Coeliac Disease, Wheat Allergy and Gluten Sensitivity

Three completely different medical conditions can be set off by eating wheat, and almost every conversation about "gluten" collapses them into one. They are not variations on a theme. One is an autoimmune disease that damages the small intestine. One is a classic allergy that can, in its most dramatic form, cause anaphylaxis on a run after lunch. The third is a real cluster of symptoms with a genuinely unsettled cause, where the best trials point away from gluten and towards a fermentable carbohydrate that happens to travel in the same slice of bread. Telling them apart changes what you should do next — and one of them has a testing trap that catches thousands of people every year, because removing wheat before you are tested destroys the evidence the test looks for.

Table of Contents

  1. Three Conditions, One Food
  2. Coeliac Disease: An Autoimmune Reaction
  3. Getting Tested — and the Mistake That Ruins It
  4. Treatment, and What "Strict" Actually Means
  5. Wheat Allergy: A Different Immune System Entirely
  6. Anaphylaxis After Exercise: WDEIA
  7. Non-Coeliac Gluten or Wheat Sensitivity
  8. The FODMAP Explanation and the Rechallenge Trials
  9. Amylase-Trypsin Inhibitors: The Other Candidate
  10. "Modern Wheat Has More Gluten Than It Used To"
  11. A Gluten-Free Diet Is Not Automatically Healthier
  12. What to Do, in Order
  13. Key Research Papers
  14. Connections
  15. Featured Videos

Three Conditions, One Food

The confusion is understandable, because all three conditions can produce bloating, cramping, loose stools, fatigue and brain fog, and all three improve when wheat is removed. What separates them is the machinery involved.

  1. Coeliac disease is an autoimmune disease. Gluten triggers an immune attack on the lining of the small intestine itself. It requires specific genes, it produces measurable antibodies, it flattens the intestinal villi, and it is diagnosed with a blood test and a biopsy. Untreated, it causes malabsorption and raises the risk of a list of long-term complications. It affects roughly one person in a hundred worldwide.
  2. Wheat allergy is an IgE-mediated allergy, the same category as peanut or shellfish allergy. The immune system makes IgE antibodies to wheat proteins; exposure releases histamine within minutes. Symptoms are allergic ones — hives, swelling, wheeze, vomiting, in severe cases anaphylaxis — not the slow intestinal damage of coeliac disease.
  3. Non-coeliac gluten or wheat sensitivity is defined by exclusion: symptoms that improve off wheat in someone who has been properly tested and does not have coeliac disease or wheat allergy. There is no blood test, no biopsy finding and, at present, no agreed mechanism.

The formal names and boundaries were settled by two consensus papers that are still the reference points — a 2012 nomenclature statement covering the whole spectrum of gluten-related disorders, and the 2013 Oslo definitions, which exist because the same words were being used to mean different things in different papers.

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Coeliac Disease: An Autoimmune Reaction

In coeliac disease, fragments of gluten that survive digestion cross into the wall of the small intestine, are chemically modified by an enzyme called tissue transglutaminase, and are then presented to the immune system by one of two specific molecules on the surface of immune cells: HLA-DQ2 or HLA-DQ8. T-cells respond as though the intestinal lining were infected, and the finger-like villi that absorb nutrients are progressively flattened. Flat villi mean less absorptive surface, which is why untreated coeliac disease so often shows up first as iron-deficiency anaemia, low folate or vitamin B12, low vitamin D, poor growth in a child or unexplained weight loss in an adult.

The genetics matter, and are widely misunderstood. Essentially everyone with coeliac disease carries HLA-DQ2 or DQ8 — but so do something like 30–40% of people of European ancestry, and the overwhelming majority of them never develop the disease. The genes are necessary but nowhere near sufficient. That asymmetry makes the genetic test useful in exactly one direction: a negative HLA result effectively rules coeliac disease out, while a positive one tells you very little on its own.

The classic picture — a thin child with diarrhoea and a distended abdomen — is now the minority presentation. Adults are more often diagnosed with anaemia, osteoporosis, fatigue, raised liver enzymes, recurrent mouth ulcers, unexplained infertility or neurological complaints, sometimes with no bowel symptoms at all. Dermatitis herpetiformis, an intensely itchy blistering rash on the elbows, knees and buttocks, is coeliac disease expressing itself in the skin; it responds to the same gluten-free diet. Because the presentation is so variable, a large share of cases go undiagnosed for years — a community-based study in Minnesota found that most people with positive coeliac serology had never been given the diagnosis, and a long-running study of stored military serum samples found that undiagnosed coeliac disease carried a substantially higher risk of death over decades of follow-up.

Prevalence has been mapped carefully. A systematic review pooling studies worldwide put the figure at about 1.4% by blood test and about 0.7% when confirmed by biopsy, with real variation between regions. A separate meta-analysis of incidence over time found new diagnoses rising steadily across recent decades in the countries with good data, more so in women and children — part better detection, but not all of it.

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Getting Tested — and the Mistake That Ruins It

This is the single most useful paragraph on this page. Coeliac testing only works while you are still eating wheat. The blood test looks for antibodies your immune system makes in response to gluten, and the biopsy looks for damage gluten is currently causing. Take gluten away and both fade — antibodies fall, villi regrow — and the tests come back negative in someone who genuinely has the disease. People who feel better on a gluten-free diet, and only then go to a doctor, routinely get a falsely reassuring result and spend years without a diagnosis they needed.

So: if you suspect coeliac disease, get tested before you cut wheat out. If you have already stopped, the standard route is a supervised gluten challenge — eating gluten-containing food daily for a period of weeks (guidelines generally ask for at least six weeks, and at minimum a couple of weeks at a meaningful dose) before repeating the tests. It is unpleasant if you are sensitive, and it is the price of a real answer.

The testing sequence itself is well standardised:

  1. tTG-IgA — the tissue transglutaminase IgA antibody. The first-line blood test, with high sensitivity and specificity in people eating gluten.
  2. Total IgA, measured at the same time. Selective IgA deficiency is several times more common in people with coeliac disease than in the general population, and someone who makes almost no IgA cannot make a positive IgA-based antibody test. If total IgA is low, the lab switches to IgG-based tests instead. Skipping this step is the second most common way a coeliac diagnosis is missed.
  3. Endoscopy with duodenal biopsies — still the confirmatory test in adults, taking multiple samples including from the duodenal bulb, because the damage can be patchy.
  4. A no-biopsy pathway for children. European paediatric guidance allows diagnosis without endoscopy when tTG-IgA is at least ten times the upper limit of normal and a second sample is positive for endomysial antibodies. Adult guidelines are more cautious, though the same principle is being evaluated.
  5. HLA-DQ2/DQ8 typing — used to exclude, particularly in someone already gluten-free who will not do a challenge, or in first-degree relatives.

First-degree relatives of someone with coeliac disease have a much higher risk than the general population and are worth testing even without symptoms. So is anyone with type 1 diabetes, autoimmune thyroid disease, unexplained iron deficiency, or early osteoporosis.

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Treatment, and What "Strict" Actually Means

The treatment is a lifelong, strict gluten-free diet: no wheat, barley or rye in any form. That includes spelt, einkorn, emmer, khorasan and durum, which are all wheat, and it includes the small quantities hidden in soy sauce, stock cubes, sausages, batter, malt vinegar, beer and many sauces. "Strict" means the crumb level: shared toasters, shared frying oil, a knife used on ordinary bread and then in the butter, flour dust in a bakery. For someone with coeliac disease, milligram quantities of gluten repeated daily are enough to keep the intestine inflamed.

Oats are a special case. Pure oats do not contain gluten, but ordinary oats are grown, transported and milled alongside wheat and are routinely contaminated; certified gluten-free oats are usually tolerated, and a small minority of people with coeliac disease react to oat protein itself.

Healing takes time. Antibody levels usually normalise within six to twelve months, but the intestinal lining can take a year or two to fully recover in adults, and some never recover completely. It is worth checking iron, zinc, B12, folate, vitamin D and calcium at diagnosis and again once the diet is established, and worth getting bone density measured if the diagnosis came late.

Naturally gluten-free whole foods do the job better than the processed gluten-free aisle: brown rice, buckwheat, quinoa, certified gluten-free oats, lentils, beans, chickpeas, potatoes, nuts, seeds, eggs, fish, meat, fruit and vegetables. Commercial gluten-free breads and biscuits are typically made from refined starches with the fibre and B-vitamins stripped out, and they are the main reason gluten-free diets so often end up lower in fibre than the diet they replaced.

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Wheat Allergy: A Different Immune System Entirely

Wheat allergy is not coeliac disease with a different name. It is an IgE-mediated food allergy, and the timing alone usually gives it away: reactions come on within minutes to two hours, not over days. The proteins involved are different too — several wheat proteins can act as allergens, and the pattern of which ones a person reacts to shapes how the allergy behaves.

It presents in three broad ways:

Diagnosis uses skin-prick testing and specific IgE blood tests, but both have a high false-positive rate for wheat, so a positive test on its own does not make the diagnosis. An allergist will interpret it against the history and, when the picture is unclear, use a supervised oral food challenge. Confirmed wheat allergy is uncommon — a small fraction of one percent of the population by challenge-confirmed criteria, well below coeliac disease — but it is the one of the three conditions where an accidental exposure can be an emergency, and where an adrenaline auto-injector may be prescribed.

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Anaphylaxis After Exercise: WDEIA

Wheat-dependent exercise-induced anaphylaxis is real, dramatic, and missed with depressing regularity, because the person eats wheat safely almost every day. Wheat alone does nothing. Exercise alone does nothing. Wheat followed within a few hours by exercise produces hives, flushing, swelling, collapse — a full anaphylactic reaction. Faced with a patient who has eaten a sandwich hundreds of times without incident, both the patient and the doctor tend to look for something more exotic than the sandwich.

The main culprit protein is omega-5 gliadin, identified and cloned in the mid-2000s; specific IgE to omega-5 gliadin is the most useful single blood test when WDEIA is suspected, and it is not part of a standard wheat allergy panel unless someone asks for it.

Exercise is not the only trigger. A prospective challenge study that tested cofactors systematically found that aspirin and other NSAIDs, and alcohol, act as cofactors in their own right, and that combining cofactors provoked reactions in people who tolerated the same amount of wheat without them. Sleep deprivation, infection and, in women, the phase of the menstrual cycle have also been reported to lower the threshold. Practically, that means the reaction is not reliably reproducible from one day to the next — which is exactly why it gets dismissed. Management is avoiding wheat within a defined window before exercise (commonly four to six hours), avoiding NSAIDs and alcohol around wheat-containing meals, never exercising alone after eating wheat, and carrying adrenaline.

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Non-Coeliac Gluten or Wheat Sensitivity

A large number of people feel meaningfully better without wheat and have neither coeliac disease nor wheat allergy. Their symptoms — bloating, abdominal pain, irregular bowels, fatigue, headache, foggy thinking, joint aches — are real, reproducible in their own experience, and unexplained by any test currently available. The label attached to this is non-coeliac gluten sensitivity, increasingly written as non-coeliac wheat sensitivity, and the change of wording is not cosmetic: it reflects genuine doubt about whether gluten is the trigger.

The honest position is that this is an open question, not a settled one and not a debunking. Three things are simultaneously true, and any account that drops one of them is misleading:

The formal research definition — the Salerno criteria — requires coeliac disease and wheat allergy to be excluded first, then a double-blind placebo-controlled crossover challenge showing a clear symptom change on the active arm. Applied strictly, that definition confirms far fewer people than self-identify, largely because the placebo arm performs so well.

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The FODMAP Explanation and the Rechallenge Trials

The most productive line of research came from a group in Melbourne who set out to prove gluten was the culprit and ended up demonstrating something else.

Their 2011 trial did what everyone expected: people with irritable-bowel-type symptoms, controlled on a gluten-free diet, were given blinded gluten or placebo, and the gluten group reported worse symptoms. That result put non-coeliac gluten sensitivity on the map.

Their 2013 follow-up is the one that changed the field. This time, before the gluten challenge, every participant was first put on a diet low in FODMAPs — fermentable oligosaccharides, disaccharides, monosaccharides and polyols, a family of short-chain carbohydrates that are poorly absorbed in the small intestine, draw in water, and are rapidly fermented by gut bacteria to gas. Symptoms improved substantially on the low-FODMAP run-in. Then gluten was reintroduced blind — and produced no specific, dose-dependent effect. Symptoms worsened on the gluten arms and on the placebo arm alike, a textbook nocebo pattern.

The point is what wheat actually contains. Wheat is one of the largest sources of fructans in the Western diet — chains of fructose units that are, by definition, FODMAPs. Cut out bread, pasta and baked goods to avoid gluten and you have also cut out most of your fructan intake, without meaning to. Two different substances left the diet on the same day, and only one of them got the blame.

A 2018 Norwegian crossover trial tested this head-on. Fifty-nine people with self-reported non-coeliac gluten sensitivity, all on a gluten-free diet, were given identical-tasting muesli bars containing gluten, fructan, or neither, in randomised order with washout periods between. Fructan produced significantly more gastrointestinal symptoms than placebo. Gluten did not.

This does not mean the symptoms were imaginary. It means the trigger was probably misidentified — and, usefully, that a low-FODMAP approach may work better than a gluten-free one for these people, while allowing foods that a gluten-free diet needlessly forbids. It also explains a common and otherwise baffling observation: that some people who react badly to ordinary bread tolerate long-fermented sourdough, where the bacteria and yeast consume a substantial share of the fructans during a long proof. That is a fructan effect, not a gluten effect — the gluten is still there.

A practical caution: the low-FODMAP diet is a short diagnostic tool, not a way of life. It is designed to be followed strictly for a few weeks, then systematically reintroduced food by food to find personal thresholds, ideally with a dietitian. Staying on it indefinitely restricts a long list of fibres your gut bacteria depend on.

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Amylase-Trypsin Inhibitors: The Other Candidate

FODMAPs are not the only alternative to gluten. Wheat also contains a family of proteins called amylase-trypsin inhibitors (ATIs), which the plant makes to deter insects and which survive digestion largely intact. Laboratory and animal work has shown that ATIs activate an innate immune receptor, toll-like receptor 4, on immune cells in the gut wall, producing an inflammatory signal that has nothing to do with the T-cell response of coeliac disease. Later work showed ATIs activating myeloid cells and worsening inflammation in mouse models of intestinal and extra-intestinal disease.

ATIs are a plausible mechanism and an active research area. They are not yet a proven cause of symptoms in people: the human trials that would show ATI-free wheat relieving symptoms in a blinded design have not been done at the scale needed. Anyone telling you that ATIs are definitely the answer is ahead of the evidence — as is anyone telling you they are irrelevant.

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"Modern Wheat Has More Gluten Than It Used To"

This is the most widely repeated claim about wheat, and it deserves a straight answer rather than a sneer, because the intuition behind it is reasonable: coeliac disease really has become more common, wheat really has been intensively bred, and it is natural to connect the two.

The data do not support a large increase in gluten. A review of United States wheat and flour protein records spanning roughly a century found no evidence that the gluten content of wheat rose as a consequence of breeding; protein content was flat or slightly declining, and the increase in total gluten consumption came from eating more wheat products and from vital wheat gluten being added to processed foods, not from the grain changing.

A German study did the cleanest possible version of the test: it grew 60 winter wheat cultivars released between 1891 and 2010 side by side in the same fields in the same years, removing the confounding effect of weather and farming practice. Yield rose sharply. Overall protein content fell slightly. Total gluten stayed essentially constant — and within it, the gliadin fraction (the part containing most coeliac-triggering sequences) went down while the glutenin fraction went up. A broader European comparison of modern and older varieties reached the same conclusion: no evidence that modern wheat is worse for health on these measures.

The semi-dwarf varieties of the Green Revolution are frequently blamed by name. What the Rht ("reduced height") genes actually do is blunt the plant's response to the growth hormone gibberellin, which makes the stem short and stiff so it does not fall over under a heavy head of grain. They change plant architecture. They were not selected for gluten content and are not known to alter it — that history is covered on the Wheat history page.

None of this means nothing changed. Milling changed enormously — roller milling from the late nineteenth century made white flour cheap and universal, stripping the bran and germ. Fermentation changed: most commercial bread is proved for an hour or two rather than overnight, leaving fructans intact. Wheat is in far more products than it used to be. Added vital gluten is common in commercial bread. Those are real changes to what people eat. They are just not changes to the plant's gluten content.

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A Gluten-Free Diet Is Not Automatically Healthier

For coeliac disease it is essential and non-negotiable. For everyone else, it carries a cost worth knowing about. Whole wheat is a major source of fibre, B-vitamins, magnesium, zinc and selenium in most Western diets, and the products that replace it are usually made from refined starch. A large prospective cohort study following adults without coeliac disease for decades found no association between long-term gluten intake and coronary heart disease, and noted that people eating the least gluten also ate the fewest whole grains — which may itself be harmful. The gluten-free aisle is not a health-food aisle; it is an allergen-management aisle.

If you are avoiding wheat by choice and feeling better for it, that is a legitimate decision. The useful version of it keeps the fibre: build the diet on brown rice, quinoa, buckwheat, certified gluten-free oats, lentils, beans, vegetables, nuts and seeds rather than on gluten-free white bread.

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What to Do, in Order

  1. Keep eating wheat until you are tested. This is the step that cannot be undone later without a gluten challenge. If you take nothing else from this page, take this.
  2. Ask for tTG-IgA and total IgA together. If tTG-IgA is positive, expect a referral for endoscopy; in children a very high titre plus a positive endomysial antibody may avoid it.
  3. If reactions come on within minutes — hives, swelling, wheeze — think allergy, not coeliac disease, and ask for allergy testing rather than coeliac serology.
  4. If the reaction only ever happens around exercise, alcohol or painkillers, ask specifically for omega-5 gliadin IgE. It will not be on a routine panel. This is the test that finds WDEIA.
  5. If coeliac disease and allergy are both excluded and you still react, try a structured low-FODMAP trial before assuming gluten. A few weeks of restriction, then systematic reintroduction, ideally with a dietitian — not indefinite avoidance.
  6. Test the fermentation variable. Genuinely long-fermented sourdough, or wheat berries and bulgur rather than fast-proved bread, distinguishes a fructan problem from a gluten one at almost no cost.
  7. Keep the fibre up whatever you conclude. Whatever wheat is doing for you or to you, a low-fibre diet is not the answer.

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Key Research Papers

  1. Lebwohl B, Sanders DS, Green PHR. Coeliac disease. The Lancet. 2018;391(10115):70-81. — doi:10.1016/S0140-6736(17)31796-8
  2. Singh P, Arora A, Strand TA, et al. Global prevalence of celiac disease: systematic review and meta-analysis. Clinical Gastroenterology and Hepatology. 2018;16(6):823-836.e2. — doi:10.1016/j.cgh.2017.06.037
  3. King JA, Jeong J, Underwood FE, et al. Incidence of celiac disease is increasing over time: a systematic review and meta-analysis. American Journal of Gastroenterology. 2020;115(4):507-525. — doi:10.14309/ajg.0000000000000523
  4. Rubio-Tapia A, Hill ID, Semrad C, et al. American College of Gastroenterology guidelines update: diagnosis and management of celiac disease. American Journal of Gastroenterology. 2023;118(1):59-76. — doi:10.14309/ajg.0000000000002075
  5. Husby S, Koletzko S, Korponay-Szabó I, et al. European Society Paediatric Gastroenterology, Hepatology and Nutrition guidelines for diagnosing coeliac disease 2020. Journal of Pediatric Gastroenterology and Nutrition. 2020;70(1):141-156. — doi:10.1097/MPG.0000000000002497
  6. Ludvigsson JF, Bai JC, Biagi F, et al. Diagnosis and management of adult coeliac disease: guidelines from the British Society of Gastroenterology. Gut. 2014;63(8):1210-1228. — doi:10.1136/gutjnl-2013-306578
  7. Ludvigsson JF, Leffler DA, Bai JC, et al. The Oslo definitions for coeliac disease and related terms. Gut. 2013;62(1):43-52. — doi:10.1136/gutjnl-2011-301346
  8. Sapone A, Bai JC, Ciacci C, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Medicine. 2012;10:13. — doi:10.1186/1741-7015-10-13
  9. Choung RS, Larson SA, Khaleghi S, et al. Prevalence and morbidity of undiagnosed celiac disease from a community-based study. Gastroenterology. 2017;152(4):830-839.e5. — doi:10.1053/j.gastro.2016.11.043
  10. Rubio-Tapia A, Kyle RA, Kaplan EL, et al. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology. 2009;137(1):88-93. — doi:10.1053/j.gastro.2009.03.059
  11. Cianferoni A. Wheat allergy: diagnosis and management. Journal of Asthma and Allergy. 2016;9:13-25. — doi:10.2147/JAA.S81550
  12. Matsuo H, Kohno K, Morita E. Molecular cloning, recombinant expression and IgE-binding epitope of omega-5 gliadin, a major allergen in wheat-dependent exercise-induced anaphylaxis. The FEBS Journal. 2005;272(17):4431-4438. — doi:10.1111/j.1742-4658.2005.04858.x
  13. Christensen MJ, Eller E, Mortz CG, Brockow K, Bindslev-Jensen C. Wheat-dependent cofactor-augmented anaphylaxis: a prospective study of exercise, aspirin, and alcohol efficacy as cofactors. The Journal of Allergy and Clinical Immunology: In Practice. 2019;7(1):114-121. — doi:10.1016/j.jaip.2018.06.018
  14. Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. American Journal of Gastroenterology. 2011;106(3):508-514. — doi:10.1038/ajg.2010.487
  15. Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013;145(2):320-328.e3. — doi:10.1053/j.gastro.2013.04.051
  16. Skodje GI, Sarna VK, Minelle IH, et al. Fructan, rather than gluten, induces symptoms in patients with self-reported non-celiac gluten sensitivity. Gastroenterology. 2018;154(3):529-539.e2. — doi:10.1053/j.gastro.2017.10.040
  17. Catassi C, Elli L, Bonaz B, et al. Diagnosis of non-celiac gluten sensitivity (NCGS): the Salerno experts' criteria. Nutrients. 2015;7(6):4966-4977. — doi:10.3390/nu7064966
  18. Fasano A, Sapone A, Zevallos V, Schuppan D. Nonceliac gluten sensitivity. Gastroenterology. 2015;148(6):1195-1204. — doi:10.1053/j.gastro.2014.12.049
  19. Junker Y, Zeissig S, Kim SJ, et al. Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4. Journal of Experimental Medicine. 2012;209(13):2395-2408. — doi:10.1084/jem.20102660
  20. Zevallos VF, Raker V, Tenzer S, et al. Nutritional wheat amylase-trypsin inhibitors promote intestinal inflammation via activation of myeloid cells. Gastroenterology. 2017;152(5):1100-1113.e12. — doi:10.1053/j.gastro.2016.12.006
  21. Kasarda DD. Can an increase in celiac disease be attributed to an increase in the gluten content of wheat as a consequence of wheat breeding? Journal of Agricultural and Food Chemistry. 2013;61(6):1155-1159. — doi:10.1021/jf305122s
  22. Pronin D, Börner A, Weber H, Scherf KA. 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. 2020;68(46):13247-13256. — doi:10.1021/acs.jafc.0c02815
  23. Shewry PR, Hassall KL, Grausgruber H, et al. Do modern types of wheat have lower quality for human health? Nutrition Bulletin. 2020;45(4):362-373. — doi:10.1111/nbu.12461
  24. Lebwohl B, Cao Y, Zong G, et al. Long term gluten consumption in adults without celiac disease and risk of coronary heart disease: prospective cohort study. BMJ. 2017;357:j1892. — doi:10.1136/bmj.j1892
  25. Ziegler JU, Steiner D, Longin CFH, Würschum T, Schweiggert RM, Carle R. Wheat and the irritable bowel syndrome — FODMAP levels of modern and ancient species and their retention during bread making. Journal of Functional Foods. 2016;25:257-266. — doi:10.1016/j.jff.2016.05.019

Further reading via topic search: PubMed: non-coeliac gluten sensitivity double-blind challenge and PubMed: wheat-dependent exercise-induced anaphylaxis.

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Connections

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