compared with the basal culture, all of the patients were challenged with the gliadin solution, and all of the patients, both those with and those without celiac disease on a gluten free diet, showed IL15 production, which indicates an immune reaction is taking place. More importantly, the IL15-mediated response in patients without celiac disease was triggered, in three of six cases, by the same toxic 19-mer gliadin peptide and, in five of six cases, by the 33-mer gliadin peptide as in those with celiac disease. Significantly, none of the basal cultures showed this result, though the ‘‘non-toxic’’ immuno-dominant 33-mer did induce an innate response that was un-foreseen. Interestingly, one patient with celiac disease and on a gluten-free diet, and three patients without celiac disease, who were also on gluten-free diets, all showed the IL15 response, which was confirmed by western blot analysis. This discounts an intracellular and non-biologically active IL15 response in patients without celiac disease. The gliadin-challenged patients with celiac disease who were on a GFD, showed increased nitrite levels, which those without celiac disease did not show. Following the biopsy mRNA isolation, only patients with celiac disease showed modifications to what are called adaptive mediators (STAT1, STAT3, IFNc). The basal samples of those celiac patients on a gluten-free diet showed IFNc mRNA levels that were 80 times higher than basal samples of those without celiac disease (p value 0.002), along with a slightly higher production of nitrites (p value 0.052). This appears to be the first time that researchers have described an IL15-mediated innate response to gliadin and gliadin peptides in people without celiac disease, as well as the first time they have described an IL15-mediated innate response to the ‘non-toxic’ deaminated immuno-dominant 33-mer peptide. What this all means is that, for the first time, scientists have documented harmful effects of gluten on people without celiac disease. This hypothesis seems to be born out by the fact that all individuals who took place in the study, both those with and those without celiac disease, showed an innate immune response to gluten, though only those with celiac disease showed an adaptive immune response to gluten. Clearly, before doctors can draw any hard and fast conclusions, they will need to do more studies on larger groups. The research team also suggests that people with celiac disease have a lower threshold for triggering an adaptive TH1 response than do non-celiacs, and that people with celiac disease need to be DQ2 positive. The reason for the differences in threshold levels between celiacs and non-celiacs might be tied to the fact that celiac patients show higher basal levels of immune mediators, such as IFNc mRNA, compared to those without celiac disease. That’s one possibility. The difference in threshold levels might also have to do with some kind of defect in permeability of the gut membrane in those with celiac disease, or even a greater IL15-sensitivity response under equal stimulus, which might be mediated by a higher density of IL15 receptor in patients with celiac disease. Gut 2007;56:889–890
  4. Celiac.com 11/29/2007 - Studies have documented the role of gut microbiotic bacteria in diseases involving chronic inflammation, such as celiac disease, yet there is scant data on such bacteria that is specific to people with celiac disease. A team of Spanish and Italian researchers from three different hospitals and universities made up of Yolanda Sanz, Ester Sanchez, Marta Marzotto, Miguel Calabuig, Sandra Torriani, and Franco Dellaglio set out to determine what differences might exist between the microbiotic bacteria in the guts of children with celiac disease compared to a healthy control group of their peers. The team conducted a denaturing gradient gel electrophoresis analysis of fecal samples from both the celiac and the control groups. They found that children with celiac disease had a more diverse profile of intestinal microbiotic bacteria than did the healthy control subjects. The children with celiac disease were characterized by the presence of Lactobacillus curvatus, Leuconostoc mesenteriodes, and Leuconostoc carnosum, whereas the members of the healthy control group were characterized by the presence of Lactobacillus casei. Conversely, the bifidobacterium population was much greater in the members of the healthy control group than among the children with celiac disease. The healthy control group showed particularly high populations of bifidobacterium adolescentis compared to the celiac patients. The team has called for more research into which populations of the various gut microbial are affected by celiac disease. This may lead to a possible role for probiotics and/or prebiotics in returning the balance of the gut microbes in those with celiac disease. FEMS Immunol Med Microbiol. 2007 Dec;51(3):562-8
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