Gluten

Last updated
Examples of sources of gluten (clockwise from top): wheat as flour, spelt, barley, and rye as rolled flakes Gluten Sources.png
Examples of sources of gluten (clockwise from top): wheat as flour, spelt, barley, and rye as rolled flakes

Gluten is a structural protein naturally found in certain cereal grains. [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. [2] The types of grains that contain gluten include all species of wheat (common wheat, durum, spelt, khorasan, emmer and einkorn), and barley, rye, and some cultivars of oat; moreover, cross hybrids of any of these cereal grains also contain gluten, e.g. triticale. [3] [4] Gluten makes up 75–85% of the total protein in bread wheat. [5]

Contents

Glutens, especially Triticeae glutens, have unique viscoelastic and adhesive properties, which give dough its elasticity, helping it rise and keep its shape and often leaving the final product with a chewy texture. [5] [6] [7] These properties, and its relatively low cost, make gluten valuable to both food and non-food industries. [7]

Wheat gluten is composed of mainly two types of proteins: the glutenins [8] and the gliadins, [9] which in turn can be divided into high molecular and low molecular glutenins and α/β, γ and Ω gliadins. Its homologous seed storage proteins, in barley, are referred to as hordeins, in rye, secalins, and in oats, avenins. [10] These protein classes are collectively referred to as "gluten". [4] The storage proteins in other grains, such as maize (zeins) and rice (rice protein), are sometimes called gluten, but they do not cause harmful effects in people with celiac disease. [3]

Bread produced from wheat grains contains gluten. Pain sans gluten a la farine de chataigne et charcuterie corse.jpg
Bread produced from wheat grains contains gluten.

Gluten can trigger adverse, inflammatory, immunological, and autoimmune reactions in some people. The spectrum of gluten related disorders includes celiac disease in 1–2% of the general population, non-celiac gluten sensitivity in 0.5–13% of the general population, as well as dermatitis herpetiformis, gluten ataxia and other neurological disorders. [11] [12] [13] [14] These disorders are treated by a gluten-free diet. [14]

Uses

Wheat, a prime source of gluten Wheat field.jpg
Wheat, a prime source of gluten

Bread products

Gluten forms when glutenin molecules cross-link via disulfide bonds to form a submicroscopic network attached to gliadin, which contributes viscosity (thickness) and extensibility to the mix. [5] [15] If this dough is leavened with yeast, fermentation produces carbon dioxide bubbles, which, trapped by the gluten network, cause the dough to rise. Baking coagulates the gluten, which, along with starch, stabilizes the shape of the final product. Gluten content has been implicated as a factor in the staling of bread, possibly because it binds water through hydration. [16] [17]

Cross-section of a baguette showing a strong gluten network Pain au levain dit a l'ancienne 02.jpg
Cross-section of a baguette showing a strong gluten network

The formation of gluten affects the texture of the baked goods. [5] Gluten's attainable elasticity is proportional to its content of glutenins with low molecular weights, as this portion contains the preponderance of the sulfur atoms responsible for the cross-linking in the gluten network. [18] [19] Using flour with higher gluten content leads to chewier doughs such as those found in pizza and bagels, while using flour with less gluten content yields tender baked goods such as pastry products. [20]

Generally, bread flours are high in gluten (hard wheat); pastry flours have a lower gluten content. Kneading promotes the formation of gluten strands and cross-links, creating baked products that are chewier (as opposed to more brittle or crumbly). The "chewiness" increases as the dough is kneaded for longer times. An increased moisture content in the dough enhances gluten development, [20] and very wet doughs left to rise for a long time require no kneading (see no-knead bread). Shortening inhibits formation of cross-links and is used, along with diminished water and less kneading, when a tender and flaky product, such as a pie crust, is desired.

The strength and elasticity of gluten in flour is measured in the baking industry using a farinograph. This gives the baker a measurement of quality for different varieties of flours when developing recipes for various baked goods. [5] [21] [22]

Added gluten

In industrial production, a slurry of wheat flour is kneaded vigorously by machinery until the gluten agglomerates into a mass. [23] [ failed verification ] This mass is collected by centrifugation, then transported through several stages integrated in a continuous process. About 65% of the water in the wet gluten is removed by means of a screw press; the remainder is sprayed through an atomizer nozzle into a drying chamber, where it remains at an elevated temperature for a short time to allow the water to evaporate without denaturing the gluten.[ 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. In the final step, the processed gluten is sifted and milled to produce a uniform product. [23]

This flour-like powder, when added to ordinary flour dough, may help improve the dough's ability to increase in volume. The resulting mixture also increases the bread's structural stability and chewiness. [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. [25] Generally, higher gluten levels are associated with higher overall protein content. [26]

Imitation meats

Gluten is often used in imitation meats (such as this mock duck) to provide supplemental protein in vegetarian diets Wheat gluten (vegetarian mock duck) 2007.jpg
Gluten is often used in imitation meats (such as this mock duck) to provide supplemental protein in vegetarian diets

Gluten, especially wheat gluten (seitan), is often the basis for imitation meats resembling beef, chicken, duck (see mock duck), fish and pork. When cooked in broth, gluten absorbs some of the surrounding liquid (including the flavor) and becomes firm to the bite. [27] [28] This use of gluten is a popular means of adding supplemental protein to many vegetarian diets. In home or restaurant cooking, wheat gluten is prepared from flour by kneading the flour under water, agglomerating the gluten into an elastic network known as a dough, and then washing out the starch. [5]

Other consumer products

Gluten is often present in beer and soy sauce, and can be used as a stabilizing agent in more unexpected food products, such as ice cream and ketchup. Foods of this kind may therefore present problems for a small number of consumers because the hidden gluten constitutes a hazard for people with celiac disease and gluten sensitivities. The protein content of some pet foods may also be enhanced by adding gluten. [29]

Gluten is also used in cosmetics, hair products and other dermatological preparations. [30]

Disorders

"Gluten-related disorders" is the umbrella term for all diseases triggered by gluten, which include celiac disease (CD), non-celiac gluten sensitivity (NCGS), wheat allergy, gluten ataxia and dermatitis herpetiformis (DH). [13]

Pathophysiological research

The gluten peptides are responsible for triggering gluten-related disorders. [31] In people who have celiac disease, the peptides trigger an immune response that causes injury of the intestines, ranging from inflammation to partial or total destruction of the intestinal villi. [32] [33] To study mechanisms of this damage, laboratory experiments are done in vitro and in vivo. [34] [33] Among the gluten peptides, gliadin has been studied extensively. [31]

In vitro and in vivo studies

In the context of celiac disease, gliadin peptides are classified in basic and clinical research as immunogenic, depending on their mechanism of action: [31] [35]

At least 50 epitopes of gluten may produce cytotoxic, immunomodulatory, and gut-permeating activities. [37]

The effect of oat peptides (avenins) in celiac people depends on the oat cultivar consumed because of prolamin genes, protein amino acid sequences, and the immunotoxicity of prolamins which vary among oat varieties. [39] [40] [41] In addition, oat products may be cross-contaminated with the other gluten-containing cereals. [40]

Incidence

As of 2017, gluten-related disorders were increasing in frequency in different geographic areas. [38] [42] [43] [44] Some suggested explanations for this increase include the following: the growing westernization of diets, [42] the increasing use of wheat-based foods included in the Mediterranean diet, [45] [46] the progressive replacement of rice by wheat in many countries in Asia, the Middle East, and North Africa, [42] the higher content of gluten in bread and bakery products due to the reduction of dough fermentation time, [47] [48] and the development in recent years of new types of wheat with a higher amount of cytotoxic gluten peptides, [47] [49] 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. "Overall, the harvest year had a more significant effect on protein composition than the cultivar. At the protein level, we found no evidence to support an increased immunostimulatory potential of modern winter wheat." [50]

Celiac disease

Medical animation still showing flattened intestinal villi. Inflammed mucous layer of the intestinal villi depicting Celiac disease.jpg
Medical animation still showing flattened intestinal villi.

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. [51] 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] [52] 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. [52] [53] [43] Added difficulties for diagnosis are the fact that serological markers (anti-tissue transglutaminase [TG2]) are not always present [54] and many people may have minor mucosal lesions, without atrophy of the intestinal villi. [55]

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. [11] [43] [56] [57] People may suffer severe disease symptoms and be subjected to extensive investigations for many years, before a proper diagnosis is achieved. [53] Untreated CD may cause malabsorption, reduced quality of life, iron deficiency, osteoporosis, an increased risk of intestinal lymphomas, and greater mortality. [58] CD is associated with some other autoimmune diseases, such as diabetes mellitus type 1, thyroiditis, [59] gluten ataxia, psoriasis, vitiligo, autoimmune hepatitis, dermatitis herpetiformis, primary sclerosing cholangitis, and more. [51] [59]

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. [51] [53] [56]

CD with "non-classic symptoms" is the most common clinical type [53] and occurs in older children (over two years old), [53] adolescents, and adults. [53] 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 [56] both in children (at least in 43% of the cases [60] ) and adults. [56]

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. Nevertheless, these individuals very often develop diseases that can be related with gluten intake. Gluten can be degraded into several morphine-like substances, named gluten exorphins. These compounds have proven opioid effects and could mask the deleterious effects of gluten protein on gastrointestinal lining and function. [61]

Non-celiac gluten sensitivity

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. [62] [63] Recognized since 2010, [64] [65] it is included among gluten-related disorders. [64] Its pathogenesis is not yet well understood, but the activation of the innate immune system, the direct negative effects of gluten and probably other wheat components, are implicated. [65] [36]

NCGS is the most common syndrome of gluten intolerance, [64] [66] with a prevalence estimated to be 6-10%. [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. [67] 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. [68] 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. [68] [69] 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. [68] [69]

People with NCGS may develop gastrointestinal symptoms, which resemble those of irritable bowel syndrome or wheat allergy, [64] [36] or a wide variety of non-gastrointestinal symptoms, such as headache, chronic fatigue, fibromyalgia, atopic diseases, allergies, neurological diseases, or psychiatric disorders, among others. [58] [65] [70] The results of a 2017 study suggest that NCGS may be a chronic disorder, as is the case with celiac disease. [71]

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. [65] As of 2019, reviews conclude that although FODMAPs present in wheat and related grains may play a role in non-celiac gluten sensitivity, they only explain certain gastrointestinal symptoms, such as bloating, but not the extra-digestive symptoms that people with non-celiac gluten sensitivity may develop, such as neurological disorders, fibromyalgia, psychological disturbances, and dermatitis. [72] [71] [65] ATIs may cause toll-like receptor 4 (TLR4)-mediated intestinal inflammation in humans. [73] [74]

Wheat allergy

People can also experience adverse effects of wheat as result of a wheat allergy. [57] As with most allergies, a wheat allergy causes the immune system to respond abnormally to a component of wheat that it treats as a threatening foreign body. This immune response is often time-limited and does not cause lasting harm to body tissues. [75] Wheat allergy and celiac disease are different disorders. [57] [76] Gastrointestinal symptoms of wheat allergy are similar to those of celiac disease and non-celiac gluten sensitivity, but there is a different interval between exposure to wheat and onset of symptoms. An allergic reaction to wheat has a fast onset (from minutes to hours) after the consumption of food containing wheat and could include anaphylaxis. [54]

Gluten ataxia

A male with gluten ataxia: previous situation and evolution after three months of gluten-free diet

Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten. [77] 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. People with gluten ataxia usually present gait abnormality or incoordination and tremor of the upper limbs. Gaze-evoked nystagmus and other ocular signs of cerebellar dysfunction are common. Myoclonus, palatal tremor, and opsoclonus-myoclonus may also appear. [78]

Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. 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. [78] [79]

Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of all ataxias. [78] [80] Less than 10% of people with gluten ataxia present any gastrointestinal symptom, yet about 40% have intestinal damage. [78]

Other neurological disorders

In addition to gluten ataxia, gluten sensitivity can cause a wide spectrum of neurological disorders, which develop with or without the presence of digestive symptoms or intestinal damage. [14] These include peripheral neuropathy, epilepsy, headache, encephalopathy, vascular dementia, and various movement disorders (restless legs syndrome, chorea, parkinsonism, Tourette syndrome, palatal tremor, myoclonus, dystonia, opsoclonus myoclonus syndrome, paroxysms, dyskinesia, myorhythmia, myokymia). [14] [81]

The diagnosis of underlying gluten sensitivity is complicated and delayed when there are no digestive symptoms. People who do experience gastrointestinal problems are more likely to receive a correct diagnosis and treatment. A strict gluten-free diet is the first-line treatment, which should be started as soon as possible. It is effective in most of these disorders. When dementia has progressed to an advanced degree, the diet has no beneficial effect. Cortical myoclonus appears to be treatment-resistant on both gluten-free diet and immunosuppression. [14]

Labeling

People with gluten-related disorders have to remove gluten from their diet strictly, so they need clear labeling rules. [82] The term "gluten-free" is generally used to indicate a supposed harmless level of gluten rather than a complete absence. [83] The exact level at which gluten is harmless is uncertain and controversial. 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. [83] Regulation of the label "gluten-free" varies. [82]

International standards

The Codex Alimentarius international standards for food labeling has a standard relating to the labeling of products as "gluten-free". It only applies to foods that would normally contain gluten. [84]

Brazil

By law in Brazil, all food products must display labels clearly indicating whether or not they contain gluten. [85]

Canada

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. [86]

European Union & United Kingdom

In the European Union, all prepackaged foods and non-prepacked foods from a restaurant, take-out food wrapped just before sale, or unpackaged food served in institutions must be identified if gluten-free. [87] "Gluten-free" is defined as 20 parts per million of gluten or less and "very low gluten" is 100 parts per million of gluten or less; only foods with cereal ingredients processed to remove gluten can claim "very low gluten" on labels. [87] It is not allowed to label food as "gluten-free" when all similar food is naturally gluten-free, such as in the case of milk. [88]

All foods containing gluten as an ingredient must be labelled accordingly as gluten is defined as one of the 14 recognised EU allergens. [89]

United States

In the United States, gluten is not listed on labels unless added as a standalone ingredient. Wheat or other allergens are listed after the ingredient line. The US Food and Drug Administration (FDA) has historically classified gluten as "generally recognized as safe" (GRAS). In August 2013, the FDA issued a final ruling, effective August 2014, that defined the term "gluten-free" for voluntary use in the labeling of foods as meaning that the amount of gluten contained in the food is below 20 parts per million. [90]

See also

Related Research Articles

<span class="mw-page-title-main">Bread</span> Food made of flour and water

Bread is a staple food prepared from a dough of flour and water, usually by baking. Throughout recorded history and around the world, it has been an important part of many cultures' diet. It is one of the oldest human-made foods, having been of significance since the dawn of agriculture, and plays an essential role in both religious rituals and secular culture.

<span class="mw-page-title-main">Coeliac disease</span> Autoimmune disorder that results in a reaction to gluten

Coeliac disease or celiac disease is a long-term autoimmune disorder, primarily affecting the small intestine, where individuals develop intolerance to gluten, present in foods such as wheat, rye and barley. Classic symptoms include gastrointestinal problems such as chronic diarrhoea, abdominal distention, malabsorption, loss of appetite, and among children failure to grow normally. Non-classic symptoms are more common, especially in people older than two years. There may be mild or absent gastrointestinal symptoms, a wide number of symptoms involving any part of the body, or no obvious symptoms. Coeliac disease was first described in childhood; however, it may develop at any age. It is associated with other autoimmune diseases, such as Type 1 diabetes mellitus and Hashimoto's thyroiditis, among others.

<span class="mw-page-title-main">Gluten-free diet</span> Diet excluding proteins found in wheat, barley, and rye

A gluten-free diet (GFD) is a nutritional plan that strictly excludes gluten, which is a mixture of prolamin proteins found in wheat, as well as barley, rye, and oats. The inclusion of oats in a gluten-free diet remains controversial, and may depend on the oat cultivar and the frequent cross-contamination with other gluten-containing cereals.

<span class="mw-page-title-main">Fructose malabsorption</span> Medical condition

Fructose malabsorption, formerly named dietary fructose intolerance (DFI), is a digestive disorder in which absorption of fructose is impaired by deficient fructose carriers in the small intestine's enterocytes. This results in an increased concentration of fructose. Intolerance to fructose was first identified and reported in 1956.

Gluten exorphins are a group of opioid peptides formed during the digestion of the gluten protein. These peptides work as external regulators for gastrointestinal movement and hormonal release. The breakdown of gliadin, a polymer of wheat proteins, creates amino acids that stop the gluten epitopes from entering the immune system to activate inflammatory reactions. During this process, gluten does not fully break down, thus increasing the presence of gluten exorphins. Because of this, researchers think this is what might lead to various diseases.

<span class="mw-page-title-main">Gliadin</span> Protein in wheat & other cereals

Gliadin is a class of proteins present in wheat and several other cereals within the grass genus Triticum. Gliadins, which are a component of gluten, are essential for giving bread the ability to rise properly during baking. Gliadins and glutenins are the two main components of the gluten fraction of the wheat seed. This gluten is found in products such as wheat flour. Gluten is split about evenly between the gliadins and glutenins, although there are variations found in different sources.

<span class="mw-page-title-main">Whole grain</span> Cereal containing endosperm, germ, and bran

A whole grain is a grain of any cereal and pseudocereal that contains the endosperm, germ, and bran, in contrast to refined grains, which retain only the endosperm.

Intestinal permeability is a term describing the control of material passing from inside the gastrointestinal tract through the cells lining the gut wall, into the rest of the body. The intestine normally exhibits some permeability, which allows nutrients to pass through the gut, while also maintaining a barrier function to keep potentially harmful substances from leaving the intestine and migrating to the body more widely. In a healthy human intestine, small particles can migrate through tight junction claudin pore pathways, and particles up to 10–15 Å can transit through the paracellular space uptake route. There is some evidence abnormally increased intestinal permeability may play a role in some chronic diseases and inflammatory conditions. The most well understood condition with observed increased intestinal permeability is celiac disease.

<span class="mw-page-title-main">Wheat allergy</span> Medical condition

Wheat allergy is an allergy to wheat which typically presents itself as a food allergy, but can also be a contact allergy resulting from occupational exposure. Like all allergies, wheat allergy involves immunoglobulin E and mast cell response. Typically the allergy is limited to the seed storage proteins of wheat. Some reactions are restricted to wheat proteins, while others can react across many varieties of seeds and other plant tissues. Wheat allergy is rare. Prevalence in adults was estimated to be 0.21% in a 2012 study in Japan.

<span class="mw-page-title-main">Triticeae</span> Tribe of grasses

Triticeae is a botanical tribe within the subfamily Pooideae of grasses that includes genera with many domesticated species. Major crop genera found in this tribe include wheat, barley, and rye; crops in other genera include some for human consumption, and others used for animal feed or rangeland protection. Among the world's cultivated species, this tribe has some of the most complex genetic histories. An example is bread wheat, which contains the genomes of three species with only one being a wheat Triticum species. Seed storage proteins in the Triticeae are implicated in various food allergies and intolerances.

<span class="mw-page-title-main">Triticeae glutens</span> Seed storage protein in mature wheat seeds

Gluten is the seed storage protein in mature wheat seeds. It is the sticky substance in bread wheat which allows dough to rise and retain its shape during baking. The same, or very similar, proteins are also found in related grasses within the tribe Triticeae. Seed glutens of some non-Triticeae plants have similar properties, but none can perform on a par with those of the Triticeae taxa, particularly the Triticum species. What distinguishes bread wheat from these other grass seeds is the quantity of these proteins and the level of subcomponents, with bread wheat having the highest protein content and a complex mixture of proteins derived from three grass species.

<span class="mw-page-title-main">Gluten-related disorders</span> Set of diseases caused by gluten exposure

Gluten-related disorders is the term for the diseases triggered by gluten, including celiac disease (CD), non-celiac gluten sensitivity (NCGS), gluten ataxia, dermatitis herpetiformis (DH) and wheat allergy. The umbrella category has also been referred to as gluten intolerance, though a multi-disciplinary physician-led study, based in part on the 2011 International Coeliac Disease Symposium, concluded that the use of this term should be avoided due to a lack of specificity.

Gluten-sensitive enteropathy–associated conditions are comorbidities or complications of gluten-related gastrointestinal distress. GSE has key symptoms typically restricted to the bowel and associated tissues; however, there are a wide variety of associated conditions. These include bowel disorders, eosinophilic gastroenteritis and increase with coeliac disease (CD) severity. With some early onset and a large percentage of late onset disease, other disorders appear prior to the coeliac diagnosis or allergic-like responses markedly increased in GSE. Many of these disorders persist on a strict gluten-free diet, and are thus independent of coeliac disease after triggering. For example, autoimmune thyroiditis is a common finding with GSE.

Anti-gliadin antibodies are produced in response to gliadin, a prolamin found in wheat. In bread wheat it is encoded by three different alleles, AA, BB, and DD. These alleles can produce slightly different gliadins, which can cause the body to produce different antibodies. Some of these antibodies can detect proteins in specific grass taxa such as Triticeae, while others react sporadically with certain species in those taxa, or over many taxonomically defined grass tribes.

Anti-transglutaminase antibodies (ATA) are autoantibodies against the transglutaminase protein. Detection is considered abnormal, and may indicate one of several conditions.

Oat sensitivity represents a sensitivity to the proteins found in oats, Avena sativa. Sensitivity to oats can manifest as a result of allergy to oat seed storage proteins either inhaled or ingested. A more complex condition affects individuals who have gluten-sensitive enteropathy in which there is an autoimmune response to avenin, the glutinous protein in oats similar to the gluten within wheat. Sensitivity to oat foods can also result from their frequent contamination by wheat, barley, or rye particles.

The immunochemistry of Triticeae glutens is important in several inflammatory diseases. It can be subdivided into innate responses, class II mediated presentation, class I mediated stimulation of killer cells, and antibody recognition. The responses to gluten proteins and polypeptide regions differs according to the type of gluten sensitivity. The response is also dependent on the genetic makeup of the human leukocyte antigen genes. In gluten sensitive enteropathy, there are four types of recognition, innate immunity, HLA-DQ, and antibody recognition of gliadin and transglutaminase. With idiopathic gluten sensitivity only antibody recognition to gliadin has been resolved. In wheat allergy, the response pathways are mediated through IgE against other wheat proteins and other forms of gliadin.

FODMAPs or fermentable oligosaccharides, disaccharides, monosaccharides, and polyols are short-chain carbohydrates that are poorly absorbed in the small intestine and ferment in the colon. They include short-chain oligosaccharide polymers of fructose (fructans) and galactooligosaccharides, disaccharides (lactose), monosaccharides (fructose), and sugar alcohols (polyols), such as sorbitol, mannitol, xylitol, and maltitol. Most FODMAPs are naturally present in food and the human diet, but the polyols may be added artificially in commercially prepared foods and beverages.

Non-celiac gluten sensitivity (NCGS) or gluten sensitivity is a controversial disorder which can cause both gastrointestinal and other problems.

The gluten challenge test is a medical test in which gluten-containing foods are consumed and (re-)occurrence of symptoms is observed afterwards to determine whether and how much a person reacts to these foods. The test may be performed in people with suspected gluten-related disorders in very specific occasions and under medical supervision, for example in people who had started a gluten-free diet without performing duodenal biopsy.

References

  1. ↑ Hervé This, « Who discovered the gluten and who discovered its production by lixiviation? », Notes Académiques de l'Académie d'Agriculture de France/Academic Notes from the French Academy of Agriculture, vol. 3, no 3, 2002, p. 1–11
    Shewry PR, Halford NG, Belton PS, Tatham AS (February 2002). "The structure and properties of gluten: an elastic protein from wheat grain". Philos Trans R Soc Lond B Biol Sci. 357 (1418): 133–42. doi:10.1098/rstb.2001.1024. PMC   1692935 . PMID   11911770.
  2. ↑ McGee, Harold (2007-03-20). On Food and Cooking. Simon and Schuster. p. 521. ISBN   978-1-4165-5637-4.
  3. 1 2 Food and Drug Administration (January 2007). "Food Labeling; Gluten-Free Labeling of Foods" (PDF). Food and Drug Administration. Archived from the original (PDF) on 2007-01-26.
  4. 1 2 3 Biesiekierski JR (2017). "What is gluten?". J Gastroenterol Hepatol (Review). 32 (Suppl 1): 78–81. doi: 10.1111/jgh.13703 . PMID   28244676. Similar proteins to the gliadin found in wheat exist as secalin in rye, hordein in barley, and avenins in oats, and are collectively referred to as 'gluten'. The gluten found in all of these grains has been identified as the component capable of triggering the immune-mediated disorder, celiac disease.
  5. 1 2 3 4 5 6 Shewry, P. R.; Halford, N. G.; Belton, P. S.; Tatham, A. S. (2002). "The structure and properties of gluten: An elastic protein from wheat grain". Philosophical Transactions of the Royal Society B: Biological Sciences. 357 (1418): 133–142. doi:10.1098/rstb.2001.1024. PMC   1692935 . PMID   11911770.
  6. ↑ Lamacchia C, Camarca A, Picascia S, Di Luccia A, Gianfrani C (Jan 29, 2014). "Cereal-based gluten-free food: how to reconcile nutritional and technological properties of wheat proteins with safety for celiac disease patients". Nutrients (Review). 6 (2): 575–90. doi: 10.3390/nu6020575 . PMC   3942718 . PMID   24481131. the distinctive feature that makes wheat unique is, precisely, the visco-elasticity of gluten. When the grain is milled and mixed with water, storage proteins form a dough, capable of retaining gas bubbles. These properties make wheat suitable for the preparation of a great diversity of food products
  7. 1 2 Day L, Augustin MA, Batey IL, Wrigley, CW (February 2006). "Wheat-gluten uses and industry needs". Trends in Food Science & Technology (Review). 17 (2): 82–90. doi:10.1016/j.tifs.2005.10.003. Given the unique properties of wheat gluten, it is not surprising that it has been the subject of intense attention by the food industry. (...) Gluten does have economic benefits over and above the more expensive milk- or soy-protein products (Table 1), and its functional properties, which other products cannot duplicate, give it a unique place among the various protein products. (...) Unlike whey and soy proteins, gluten or wheat proteins are not high in biological value and have not been widely researched for nutritional advantages.
  8. ↑ Payne, P. I. (2012-12-06). "Endosperm Proteins". In Blonstein, A. D.; King, P. J. (eds.). A Genetic Approach to Plant Biochemistry. Springer. p. 210. ISBN   978-3-7091-6989-6.
  9. ↑ Zhao, Hefei (February 2020). "Comparison of wheat, soybean, rice, and pea protein properties for effective applications in food products". Journal of Food Biochemistry. (44)4 (4): e13157. doi: 10.1111/jfbc.13157 . PMID   32020651. S2CID   211034183.
  10. ↑ Rosentrater, Kurt A.; Evers, A.D. (2018). "Chemical components and nutrition". Kent's Technology of Cereals. pp. 267–368. doi:10.1016/B978-0-08-100529-3.00004-9. ISBN   978-0-08-100529-3.
  11. 1 2 3 Lundin KE, Wijmenga C (Sep 2015). "Coeliac disease and autoimmune disease-genetic overlap and screening". Nat Rev Gastroenterol Hepatol. 12 (9): 507–15. doi:10.1038/nrgastro.2015.136. PMID   26303674. S2CID   24533103.
  12. 1 2 Molina-Infante J, Santolaria S, Montoro M, Esteve M, Fernández-Bañares F (2014). "[Non-celiac gluten sensitivity: a critical review of current evidence] [Article in Spanish]". Gastroenterol Hepatol. 37 (6): 362–71. doi:10.1016/j.gastrohep.2014.01.005. PMID   24667093.
  13. 1 2 Ludvigsson JF, Leffler DA, Bai JC, Biagi F, Fasano A, Green PH, Hadjivassiliou M, Kaukinen K, Kelly CP, Leonard JN, Lundin KE, Murray JA, Sanders DS, Walker MM, Zingone F, Ciacci C (January 2013). "The Oslo definitions for coeliac disease and related terms". Gut (Review). 62 (1): 43–52. doi:10.1136/gutjnl-2011-301346. PMC   3440559 . PMID   22345659.
  14. 1 2 3 4 5 Zis P, Hadjivassiliou M (26 February 2019). "Treatment of Neurological Manifestations of Gluten Sensitivity and Coeliac Disease". Curr Treat Options Neurol (Review). 21 (3): 10. doi: 10.1007/s11940-019-0552-7 . PMID   30806821.
  15. ↑ Woychick, JH; et al. "The Gluten Proteins and Deamidated Soluble Wheat Protein". Archived from the original on 12 August 2009. Retrieved 8 September 2009.
  16. ↑ Sahlström, S.; Bråthen, E. (January 1997). "Effects of enzyme preparations for baking, mixing time and resting time on bread quality and bread staling". Food Chemistry. 58 (1–2): 75–80. doi:10.1016/S0308-8146(96)00216-6.
  17. ↑ Magnus, E.M.; Bråthen, E.; Sahlström, S.; Færgestad, E.Mosleth; Ellekjær, M.R. (May 1997). "Effects of Wheat Variety and Processing Conditions in Experimental Bread Baking Studied by Univariate and Multivariate Analyses". Journal of Cereal Science. 25 (3): 289–301. doi:10.1006/jcrs.1996.0094.
  18. ↑ Edwards, N. M.; Mulvaney, S. J.; Scanlon, M. G.; Dexter, J. E. (November 2003). "Role of Gluten and Its Components in Determining Durum Semolina Dough Viscoelastic Properties". Cereal Chemistry. 80 (6): 755–763. doi:10.1094/CCHEM.2003.80.6.755.
  19. ↑ Tosi, Paola; Masci, Stefania; Giovangrossi, Angela; D’Ovidio, Renato; Bekes, Frank; Larroque, Oscar; Napier, Johnathan; Shewry, Peter (September 2005). "Modification of the Low Molecular Weight (LMW) Glutenin Composition of Transgenic Durum Wheat: Effects on Glutenin Polymer Size and Gluten Functionality". Molecular Breeding. 16 (2): 113–126. doi:10.1007/s11032-005-5912-1. S2CID   24914227.
  20. 1 2 "Baking Technology, Bread". Bakersassist. Archived from the original on 2007-08-23. Retrieved 2007-08-14.
  21. ↑ "Farinograph". Wheat Quality and Carbohydrate Research. North Dakota State University. 22 September 2014. Archived from the original on 23 December 2014. Retrieved 8 December 2014.
  22. ↑ Oliver, JR; Allen, HM (January 1992). "The prediction of bread baking performance using the farinograph and extensograph". Journal of Cereal Science. 15 (1): 79–89. doi:10.1016/S0733-5210(09)80058-1.
  23. 1 2 Sakhare, S. D.; Inamdar, A. A.; Soumya, C; Indrani, D; Rao, G. V. (2013). "Effect of flour particle size on microstructural, rheological and physico-sensory characteristics of bread and south Indian parotta". Journal of Food Science and Technology. 51 (12): 4108–13. doi:10.1007/s13197-013-0939-5. PMC   4252461 . PMID   25477689.
  24. ↑ Amendola, J.; Rees, N.; Lundberg, D. E. (2002). Understanding Baking.
  25. ↑ Eckhardt, L.W.; Butts, D.C. (1997). Rustic European Breads from your Bread Machine.
  26. ↑ "Against the Grain". The New Yorker. 3 November 2014. Retrieved 8 December 2014.
  27. ↑ Bates, Dorothy R.; Wingate, Colby (1993). Cooking with Gluten and Seitan. Book Publishing Company. p. 128. ISBN   978-0-913990-95-7.
  28. ↑ Abramowski, Nicole (11 March 2011). "How to Make Seitan: An Illustrated Guide". Vegan Nom Noms. Retrieved 8 December 2014.
  29. ↑ "Pet Foods". International Wheat Gluten Association. Archived from the original on 2007-10-07. Retrieved 14 August 2007.
  30. ↑ Humbert, Philippe; Pelletier, Fabien; Dreno, Brigitte; Puzenat, Eve; Aubin, François (1 January 2006). "Gluten intolerance and skin diseases". European Journal of Dermatology. 16 (1): 4–11. PMID   16436335.
  31. 1 2 3 4 5 6 Lammers KM, Herrera MG, Dodero VI (2018). "Translational Chemistry Meets Gluten-Related Disorders". ChemistryOpen (Review). 7 (3): 217–232. doi:10.1002/open.201700197. PMC   5838388 . PMID   29531885.
  32. ↑ Dickson BC, Streutker CJ, Chetty R (2006). "Coeliac disease: an update for pathologists". J Clin Pathol (Review). 59 (10): 1008–16. doi:10.1136/jcp.2005.035345. PMC   1861744 . PMID   17021129.
  33. 1 2 Stoven S, Murray JA, Marietta EV (2013). "Latest in vitro and in vivo models of celiac disease". Expert Opin Drug Discov (Review). 8 (4): 445–57. doi:10.1517/17460441.2013.761203. PMC   3605231 . PMID   23293929.
  34. ↑ Kupfer SS, Jabri B (2012). "Pathophysiology of celiac disease". Gastrointest Endosc Clin N Am (Review). 22 (4): 639–60. doi:10.1016/j.giec.2012.07.003. PMC   3872820 . PMID   23083984.
  35. 1 2 Silano M, Vincentini O, De Vincenzi M (2009). "Toxic, immunostimulatory and antagonist gluten peptides in celiac disease". Curr Med Chem (Review). 16 (12): 1489–98. doi:10.2174/092986709787909613. PMID   19355902.
  36. 1 2 3 4 Elli L, Roncoroni L, Bardella MT (2015). "Non-celiac gluten sensitivity: Time for sifting the grain". World J Gastroenterol (Review). 21 (27): 8221–6. doi: 10.3748/wjg.v21.i27.8221 . PMC   4507091 . PMID   26217073.
  37. 1 2 Fasano A (Jan 2011). "Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer". Physiol. Rev. (Review). 91 (1): 151–75. CiteSeerX   10.1.1.653.3967 . doi:10.1152/physrev.00003.2008. PMID   21248165. There are at least 50 toxic epitopes in gluten peptides exerting cytotoxic, immunomodulatory, and gut-permeating activities.
  38. 1 2 Leonard MM, Sapone A, Catassi C, Fasano A (2017). "Celiac Disease and Nonceliac Gluten Sensitivity: A Review". JAMA (Review). 318 (7): 647–656. doi:10.1001/jama.2017.9730. PMID   28810029. S2CID   205094729. Previous studies have shown that gliadin can cause an immediate and transient increase in gut permeability. This permeating effect is secondary to the binding of specific undigestible gliadin fragments to the CXCR3 chemokine receptor with subsequent release of zonulin, a modulator of intercellular tight junctions. This process takes place in all individuals who ingest gluten. For the majority, these events do not lead to abnormal consequences. However, these same events can lead to an inflammatory process in genetically predisposed individuals when the immunologic surveillance system mistakenly recognizes gluten as a pathogen.
  39. ↑ Penagini F, Dilillo D, Meneghin F, Mameli C, Fabiano V, Zuccotti GV (Nov 18, 2013). "Gluten-free diet in children: an approach to a nutritionally adequate and balanced diet". Nutrients (Review). 5 (11): 4553–65. doi: 10.3390/nu5114553 . PMC   3847748 . PMID   24253052.
  40. 1 2 de Souza MC, Deschênes ME, Laurencelle S, Godet P, Roy CC, Djilali-Saiah I (2016). "Pure Oats as Part of the Canadian Gluten-Free Diet in Celiac Disease: The Need to Revisit the Issue". Can J Gastroenterol Hepatol (Review). 2016: 1–8. doi: 10.1155/2016/1576360 . PMC   4904650 . PMID   27446824.
  41. ↑ Comino I, Moreno Mde L, Sousa C (Nov 7, 2015). "Role of oats in celiac disease". World J Gastroenterol. 21 (41): 11825–31. doi: 10.3748/wjg.v21.i41.11825 . PMC   4631980 . PMID   26557006. It is necessary to consider that oats include many varieties, containing various amino acid sequences and showing different immunoreactivities associated with toxic prolamins. As a result, several studies have shown that the immunogenicity of oats varies depending on the cultivar consumed. Thus, it is essential to thoroughly study the variety of oats used in a food ingredient before including it in a gluten-free diet.
  42. 1 2 3 Tovoli F, Masi C, Guidetti E, Negrini G, Paterini P, Bolondi L (Mar 16, 2015). "Clinical and diagnostic aspects of gluten related disorders". World J Clin Cases (Review). 3 (3): 275–84. doi: 10.12998/wjcc.v3.i3.275 . PMC   4360499 . PMID   25789300.
  43. 1 2 3 Lionetti E, Gatti S, Pulvirenti A, Catassi C (Jun 2015). "Celiac disease from a global perspective". Best Pract Res Clin Gastroenterol (Review). 29 (3): 365–79. doi:10.1016/j.bpg.2015.05.004. PMID   26060103.
  44. ↑ Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH, Hadjivassiliou M, Kaukinen K, Rostami K, Sanders DS, Schumann M, Ullrich R, Villalta D, Volta U, Catassi C, Fasano A (2012). "Spectrum of gluten-related disorders: consensus on new nomenclature and classification". BMC Medicine (Review). 10: 13. doi: 10.1186/1741-7015-10-13 . PMC   3292448 . PMID   22313950. Open Access logo PLoS transparent.svg
  45. ↑ Volta U, Caio G, Tovoli F, De Giorgio R (2013). "Non-celiac gluten sensitivity: questions still to be answered despite increasing awareness". Cellular and Molecular Immunology (Review). 10 (5): 383–392. doi:10.1038/cmi.2013.28. PMC   4003198 . PMID   23934026.
  46. ↑ Guandalini S, Polanco I (Apr 2015). "Nonceliac gluten sensitivity or wheat intolerance syndrome?". J Pediatr (Review). 166 (4): 805–11. doi:10.1016/j.jpeds.2014.12.039. PMID   25662287. The increase in world-wide consumption of a Mediterranean diet, which includes a wide range of wheat-based foods, has possibly contributed to an alarming rise in the incidence of wheat (gluten?)-related disorders.1, 2
  47. 1 2 Volta U, Caio G, Tovoli F, De Giorgio R (September 2013). "Non-celiac gluten sensitivity: questions still to be answered despite increasing awareness". Cellular & Molecular Immunology (Review). 10 (5): 383–92. doi:10.1038/cmi.2013.28. PMC   4003198 . PMID   23934026. mechanization of farming and the growing industrial use of pesticides have favored the development of new types of wheat with a higher amount of toxic gluten peptides that cause the development of gluten-related disorders
  48. ↑ Gobbetti M, Giuseppe Rizzello C, Di Cagno R, De Angelis M (Apr 2007). "Sourdough lactobacilli and celiac disease". Food Microbiol (Review). 24 (2): 187–96. doi:10.1016/j.fm.2006.07.014. PMID   17008163.
  49. ↑ Belderok B (2000). "Developments in bread-making processes". Plant Foods Hum Nutr (Review). 55 (1): 1–86. doi:10.1023/A:1008199314267. PMID   10823487. S2CID   46259398.
  50. ↑ Pronin, Darina; Borner, Andreas; Weber, Hans; Scherf, Ann (10 July 2020). "Wheat (Triticum aestivum L.) Breeding from 1891 to 2010 Contributed to Increasing Yield and Glutenin Contents but Decreasing Protein and Gliadin Contents". Journal of Agricultural and Food Chemistry . 68 (46): 13247–13256. doi:10.1021/acs.jafc.0c02815. PMID   32648759. S2CID   220469138.
  51. 1 2 3 Caio, Giacomo; Volta, Umberto; Sapone, Anna; Leffler, Daniel A.; De Giorgio, Roberto; Catassi, Carlo; Fasano, Alessio (2019-07-23). "Celiac disease: a comprehensive current review". BMC Medicine. 17 (1): 142. doi: 10.1186/s12916-019-1380-z . PMC   6647104 . PMID   31331324.
  52. 1 2 "Celiac disease". World Gastroenterology Organisation Global Guidelines. July 2016. Retrieved 23 April 2017.
  53. 1 2 3 4 5 6 Ludvigsson JF, Card T, Ciclitira PJ, Swift GL, Nasr I, Sanders DS, Ciacci C (Apr 2015). "Support for patients with celiac disease: A literature review". United European Gastroenterol J. 3 (2): 146–59. doi:10.1177/2050640614562599. PMC   4406900 . PMID   25922674.
  54. 1 2 Fasano, A; Catassi, C (December 2012). "Clinical practice. Celiac disease". The New England Journal of Medicine. 367 (25): 2419–26. doi:10.1056/NEJMcp1113994. PMID   23252527.
  55. ↑ Bold J, Rostami K (2011). "Gluten tolerance; potential challenges in treatment strategies". Gastroenterol Hepatol Bed Bench. 4 (2): 53–7. PMC   4017406 . PMID   24834157.
  56. 1 2 3 4 Fasano A (Apr 2005). "Clinical presentation of celiac disease in the pediatric population". Gastroenterology. 128 (4 Suppl 1): S68–73. doi:10.1053/j.gastro.2005.02.015. PMID   15825129.
  57. 1 2 3 Elli L, Branchi F, Tomba C, Villalta D, Norsa L, Ferretti F, Roncoroni L, Bardella MT (Jun 2015). "Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity". World J Gastroenterol. 21 (23): 7110–9. doi: 10.3748/wjg.v21.i23.7110 . PMC   4476872 . PMID   26109797.
  58. 1 2 Lebwohl B, Ludvigsson JF, Green PH (Oct 2015). "Celiac disease and non-celiac gluten sensitivity". BMJ (Review). 351: h4347. doi:10.1136/bmj.h4347. PMC   4596973 . PMID   26438584.
  59. 1 2 Lundin KE, Wijmenga C (Sep 2015). "Coeliac disease and autoimmune disease-genetic overlap and screening". Nat Rev Gastroenterol Hepatol. 12 (9): 507–15. doi:10.1038/nrgastro.2015.136. PMID   26303674. S2CID   24533103.
  60. ↑ Vriezinga SL, Schweizer JJ, Koning F, Mearin ML (Sep 2015). "Coeliac disease and gluten-related disorders in childhood". Nature Reviews. Gastroenterology & Hepatology (Review). 12 (9): 527–36. doi:10.1038/nrgastro.2015.98. PMID   26100369. S2CID   2023530.
  61. ↑ Pruimboom, Leo; de Punder, Karin (24 November 2015). "The opioid effects of gluten exorphins: asymptomatic celiac disease". Journal of Health, Population, and Nutrition (Review). 33: 24. doi: 10.1186/s41043-015-0032-y . PMC   5025969 . PMID   26825414.
  62. ↑ Mooney, P; Aziz, I; Sanders, D (2013). "Non-celiac gluten sensitivity: clinical relevance and recommendations for future research". Neurogastroenterology & Motility. 25 (11): 864–871. doi:10.1111/nmo.12216. PMID   23937528. S2CID   9277897.
  63. ↑ Nijeboer, P; Bontkes, H; Mulder, C; Bouma, G (2013). "Non-celiac gluten sensitivity. Is it in the gluten or the grain?". Journal of Gastrointestinal and Liver Disorders. 22 (4): 435–40. PMID   24369326.
  64. 1 2 3 4 Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A (Sep 2013). "Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders". Nutrients. 5 (10): 3839–53. doi: 10.3390/nu5103839 . PMC   3820047 . PMID   24077239.
  65. 1 2 3 4 5 Fasano, Alessio; Sapone, Anna; Zevallos, Victor; Schuppan, Detlef (May 2015). "Nonceliac Gluten Sensitivity". Gastroenterology. 148 (6): 1195–1204. doi: 10.1053/j.gastro.2014.12.049 . PMID   25583468.
  66. ↑ Czaja-Bulsa G (Apr 2015). "Non coeliac gluten sensitivity - A new disease with gluten intolerance". Clin Nutr. 34 (2): 189–94. doi: 10.1016/j.clnu.2014.08.012 . PMID   25245857.
  67. ↑ Igbinedion SO, Ansari J, Vasikaran A, Gavins FN, Jordan P, Boktor M, Alexander JS (Oct 2017). "Non-celiac gluten sensitivity: All wheat attack is not celiac". World Journal of Gastroenterology (Review). 23 (20): 7201–10. doi: 10.3748/wjg.v23.i40.7201 . PMC   5677194 . PMID   29142467.
  68. 1 2 3 Verdu EF, Armstrong D, Murray JA (2009). "Between celiac disease and irritable bowel syndrome: the "no man's land" of gluten sensitivity". Am J Gastroenterol (Review). 104 (6): 1587–94. doi:10.1038/ajg.2009.188. PMC   3480312 . PMID   19455131.
  69. 1 2 Mansueto, Pasquale; Seidita, Aurelio; D'Alcamo, Alberto; Carroccio, Antonio (2014). "Non-Celiac Gluten Sensitivity: Literature Review". Journal of the American College of Nutrition (Review). 33 (1): 39–54. doi:10.1080/07315724.2014.869996. hdl: 10447/90208 . PMID   24533607. S2CID   22521576.
  70. ↑ Volta U, Caio G, De Giorgio R, Henriksen C, Skodje G, Lundin KE (Jun 2015). "Non-celiac gluten sensitivity: a work-in-progress entity in the spectrum of wheat-related disorders". Best Pract Res Clin Gastroenterol. 29 (3): 477–91. doi:10.1016/j.bpg.2015.04.006. PMID   26060112.
  71. 1 2 Volta U, De Giorgio R, Caio G, Uhde M, Manfredini R, Alaedini A (March 2019). "Nonceliac Wheat Sensitivity: An Immune-Mediated Condition with Systemic Manifestations". Gastroenterol Clin North Am (Review). 48 (1): 165–182. doi:10.1016/j.gtc.2018.09.012. PMC   6364564 . PMID   30711208. Furthermore, a role for the FODMAP (eg, fructans) component of wheat as the sole trigger for symptoms is somewhat doubtful, because many patients with NCWS report resolution of symptoms after the withdrawal of wheat and related cereals, while continuing to ingest vegetables and fruits with high FODMAP content in their diets.59 On the whole, it is conceivable that more than one culprit may be involved in symptoms of NCWS (as they are currently defined), including gluten, other wheat proteins, and FODMAPs.60–62
  72. ↑ Verbeke, K (February 2018). "Nonceliac Gluten Sensitivity: What Is the Culprit?". Gastroenterology. 154 (3): 471–473. doi: 10.1053/j.gastro.2018.01.013 . PMID   29337156. Although intolerance to fructans and other FODMAPs may contribute to NCGS, they may only explain gastrointestinal symptoms and not the extraintestinal symptoms observed in NCGS patients, such as neurologic dysfunction, psychological disturbances, fibromyalgia, and skin rash.15 Therefore, it is unlikely that they are the sole cause of NCGS.
  73. ↑ Barone, Maria; Troncone, Riccardo; Auricchio, Salvatore (2014). "Gliadin Peptides as Triggers of the Proliferative and Stress/Innate Immune Response of the Celiac Small Intestinal Mucosa". International Journal of Molecular Sciences (Review). 15 (11): 20518–20537. doi: 10.3390/ijms151120518 . PMC   4264181 . PMID   25387079.
  74. ↑ Junker, Y.; Zeissig, S.; Kim, S.-J.; Barisani, D.; Wieser, H.; Leffler, D. A.; Zevallos, V.; Libermann, T. A.; Dillon, S.; Freitag, T. L.; Kelly, C. P.; Schuppan, D. (2012). "Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4". Journal of Experimental Medicine. 209 (13): 2395–2408. doi:10.1084/jem.20102660. PMC   3526354 . PMID   23209313.
  75. ↑ "What's the difference between celiac disease, gluten intolerance, non-celiac gluten sensitivity and wheat allergy?". The University of Chicago Celiac Disease Center. 2015. Retrieved 4 January 2015.
  76. ↑ "Food intolerance and coeliac disease" (PDF). Food Standards Agency. September 2006. Archived from the original (PDF) on 15 October 2012. Retrieved 8 September 2009.
  77. ↑ Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PH, Hadjivassiliou M, Kaukinen K, Rostami K, Sanders DS, Schumann M, Ullrich R, Villalta D, Volta U, Catassi C, Fasano A (2012). "Spectrum of gluten-related disorders: consensus on new nomenclature and classification". BMC Medicine (Review). 10: 13. doi: 10.1186/1741-7015-10-13 . PMC   3292448 . PMID   22313950.
  78. 1 2 3 4 Hadjivassiliou M, Sanders DD, Aeschlimann DP (2015). "Gluten-related disorders: gluten ataxia". Dig Dis (Review). 33 (2): 264–8. doi:10.1159/000369509. PMID   25925933. S2CID   207673823.
  79. ↑ Mitoma H, Adhikari K, Aeschlimann D, Chattopadhyay P, Hadjivassiliou M, Hampe CS, et al. (2016). "Consensus Paper: Neuroimmune Mechanisms of Cerebellar Ataxias". Cerebellum (Review). 15 (2): 213–32. doi:10.1007/s12311-015-0664-x. PMC   4591117 . PMID   25823827.
  80. ↑ Hadjivassiliou M, Grünewald R, Sharrack B, Sanders D, Lobo A, Williamson C, Woodroofe N, Wood N, Davies-Jones A (March 2003). "Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics". Brain. 126 (Pt 3): 685–91. doi: 10.1093/brain/awg050 . PMID   12566288.
  81. ↑ Vinagre-Aragón A, Zis P, Grunewald RA, Hadjivassiliou M (2018). "Movement Disorders Related to Gluten Sensitivity: A Systematic Review". Nutrients (Review). 10 (8): 1034. doi: 10.3390/nu10081034 . PMC   6115931 . PMID   30096784.
  82. 1 2 Diaz-Amigo C, Popping B (2012). "Gluten and gluten-free: issues and considerations of labeling regulations, detection methods, and assay validation". J AOAC Int (Review). 95 (2): 337–48. doi: 10.5740/jaoacint.SGE_Diaz-Amigo . PMID   22649917.
  83. 1 2 Akobeng AK, Thomas AG (June 2008). "Systematic review: tolerable amount of gluten for people with coeliac disease". Aliment. Pharmacol. Ther. 27 (11): 1044–52. doi: 10.1111/j.1365-2036.2008.03669.x . PMID   18315587. S2CID   20539463.
  84. ↑ "Codex Standard For "Gluten-Free Foods" CODEX STAN 118-1981" (PDF). Codex Alimentarius. February 22, 2006.
  85. ↑ "General labeling for Packaged Foods (free translation)". Anvisa. July 2014. Archived from the original on 2007-12-06. Retrieved 2014-07-22.
  86. ↑ "Health Canada's Position on Gluten-Free Claims". Health Canada. 29 June 2012. Retrieved 28 January 2015.
  87. 1 2 "Labelling of 'gluten free' foods" (PDF). Food Standards Agency. 31 October 2016.
  88. ↑ 'Gluten-free' and 'Very Low Gluten' Declarations (Guidance Note 24). Food Safety Authority of Ireland. 2017. ISBN   978-1-904465-71-3. Archived from the original on 16 July 2020. Retrieved 20 February 2023.
  89. ↑ "EU Food Information for Consumers Regulation (EU FIC)" (link). Food Standards Agency. March 2016.
  90. ↑ "Questions and Answers: Gluten-Free Food Labeling Final Rule". US Food and Drug Administration. 5 August 2014. Retrieved 4 January 2015.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.