Gluten sensitivity: problems of an emerging condition separate from celiac disease.
ABSTRACT Gluten sensitivity appears to be emerging as a separate condition from celiac disease, yet no clear definition or diagnosis exists. As a result, patients with gluten sensitivity experience delayed diagnosis and continuing symptoms if they consume gluten. This emerging medical problem may involve human genetics, plant genetic modifications, gluten as a food additive, environmental toxins, hormonal influences, intestinal infections and autoimmune diseases. The treatment is similar to that for celiac disease - a gluten-free diet. The use of a gluten-free diet or an elimination diet is encouraged in assisting people to determine whether or not they are gluten sensitive. It is time to not only recognize, but to treat and further research gluten sensitivity, as unconfirmed environmental factors continue to spread this problem further into the general population.
Article: Non-coeliac gluten sensitivity.[Show abstract] [Hide abstract]
ABSTRACT: This patient reflects on his 20 years of unexplained ill health with multiple symptoms before a chance conversation in an internet chat room led to his initial self diagnosis.BMJ (online) 11/2012; 345:e7982. · 16.38 Impact Factor
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ABSTRACT: There is an increase in the number of people adopting a gluten-free diet, with one-fifth of Australian consumers avoiding certain food or drinks for allergy or intolerance reasons. For most consumers, the belief that a gluten-free diet is healthier than a gluten containing diet is unsupported by a formal diagnosis. However, for a small group of subjects who have gluten sensitive disorder, a lifelong, gluten-free diet is required, including avoidance of beer. Prolylendopeptidase enzymes (PEP) cleave gluten proteins after the abundant proline residues and have the potential to destroy gluten proteins and remove or minimize immunoreactive peptides from food. However, PEP treatment may also confound measurement of gluten concentration in food and beverages by destroying epitopes that are used to enumerate gluten peptides – we ask, “does PEP treatment destroy celiac reactive epitopes or merely disguise them from ELISA enumeration?” There is now sufficient data to show that treatment of gluten peptides with bacterial PEP in combination with other proteases, or the fungal Aspergillus niger PEP alone, reduces the immunoreactivity of gluten peptides, with celiac T-cells to near zero. This is also accompanied by destruction of key epitopes that are used by antibodies to enumerate gluten peptides during ELISA reactions. Thus, both immunoreactivity and ELISA measurements are reduced to near zero by PEP treatment. However, definitive evidence of the safety of treated beer for celiacs ideally requires a double-blind crossover, dietary challenge. Consuming sufficient beer to present a suitable load of hordein peptides is not possible, and presenting hordeins in the same form as encountered in treated beer is difficult. The effect of protease treatments on the safety of treated gluten for the remainder the celiac-like diseases, including gluten ataxia and dermatitis herpetiformis, and the larger spectrum of glutenrelated disorders, including gluten intolerance and the IgE-mediated allergic responses Bakers asthma, gluten allergy, WDEIA, and urticaria, cannot be definitively assessed until the epitopes involved have been defined. The gluten sensitive disorders and the gluten proteins are reviewed, and the effects of proteolysis on several archetypal gluten peptides are examined. Keywords: Beer, celiac disease, gluten, hordeins, prolylendopeptidase.Journal of the American Society of Brewing Chemists 02/2014; 72(1):36-50. · 0.86 Impact Factor
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ABSTRACT: Recently, the increasing number of patients worldwide who are sensitive to dietary gluten without evidence of celiac disease or wheat allergy has contributed to the identification of a new gluten-related syndrome defined as non-celiac gluten sensitivity. Our knowledge regarding this syndrome is still lacking, and many aspects of this syndrome remain unknown. Its pathogenesis is heterogeneous, with a recognized pivotal role for innate immunity; many other factors also contribute, including low-grade intestinal inflammation, increased intestinal barrier function and changes in the intestinal microbiota. Gluten and other wheat proteins, such as amylase trypsin inhibitors, are the primary triggers of this syndrome, but it has also been hypothesized that a diet rich in fermentable monosaccharides and polyols may elicit its functional gastrointestinal symptoms. The epidemiology of this condition is far from established; its prevalence in the general population is highly variable, ranging from 0.63% to 6%. From a clinical point of view, non-celiac gluten sensitivity is characterized by a wide array of gastrointestinal and extraintestinal symptoms that occur shortly after the ingestion of gluten and improve or disappear when gluten is withdrawn from the diet. These symptoms recur when gluten is reintroduced. Because diagnostic biomarkers have not yet been identified, a double-blind placebo-controlled gluten challenge is currently the diagnostic method with the highest accuracy. Future research is needed to generate more knowledge regarding non-celiac gluten sensitivity, a condition that has global acceptance but has only a few certainties and many unresolved issues.Cellular & Molecular Immunology advance online publication, 12 August 2013; doi:10.1038/cmi.2013.28.Cellular & molecular immunology 08/2013; · 4.19 Impact Factor