Gluten
[1] The term gluten usually refers to the elastic network of a wheat grain's proteins, gliadin and glutenin primarily, that forms readily with the addition of water and often kneading in the case of bread dough.
Kneading promotes the formation of gluten strands and cross-links, creating baked products that are chewier (as opposed to more brittle or crumbly).
[citation needed] The process yields a flour-like powder with a 7% moisture content, which is air cooled and pneumatically transported to a receiving vessel.
[24] Gluten-added dough must be worked vigorously to induce it to rise to its full capacity; an automatic bread machine or food processor may be required for high-gluten kneading.
[33] In the context of celiac disease, gliadin peptides are classified in basic and clinical research as immunogenic, depending on their mechanism of action:[33][37] At least 50 epitopes of gluten may produce cytotoxic, immunomodulatory, and gut-permeating activities.
[40][44][45][46] Some suggested explanations for this increase include the following: the growing westernization of diets,[44] the increasing use of wheat-based foods included in the Mediterranean diet,[47][48] the progressive replacement of rice by wheat in many countries in Asia, the Middle East, and North Africa,[44] the higher content of gluten in bread and bakery products due to the reduction of dough fermentation time,[49][50] and the development in recent years of new types of wheat with a higher amount of cytotoxic gluten peptides,[49][51] However, a 2020 study that grew and analyzed 60 wheat cultivars from between 1891 and 2010 found no changes in albumin/globulin and gluten contents over time.
"[52] Celiac disease (CD) is a chronic, multiple-organ autoimmune disorder primarily affecting the small intestine caused by the ingestion of wheat, barley, rye, oats, and derivatives, that appears in genetically predisposed people of all ages.
[53] CD is not only a gastrointestinal disease, because it may involve several organs and cause an extensive variety of non-gastrointestinal symptoms, and most importantly, it may be apparently asymptomatic.
[4][54] Many asymptomatic people become accustomed to living with a chronic bad health status as if it were normal, but they are able to recognize that they actually had symptoms related to celiac disease after starting a gluten-free diet and improvement occurs.
[54][55][45] Added difficulties for diagnosis are the fact that serological markers (anti-tissue transglutaminase [TG2]) are not always present[56] and many people may have minor mucosal lesions, without atrophy of the intestinal villi.
[57] CD affects approximately 1–2% of the general population,[11] but most cases remain unrecognized, undiagnosed and untreated, and at risk for serious long-term health complications.
[55] Untreated CD may cause malabsorption, reduced quality of life, iron deficiency, osteoporosis, an increased risk of intestinal lymphomas, and greater mortality.
[53][61] CD with "classic symptoms", which include gastrointestinal manifestations such as chronic diarrhea and abdominal distention, malabsorption, loss of appetite, and impaired growth, is currently the least common presentation form of the disease and affects predominantly small children generally younger than two years of age.
[55] It is characterized by milder or even absent gastrointestinal symptoms and a wide spectrum of non-intestinal manifestations that can involve any organ of the body, and very frequently may be completely asymptomatic[58] both in children (at least in 43% of the cases[62]) and adults.
[58] Asymptomatic CD (ACD) is present in the majority of affected patients and is characterized by the absence of classical gluten-intolerance signs, such as diarrhea, bloating, and abdominal pain.
[63] Non-celiac gluten sensitivity (NCGS) is described as a condition of multiple symptoms that improves when switching to a gluten-free diet, after celiac disease and wheat allergy are excluded.
[12] NCGS is becoming a more common diagnosis, but its true prevalence is difficult to determine because many people self-diagnose and start a gluten-free diet, without having previously tested for celiac disease or having the dietary prescription from a physician.
[69] People with NCGS and gastrointestinal symptoms remain habitually in a "no man's land", without being recognized by the specialists and lacking the adequate medical care and treatment.
[70] Most of these people have a long history of health complaints and unsuccessful consultations with numerous physicians, trying to get a diagnosis of celiac disease, but they are only labeled as irritable bowel syndrome.
[70][71] A consistent although undefined number of people eliminate gluten because they identify it as responsible for their symptoms and these improve with the gluten-free diet, so they self-diagnose as NCGS.
[73] Besides gluten, additional components present in wheat, rye, barley, oats, and their derivatives, including other proteins called amylase-trypsin inhibitors (ATIs) and short-chain carbohydrates known as FODMAPs, may cause NCGS symptoms.
[79] With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing, with loss of Purkinje cells.
The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible.
A 2008 systematic review tentatively concluded that consumption of less than 10 mg of gluten per day is unlikely to cause intestinal damage in people with celiac disease, although it noted that few reliable studies had been done.
[87] Labels for all food products sold in Canada must clearly identify the presence of gluten if it is present at a level greater than 20 parts per million.
