Everything You’ve Always Wanted to Know about Wheat Allergy

image by Melissa Askew on Unsplash

Wheat was one of the first crops to be cultivated by humans and we’ve had thousands of years to develop a whole range of adverse reactions to it. There’s the ‘classic’ form of food allergy, which produces everything from rashes to anaphylaxis, and there’s wheat-dependent exercise-induced anaphylaxis (WDEIA), which requires both wheat and exercise to produce reactions (which aren’t always anaphylactic, but often are). There’s the occupational form of wheat allergy, called baker’s asthma, which affects people who work with wheat, and there’s a relatively new form of wheat allergy that can cause severe reactions and appears in people who use certain hydrolised wheat-containing beauty products.

There are also a range of non-IgE-mediated forms of wheat allergy like eosinophilic oesophagitis (EoE) and food protein-induced enterocolitis syndrome (FPIES). And that’s not even counting the gluten-related disorders like coeliac disease and non-coeliac gluten sensitivity (NCGS), which this page doesn’t actually deal with.

And now for the details, which include:

What is an allergy to wheat?

Wheat is a grass plant that belongs to the genus Triticum and the family Poaceae. It was one of the first crops to be domesticated and cultivated. Its domestication is thought to have occurred in the ancient Middle Eastern territory known as the Fertile Crescent—modern-day south-eastern Turkey, Syria, Lebanon, Jordan, Palestine, Israel, northern Iraq, western Iran and northern Kuwait—about 10,000 years ago. The first farmers then spread it to all parts of the world, adapting the domesticated varieties to different environments.

The earliest cultivated species were einkorn (Triticum monococcum), emmer (Triticum Dicoccum) and spelt (Triticum spelta), and their corresponding wild ancestors are still found in the region of the Fertile Crescent.

The most commercially important species today are bread (aka common) wheat (Triticum aestivum)—which accounts for 95% of the world’s production—and durum wheat (Triticum turgidum)—which accounts for the other 5%. (Strictly speaking, a bit less, since some forms of ancient wheat are still cultivated.)

Due to its enormous genetic diversity— there are well over 25,000 varieties of Triticum aestivum—bread wheat can be grown in warm and humid climates as well as cold and dry ones. Today, it’s grown on more land area than any other commercial crop. That said, the amount of land used has stayed the same since the 1960s, but production has increased significantly, in part because of the introduction of hybrid varieties which produce a higher yield.

World trade in wheat is greater than all other crops combined. The top five producers (according to 2022 data) are China, India, Russia, the US and Australia, who grow just over half of the world’s wheat.

Wheat has been hugely successful because of its high nutritional value and high palatability, and the fact that it can be processed into many types of foods and drink.

Bread wheat is generally milled into (refined and whole meal) flour and used to make (fermented, crushed, steamed and flat) breads, pasta, biscuits, and cake—indeed one of wheat’s main advantages is the unique ability of its gluten proteins to form a viscoelastic dough that traps minute bubbles of gas and allows wheat flour to be processed into a wide variety of leavened bakery products. Wheat is also used as a binding agent in deli meats, soups, sauces, puddings, ice cream and cream. Wheat starch is used to coat pralines, roasted coffee grains and pills, and for a variety of other purposes by the cosmetic and chemical industries.

Wheat is also used as animal feed, particularly in wet years when harvests are badly affected by rain and large quantities of grain are made unsuitable for food use. This low-grade grain is also used to make products like glue, paper additives and alcohol.

Durum wheat is widely used to make regional foods such as pasta in Italy, sweet noodle kugel in Germany, flat bread in Turkey and couscous in North African countries, as well as breakfast cereals and burger buns in North America. Durum wheat flour, used alone or mixed with other flours, is widely used in Mediterranean countries to make bread.

Increased awareness of the health benefits of consuming of complex rather than simple carbohydrates is leading to an increase in consumption of bread made with whole wheat and multigrain flour in developed countries. Somewhat ironically, despite modern varieties of wheat having a higher yield potential and superior bread-making quality, compared to older varieties, they are less able to withstand the onslaught of pests, disease, drought, heat, cold, soil pollution and shortage of nutrients, so they require more chemical help in the form of fertilisers, pesticides and herbicides.

Ancient wheat varieties also have a nutritional composition that can be somewhat different to modern wheat varieties. However, although ancient varieties of wheat are considered by some to be more nutritious and less likely to cause allergic reactions than modern varieties, this is probably not the case.

Nevertheless, a growing demand for sustainable, artisanal products is leading to increased interest in using old wheat varieties—namely spelt, emmer, einkorn and Khorasan—to increase the nutrient content of bread made from modern wheat flour and to make different types of fermented bread, unleavened bread, pancakes and pasta products.

Most people eat wheat in some form or another at every meal, perhaps in the form of cereal or toast for breakfast, a sandwich or wrap for lunch and pizza or pasta for dinner. Not to mention snacks.

Although wheat tends to be regarded as a source of unhealthy carbohydrate calories, it’s a major source of nutrients beneficial to our health, including dietary fibre, as well as B vitamins, minerals (iron, zinc), phytochemicals and high-quality protein (containing most of the essential amino acids)

Wheat actually contains more vegetable protein than the two other major cereals (corn and rice); about 10 to 15% of the wheat grain is made up of protein. This is a problem for some people whose immune system mistakes one or more of those harmless proteins for toxic invaders and creates IgE antibodies against them. The next time they eat wheat, the antibodies recognise the proteins and prompt a response from immune system cells. These, in turn, release a variety of chemicals into the bloodstream, including histamine, the chemical that is primarily responsible for the symptoms of allergy.

The many wicked faces of wheat hypersensitivity

Wheat allergy is the most common of the cereal grain allergies and it causes problems that can be loosely classified into 3 major groups: allergic reactions to wheat, autoimmune disorders (coeliac disease, dermatitis herpetiformis and gluten ataxia) and ‘none of the above’ (gluten sensitivity).

Wheat allergy; IgE mediated reactions

Wheat allergic reactions are characterised by the presence of wheat-specific IgE antibodies. They can be provoked either by eating wheat proteins, inhaling them or touching them, and they manifest in 4 major forms.

There is the classic form of food allergy, which is more common in children than in adults. Symptoms range from skin rashes to anaphylaxis and occur minutes to hours after exposure to wheat proteins in food.

There is Wheat-Dependent, Exercise-Induced Anaphylaxis (WDEIA), a condition in which eating wheat either before or after exercise provokes a range of symptoms ranging from hives to anaphylaxis. This form of wheat allergy is more common in adults and adolescents than in younger children. Although any kind of food can trigger exercise-induced anaphylaxis, wheat is the most well-known trigger and has been reported to be the most common cause of exercise-induced anaphylaxis in adults.

The amount of wheat that needs to be eaten to provoke a reaction varies widely between individuals, and as one group of researchers—who call the condition ‘Omega-5 gliadin allergy’, after the wheat allergen that often (but not always) provokes it—have pointed out, people with WDEIA can consume wheat regularly without necessarily having symptoms, and when they do, the symptoms can be very varied, all of which makes it more difficult to identify the condition.

A subtype of WDEIA caused by using soap containing hydrolysed wheat proteins has also been reported in Japan. In this case, the wheat proteins are either absorbed through the skin or inhaled. About half of the people with this form of allergy seem to develop a contact allergy after using the soap for a few months, which is then followed by an allergy to the food itself, and the other half develop reactions to the food immediately. The most common symptom is oedema (swelling) of the eyelids.

To complicate matters further, episodes of WDEIA don’t necessarily result in anaphylaxis and some experts have suggested a different name for the syndrome, such as ‘activity-dependent wheat allergy’.

But that term is also misleading. The intensity of exercise that provokes a reaction varies widely—from performing cardiopulmonary resuscitation at work, to taking a brisk walk, dancing, jogging or taking part in team sports—and exercise even isn’t necessary to provoke reactions in a good number of people; although the exercise makes an allergic reaction more likely and the symptoms more severe, simply eating a lot of wheat would work. Or taking an aspirin, or drinking alcohol. Meaning that the ‘exercise’ part of the name is subjective and even ‘activity’ can be inaccurate.

So some experts have suggested the term ‘augmentation factor–triggered food allergy’ or’ wheat anaphylaxis dependent on augmentation (factors) (or WANDA)’ or wheat allergy dependent on augmentation (factors)—WALDA—to reflect that it doesn’t necessarily involve anaphylaxis and can be provoked by cofactors other than exercise.

Right now, however, Wheat-Dependent, Exercise-Induced Anaphylaxis is still the most popular term used to group together people who can normally eat wheat without problems but tend to have an allergic reaction to it after exercising, and/or taking medicine, and/or drinking alcohol, and/or using a certain soap, or simply eating a large portion of it.

On the bright side, since WDEIA generally requires both exercise and wheat to provoke reactions, eliminating wheat from your diet (or at least avoiding it around exercise) tends to eliminate the symptoms.

Another form of wheat allergy is respiratory; occupational asthma (aka baker’s asthma) and rhinitis (aka hay fever). This form of wheat allergy has been recognised since the time of the Roman Empire—when slaves who worked with flour and dough were made to wear masks—and is caused by the frequent inhalation of wheat flour and dusts. As such, this form of the allergy mostly affects millers, bakers, confectioners, pastry factory workers, pizza makers, farmers and cereal handlers who tend to develop respiratory symptoms and, very occasionally, a food allergy.

Finally, there are skin rashes; contact urticaria and contact dermatitis. The first is a localised skin rash often provoked by exposure to wheat-containing cosmetics which tends to manifest as a raised, burning, and/or itchy swelling that appears within 10–30 min after exposure to the allergen and fades away within hours. The second manifests as a large, burning and itchy rash, with blisters and weals that can take several days to weeks to heal and most often affects people who handle wheat such as millers, bakers and flour handlers.

Wheat allergy; non-IgE-mediated and mixed reactions

Non-IgE-mediated reactions can occur hours to days after eating wheat and tend not to be life-threatening (just extremely unpleasant and inconvenient).

The two most common are:

• Eosinophilic oesophagitis (EoE), which involves chronic inflammation of the oesophagus caused by the wheat-triggered activity of eosinophils, a kind of white blood cell. It produces the kind of symptoms you would associate with a problematic “food tube” such as reflux and difficulty swallowing, as well as other symptoms
• Eosinophilic gastritis (EG), which involves chronic inflammation of the stomach caused by the wheat-triggered activity of eosinophils. It produces symptoms associated with the stomach, such as nausea and stomach pain, and other symptoms

Another non-IgE-mediated and mixed (can also involve IgE antibodies) allergy that can be provoked by wheat is food protein-induced enterocolitis syndrome (FPIES). It involves chronic inflammation of the small intestine and large intestine (colon) and is considered is the most serious of the non-IgE-mediated gastrointestinal food allergies. It comes in two main flavours: chronic, the less common version which tends to affects infants and acute, the more common version, which affects older children and adults. So-called ‘atypical’ cases of FPIES involve IgE-mediated mechanisms and may be more persistent. Although wheat is not the most common trigger of this condition—possibly because of the common practice of delaying the introduction of wheat in an infant’s diet until after 12 months—cases of FPIES in both children and adults are on the rise, so wheat-induced FPIES is also becoming more frequent.

Gluten related disorders (GRD)

And then there are the gluten related disorders (GRD), an umbrella term proposed by an international, multidisciplinary task force known as the Oslo group to describe all gluten triggered diseases. These include autoimmune diseases and reactions that are neither allergic nor autoimmune; now covered by the term Non Coeliac Gluten Sensitivity (NCGS).

Autoimmune diseases include:

• Coeliac disease (CD), a disease with a strong genetic component. Symptoms are very varied and although they are often intestinal, they can also be extraintestinal (e.g. anaemia, osteoporosis, depression). The onset of symptoms is usually gradual and can happen months or years after exposure to gluten. Often treated by gastroenterologists rather than allergists. The Oslo group also has a lot of different categories for CD, depending on the symptoms:
  • Classical: has the signs and symptoms of malabsorption (difficulty digesting or absorbing nutrients), including diarrhoea, steatorrhoea (abnormal quantities of fat in the faeces), malnutrition, anaemia, weight loss or growth failure, oedema (swelling) secondary to hypoalbuminemia (too much albumin in your urine or stool). The paediatric versions is often characterised by diarrhoea, poor appetite, abdominal distension, failure to thrive (I.e. develop and grow normally) and muscle wasting. It’s diagnosed with the introduction of a gluten-free diet, measurement of various types of IgA antibodies and an intestinal biopsy
  • Non-classical: without signs and symptoms of malabsorption; e.g. constipation and abdominal pain but none of the symptoms listed above
  • Subclinical: essentially asymptomatic or ‘below the threshold of clinical detection’. This condition does not show any signs or symptoms which would trigger CD testing in routine practice, although minor symptoms like fatigue might show up after the introduction of a gluten-free diet. These people are often diagnosed if the enrol in screening programs designed to test a population
  • Other versions of CD include symptomatic, refractory, latent and potential, which can include other symptoms like osteoporosis and neurological disturbances
• Dermatitis herpetiformis (DH), a blistering skin rash associated with coeliac disease. Named in 1884, it normally occurs in people of European origin. The prevalence is approximately 1 in 10,000 in the UK and the same in Americans of European origin. Higher rates of 4 and 6 per 10,000 have been reported in Sweden and Finland, respectively. Diagnosis consists of finding IgA in the skin with biopsies
• Gluten ataxia, a gluten-related autoimmune disease characterised by damage to the cerebellum resulting in ataxia (loss of muscle control in arms and legs). Of 635 patients with sporadic ataxia evaluated in the UK, 148 (23%) showed evidence of gluten sensitisation. Treatment is only possible if a person has not had the condition too long, otherwise it is irreversible and symptoms can only be improved or stabilised. Diagnosis is not simple and involves trying to find a certain type of IgA antibody only present in about a third of patients

Nonceliac gluten sensitivity (NCGS), or just gluten sensitivity, is provoked by eating gluten-containing foods but, unlike other gluten-related disorders, seems to involve neither allergic nor autoimmune mechanisms.

Symptoms occur hours to days after eating gluten and often resemble those of coeliac disease or Irritable Bowel Syndrome (IBS); that is, gastrointestinal (GI) symptoms including abdominal pain, bloating, chronic diarrhoea and constipation, as well as extra-intestinal symptoms such as headache, ‘brain fog’, chronic fatigue, anxiety, depression, joint and muscle pain, numbness in the legs, arms or fingers, skin rash, anaemia and weight loss.

How many people actually have this kind of condition is unknown. However, of 5,896 patients seen at the Center for Celiac Research at the University of Maryland between 2004 and 2010, 347 (6%) were diagnosed with ‘gluten sensitivity’. 68% of them complained of abdominal pain, 40% of eczema and/or skin rash, 35% of headaches, 34% of a ‘foggy mind’, 33% of fatigue, 33% had diarrhoea, 22% were depressed, 20% had anaemia, 20% had numbness in the legs, arms or fingers and 11% had joint pain.

It’s generally difficult to differentiate NCGS from other gluten-related disorders because they all have similar triggers and similar avoidance strategies. Because of this and the fact that there are no reliable diagnostic tests for the condition, it’s diagnosed by exclusion. What this means is that, if you seem to have a gluten-related disorder but tests show that you do not have coeliac antibodies and your small intestine doesn’t show anything worse than mild irritation—i.e. you don’t have CD—and you also test negative for any kind of wheat-specific IgE antibodies— i.e. you don’t have wheat allergy—you are left with a probable diagnosis of NCGS.

This can be confirmed by a gluten challenge, in which you follow a gluten-free diet for six weeks; if your symptoms improve or disappear, but then reappear when you eat gluten again, you are diagnosed with NCGS.

The possible triggers and, indeed, the existence of NCGS remain controversial. Some researchers have found that it is caused by wheat carbohydrates—notably fructans—and not gluten. Some have reported that people who claim to have NCGS actually get better when put on low-FODMAP diets, leading some doctors to claim that NCGS is, therefore, just a subset of irritable bowel syndrome (IBS).

From an allergist’s perspective, NCGS is a condition that is frequently self-diagnosed and of unknown prevalence and unknown, non-validated origin. There are no validated methods to diagnose it and no reliable biomarkers. As a result, not all allergists are on board with the idea that the conditions exists.

From the average person’s point of view, the whole subject area of wheat allergy and gluten sensitivity is confusing. The important thing to remember is that they are not the same thing and that there are a whole range of different reactions to gluten that do not involve what is defined as an allergic reaction, nor do they have the same biomarkers, such as the presence of IgE antibodies, even if they have similar digestive symptoms. So they will also not be picked up by an allergist. In the end, you will probably have to listen to your body and do what’s best for it.

People with a gluten sensitivity must avoid all grains that contain gluten; that is wheat, rye and barley. People with a wheat allergy only need to avoid wheat; they can tolerate gluten from other grains.

This page only covers wheat allergy.

Identified allergens

The proteins (and occasionally carbohydrates) in a food that are capable of provoking allergic reactions are called allergens. Allergens are named using the first three letters of the genus—Triticum—the first letter of the species—aestivum—and a number generally reflecting the order in which they were identified.

As of March 2026, 28 wheat allergens have been added to the WHO/IUIS allergen database (the official, peer-reviewed database of allergens maintained by the World Health Organisation and International Union of Immunological Societies):

The clinical relevance of many of them has not yet been determined.

Image by DS stories on Pexels

How common is wheat allergy?

A definitive diagnosis of allergy can currently only be established with a food challenge, but challenges are costly in terms of both time and resources, as well as potentially risky. So many prevalence studies measure sensitisation—using skin or blood test data—but sensitisation is not allergy. Being sensitised to something simply means that your immune system recognises it, but you may not actually react to it; in fact, many people don’t react to whatever it is they are sensitised to. Studies that use sensitisation data therefore tend to produce allergy prevalence numbers that are larger than they should be.

In a similar vein, studies that estimate allergy prevalence using questionnaires usually produce somewhat inflated numbers as people can self-report allergies that they do not actually have, although robust studies will use certain criteria to evaluate respondents’ answers and determine whether their symptoms suggest an allergy or not.

IgE-mediated allergy

In most countries, allergy to milk and egg are the two most common food allergies, with wheat coming third in many countries including Finland, Germany, the United States (US) (in preschool children), Japan and Korea. That said, there are surprisingly few studies around looking at the prevalence of wheat allergy in the general population, although more research has been done into wheat allergy in food-allergic populations.

A 2023 meta-analysis of 56 studies including over 100,000 people from all over the world put the prevalence of global, physician-diagnosed wheat allergy at 0.7%. The prevalence of people sensitised to wheat (i.e. had wheat-specific IgE antibodies) was 0.97%.

The analysis also revealed that the prevalence of physician-diagnosed wheat allergy in adults (1.34%) was higher than in children (0.88%), but more children (2.16%) than adults (0.16%) were sensitised to wheat (i.e. had IgE antibodies).

Physician-diagnosed wheat allergy was higher in so-called developed countries (1.14%) than developing ones (0.27%) and highest in Europe (1.93%), followed by Eastern Mediterranean regions (0.71%), the Americas (0.35%) and Western Pacific regions (0.22%). There was no data for South-East Asia.

The pattern was reversed when it came to sensitisation, with the highest prevalence being in the Americas (3.35%), followed by Western Pacific regions (1.93%), European regions (0.76%) and South-East Asia (0.35% (95%CI: 0–1.35%))> There was no data for Africa or the Eastern Mediterranean.

In 2023, a team of researchers investigating the prevalence of the 8 biggest food allergens in Europe reviewed 47 wheat-related studies carried out in the whole region and calculated that around 0.47% of Europeans had been diagnosed with wheat allergy during their lifetimes.

An earlier review involving 25 European studies reported an estimated prevalence of 0.3% across all age groups, based either on food challenges or a history of wheat allergy.

In the UK, a study following 827 children from birth confirmed wheat allergy in 0.48% of 10-year-olds. Among allergic 6-year-olds undergoing food challenges, wheat has been found to be the third most common food allergy

In Iceland infants, wheat allergy was confirmed in 0.15% of infants in the general population.

In the US, parental reports of food allergy put wheat in 6^th place (tied with fish and soy), affecting around 0.4 million children. In a 2009 survey of college students, 4.2% reported having allergic reactions to wheat. A 2019 survey study of American adults reported that around 2 million had a probable allergy to wheat, or 0.8%.

In Brazil, wheat sensitisation was shown to be 20% in allergic children versus 8.1% in healthy controls.

In Australia, a 1998 study of 620 healthy children under 2 years old reported that wheat was the 4^th most common food allergen and that 0.16% of the children were sensitised to it.

In China, a 2011 study focussing on 2632 infants in 8 different cities reported that wheat was the 5^th most common allergen, with 4.05% being sensitised to the grain. Among 96 toddlers with hay fever aged between 1 and 3 referred to Beijing Children’s Hospital over the period of a year, wheat was found to be the 6^th most common allergen, with 18.8% sensitised to wheat. A 2013 study of 5 473 allergic patients of all ages seen in one hospital located in China’s northernmost province reported that 3.1% were sensitised to wheat, the 2^nd most common allergen.

A 2023 meta-analysis of 13 studies examining the presence of wheat allergy in China reported a prevalence of 7.3% among the food-allergic. Splitting data into regions revealed a large disparity in the numbers, with 2.74% being sensitised in the south of the country while 11.47% were sensitised in the north (with the rate of sensitisation reaching 23.1% in the Shaanxi province and 18.1% in Henan). This is explained by the fact that the north is the main wheat-growing area in China and wheat is the main food staple in those regions. The presence of flour-mites in home-stored wheat has also been shown to increase the risk of developing an allergy to wheat in those areas.

The meta-analysis also noted a gradual increase in reported cases of wheat allergy in China over the past 2 decades, with wheat now being ranked third among the most common allergens among the food-allergic.

In Japan, research has found a prevalence of wheat allergy of 0.37% in children and 0.21%.in adults.

In Malaysia, a 2016 study examined 192 food-allergic children and reported a prevalence of wheat allergy in 10.4% them, 17.1% in the under 2s and 8.9% in those aged between 2 and 10. In Singapore, the prevalence of wheat allergy among allergic children was found to be 5.7%.

In Korea, a survey study carried out 2 years earlier including 29,842 children schoolchildren aged between 6 and 16 reported a prevalence of wheat allergy of 0.04%. In this study, wheat was the 9^th most common allergen among all age groups. The prevalence peaked between the ages of 9 and 10 (at 0.07%).

A 2017 multicenter study involving 1353 food-allergic children (93% of whom were younger than 7 years old) reported that wheat was the 3^rd most common food allergen across all age groups (affecting 7.9%). However, looking at the various age groups separately revealed that wheat was the 3^rd most common allergen in the under-2s, the 5^th most common in children aged between 2 and 6, the 4^th most common in those aged 7 to 12 and the second most common allergen in adolescents.

A 2018 study carried out in a major teaching hospital in Thailand found that wheat was second only to shellfish when it came to positive oral food challenges. It also provoked the most positive challenges among children younger than 3. The study also noted a possible increase in wheat allergy in Thailand.

In Lebanon, a 2020 study reported that wheat was the no.1 problem food among the food-allergic, with 15.7% of the patients surveyed by the researchers reporting an allergy to wheat.

In Iran, a 2016 study of young, symptomatic food-allergic children in the Northeast of the country reported 2.2% were allergic to wheat, with 4.5% of the under 2s having a positive skin prick test to wheat and 1.5% of the children aged between 2 and 7 having a positive result. A separate study focussing on 79 children with asthma found that wheat was the 3^rd most common allergen in that group, affecting 15.2% of the children.

A study carried out in India on 4680 allergic patients of all ages who attended a clinic in Kolkata reported that 21.8% were sensitised to wheat, the 3^rd most common allergen.

In Pakistan, a 2016 study of 689 allergic adults reported that 22.6 % were sensitised to wheat, the most commonly eaten staple and the most common food allergen. A food challenge confirmed that at least 1.6% of the study population were allergic.

Non-IgE-mediated and mixed allergies

Specific prevalence information for non-IgE-mediated conditions is (even) more difficult to find.

One type of mixed allergy that’s associated with wheat is atopic dermatitis (AD), aka allergic eczema, which I shall now just call eczema (although, strictly-speaking, AD is the most common subtype of eczema).

About 2.6% of the global population is estimated to be affected by eczema, which is just over 204 million people. It’s a condition that’s more likely to affect young children and females, and food is thought to be a trigger in 20% to 30% of the cases, with the most common allergens being milk, egg, soy, wheat, peanut and fish.

Although food-triggered eczema affects children more than adults, quite a few adults still have the condition. The prevalence of food allergy in children with eczema is estimated to be somewhere in the range of 15% to 30% and the prevalence of food allergy in adults with eczema is thought by most experts to be between 1% and 3%, with between 9% and up to 24.5% of that number estimated to be new, adult-onset cases.

A 2011 study carried out on Czech adolescents and adults with eczema revealed that, of the 179 people, at least 20 were sensitised to wheat, but only 8 (4.5%) of them had wheat allergy confirmed with a food challenge, and they all seemed to experienced an improvement in their skin condition after eliminating wheat from their diet.

However, not everyone with eczema and wheat allergy will suffer from a worsening of their skin condition after eating wheat; in general, about 1 in 2 people with eczema and food allergy may experience a worsening of their skin condition after eating their food trigger, often after experiencing immediate-type symptoms. Only around 1 in 10 will experience worsening eczema as their only symptom.

A 2012 German review of 1843 oral food challenges given to children with suspected food allergies revealed that soy and wheat were the two triggers most likely to cause a worsening of the skin condition, with wheat worsening the eczema of just over half (52%) of the children with wheat allergy.

Cases of eosinophilic oesophagitis (EoE) have reportedly been on the rise since the turn of the century. EoE is now thought to affect 1or 2 people in 2000 but, in those with food allergies, the number is more like 1 in 20. Prevalence rates are also higher in studies from America than in those carried out in Europe.

Eosinophilic oesophagitis is more common in males and can occur at any age, but it becomes more common as people get older, peaking in adults aged between 30 and 50.

EoE to a food often develops in someone who already has a standard, IgE-mediated allergy to that food. Wheat/gluten is currently thought to be the second or third most common trigger of EoE in children and adults in the United States, Spain, and Australia. In Poland, a study which followed 50 children with wheat allergy over 12 years reported that 5 (10%) of them developed eosinophilic oesophagitis.

Eosinophilic gastritis is a very rare disease (although cases are on the increase) and, because of that, very understudied. According to American research, it affects about 6.3 in 100,000 individuals, but the lack of typical symptoms and standardised guidelines for diagnosis means that it’s probably underdiagnosed. EG can occur at any age and, unlike the male predominance reported in EoE, there may be a slight female predominance in EG.

Experts do not know the exact prevalence of food protein–induced enterocolitis syndrome (FPIES) but it’s estimated to occur in the general population at a prevalence ranging from 0.015% in Australia to 0.7% in Spain and reports of cases have been on the increase in recent years, either because of an increase in new cases or because of an increased awareness of the condition among doctors. A study using American 2016 Census data estimated the prevalence to be 0.51 % amongst children and 0.22 % among adults.

Food triggers depend on cultural eating habits and grains (rice, oats, wheat) are more likely to a problem in the UK, Canada, the US and Australia.

Research looking into which foods cause FPIES has found that wheat is the fifth most common trigger in British children, the third most common trigger in Canadian adults and the 5^th or 6^th most common trigger in American children, and that ‘grains’ are the most common trigger in Australian children and the most common trigger in Americans (children and adults). In France, a small study has reported that wheat is the 4^th most common trigger of FPIES.

Image by Jaqor Q.I. on Pexels

Will it go away?

IgE-mediated allergy

Wheat allergy usually rears its ugly head in the first few months of life, generally when we’re first exposed to wheat in our diets. Infants can become sensitised to wheat via allergens present in breast milk, which means that they often have an allergic reaction during their first 12 months, either the first time they actually eat wheat or while they’re breastfeeding.

Happily, wheat allergy has a good prognosis. In the general population, it is often outgrown by the time the child goes to school, around the age of 6. Tolerance generally develops more slowly among atopic children (children prone to developing allergies), although most children outgrow their allergy by the time they reach adolescence.

In 1995, Finnish researchers looked at the medical records of 28 children with both IgE-mediated and non-IgE-mediated wheat allergy. They reported that 59% of the children were able to eat wheat by the age of 4, 69% by the age of 6, 84% by the age of 10 and 96% by the age of 16.

In 2009, American researchers examined the medical data of 103 children who had been admitted to Johns Hopkins Pediatric Allergy Clinic over 14 years and diagnosed as having wheat allergy. They reported that, based on the strictest definition of tolerance (the child had passed a food challenge and started eating wheat regularly), 29% were able to tolerate wheat by the age of 4, 45% by the age of 6, 56% by the age of 8, 62% by the age of 10 and 70% by the age of 14.

The average age at which the children outgrew their allergy was 6 and a half years. Under the least strict definition of tolerance (a reduced wheat IgE level and a year without showing symptoms), the average age at which tolerance was achieved was 4 years and 9 months. Unlike with other food allergies, the presence of other allergic disease did not affect the rate of resolution.

Similarly, a Thai study of 55 wheat-allergic children reported that the allergy was resolved in 14.7% by the age of 2, 27% by the age of 4, 45.7% by the age of 5 and 69% by the age of 9. The average age at which the children outgrew their allergy was 6 years and 4 months.

A Polish study that followed 50 wheat-allergic children with predominant gastrointestinal symptoms reported that 20% of children had outgrown their allergy by the age of 4, 52% by the age of 8, 66% by the age of 12 and 76% by the age of 18. The average age at which the children outgrew their allergy was slightly earlier, around 5 years and 10 months.

A slightly quicker rate of resolution was also noted by Japanese researchers following the fortunes of of 83 wheat-allergic children who were regularly tested with wheat-based udon noodles until the age of 6; they reported a tolerance rate of 20.5% at 3 years old, 54.2% at 5 years old and 66.3% at 6 years old.

Initial reactions to wheat can be quite serious, as illustrated by a report describing the case of a 10-week-old infant going into anaphylactic shock after eating semolina pudding. However, his allergy resolved quickly and he was able to eat wheat without problems by the age of 14 months.

In general, the prognosis for children who show serious symptoms seems somewhat worse, as illustrated by an Iranian study of 21 children with severe wheat allergy referred to a hospital clinic. Of 8 children who were followed for a period of at least six years, only 3 outgrew their allergies.

These results are backed up by the results of a Polish study designed to examine the natural course of wheat allergy in children with dominant gastrointestinal symptoms. It found that those who ended up with a persistent wheat allergy were more likely to have anaphylactic reactions (50%) and bronchospasm (40-45%) than skin or GI reactions.

These studies have all shown that blood or skin tests that measure the level of specific IgE antibodies to wheat (or the omega-5 gliadin allergen) can be used to predict how likely a child is to outgrow their allergy; as a rule of thumb, the higher the level (or the larger your skin weal), the longer the allergy will probably last. The age at which you reach peak levels of specific IgE are similarly predictive; the older you are, the longer it will probably take for you to outgrow your allergy.

That said, there is always hope; even children with the highest wheat IgE levels may outgrow their allergy, as shown by an American study which noted that 1 in 5 children who had the highest levels measured still outgrew their allergy during the study period.

Japanese research has also identified several factors which can help to predict whether or not a child will outgrow their wheat allergy. Those who are less likely to outgrow their allergy:

• have had an anaphylactic reaction to any food before the age of 3
• cannot tolerate low doses of wheat during oral food challenges
• have a prolonged history of eczema and/or allergies to several foods

Although most studies on wheat allergy are carried out on children, wheat is also an important allergen in the adult population.

Although many adults with wheat allergy are people who did not outgrow their childhood allergy, you can also develop an allergy to wheat during adulthood.

In fact, according to an American study carried out in 2019, wheat allergy is the most common adult onset allergy. Their survey of 40 443 US adults found that 52.6% who reported an allergy to wheat had developed it after the age of 18. The prevalence of wheat allergy among adults decreased as they got older, from a high of 1% among those in the 18 to 29 group to 0.6% in the over 60s.

The title for oldest person to get an adult-onset wheat allergy probably belongs to a Japanese man who developed WDEIA when he was 82 years old. He discovered his new allergy when he had an anaphylactic attack while playing tennis after eating bread for breakfast. The attack was preceded by a month’s worth of episodes of hives and was probably triggered by a newly prescribed medicine for high blood pressure. He was given antihistamines to take before exercise and they prevented further symptoms.

An Italian study of 13 wheat-allergic adults (average age of 40) reported an excellent prognosis. After being diagnosed, they all adhered to a wheat-free diet and 10 of them were followed for 5 years. During that time, 9 of them regained tolerance, and they were still able to eat wheat when they were contacted 7 years later.

The authors of the study concluded that ‘IgE-mediated wheat allergy in adults is benign and represents a temporary break in gastrointestinal tolerance’ probably brought on by known cofactors (things that can aggravate allergic reactions) such as medications (antacids, nonsteroidal anti-inflammatory drugs like aspirin) and alcohol and the use of wheat-protein containing soaps by people with skin problems like eczema.

The only person who did no regain tolerance was allergic to the heat-resistant LTP allergen (Tri a 14) and also allergic to grass pollen.

Finally, the prognosis is not good for people who either have severe anaphylactic reactions to wheat (including WDEIA) or those who have chronic forms of wheat allergy, such as eosinophilic gastritis, eosinophilic oesophagitis (EoE) or the occupational allergy baker’s asthma. These forms of allergy all tend to be persistent, although people who have exercise-induced anaphylaxis tend to have fewer reactions over time, as they learn to better manage their allergy by either avoiding eating wheat around exercise or avoiding wheat altogether, and people with eosinophilic gastritis tend to go through periods of remission between experiencing flare-ups.

That said, a small Japanese study that followed 7 infants with wheat-induced FPIES for 5 years reported that 6 of them were able to tolerate wheat by the age of 5, implying that infants who develop a chronic allergy to wheat have a better prognosis than do older children and adults.

Image by onlyyouqj on Freepik

Cross-reactions to wheat

Technically-speaking, a person can be allergic to wheatand another food (or foods, or aeroallergen(s)) either by cross-reactivity—the immune system mistakes the proteinin one allergen for aprotein with a similar structure inthe other—or by an independent sensitisation to each food and/or aeroallergen(a co-sensitisation or co-allergy), in which case the immune system has developed specific IgE antibodies against each allergen. It can be difficult to determine whether reactions are caused by cross-reactions or co-allergies,but the end result is the same; problems, problems.

Cereals are part of the Gramineae (grasses) family and are divided into four subfamilies: the Panicoideae (most millets, maize and sorghum), the Chloridoideae (including finger millet, aka ragi, and teff), the Bambusoideae (rice), and the Pooideae, which are further divided into the Triticeae tribe (wheat, barley and rye) and the Aveneae (oats).

As a result, wheat is highly cross-reactive with rye and barley and less so with oats, which is a more distant relation.

This is because plants in the same family contain proteins with similar amino acid sequences and structures and these similar proteins/allergens provoke similar reactions in people allergic to wheat.

Wheat is particularly likely to cross react with barley, as demonstrated by a study in which 18 Iranian children with wheat allergy were given food challenges with various cereals and 10 of them were shown to also be allergic to barley. In another study conducted on 20 barley-allergic children in Korea, 15 were found to also be allergic to wheat. Both studies noted a remarkable correlation between the levels of IgE antibodies to both cereals when testing the children.

Co-sensitisations to wheat and rye have also been reported in asthmatic bakers in Denmark, Germany, Spain and Australia, as well as in Danish children and Italian adults with oral wheat allergy. A large European study of baker’s asthma also noted a large correlation between the levels of IgE antibodies to both wheat and rye flour.

In fact, lab tests using the blood of the wheat-allergic have often demonstrated a very high potential for cross reactions between wheat, barley and rye. In a Finnish study conducted on 23 patients with WDEIA who were specifically allergic to the wheat protein omega-5 gliadin, 21 blood samples showed reactivity against allergens in rye and barley. Skin prick tests on the subjects were positive for various rye and barley allergens between 20% and 67% of the time.

On the basis of these kinds of results, some (predominantly European) allergists recommend that people with eosinophilic oesophagitis (EoE) who undergo elimination diets including wheat also eliminate all foods containing gluten (i.e. barley and rye), in part because of the possibility of cross-contamination during processing, but also because IgE antibodies to rye have been found in the blood of some patients with EoE, suggesting the potential for cross-reactivity between gluten-containing grains.

However, this approach is not recommended by American experts, possibly because it’s a more difficult diet to manage in America, where labelling laws cover only wheat and not gluten-containing cereals as in other English-speaking countries, but also because there are no studies showing whether or not excluding all gluten-containing grains would actually help.

In fact, food allergy research in general tends to show a lot of potential for cross-reactivity when tests are carried out in test tubes (so-called in vitro testing) but not when actual food challenges are carried out in a person (so-called in vivo testing). This is certainly the case for cereals grains which show low rates of actual cross-reactions in people compared to other food families.

In one of the earliest investigations of its kind, 145 American children with eczema and a suspected allergy to cereal grains based on skin prick tests were asked to undergo food challenges. Only 31 of them reacted. 25 of them reacted to only one grain (19 to wheat, 3 to corn and 1 each to barley, rye and rice). 3 reacted to 2 grains (2 to wheat and oat, 1 to wheat and rye). 3 reacted to 4 grains (1 to wheat, oat, barley, and corn, 1 to wheat, oat, rye, and corn and 1 to wheat, oat, barley, and rye). They also carried out lab tests on the blood of their subjects and found a very high degree of cross-reactions that were not reflected by the results of their food challenges and concluded that food challenges were essential to prove allergy and that ‘elimination of all grains from the diet of a patient with grain allergy is unwarranted.’

Similarly, a recent study carried out in 15 Finnish children with a history of severe wheat allergy who were sensitised to oats carried out food challenges which 14 children passed. One child experienced ‘mild abdominal discomfort’ which was successfully treated with an antihistamine.

However, just because cross-reactions are unlikely does not mean that they are impossible. Sometimes they can present themselves in unusual ways, as was the case for a Japanese woman who used a soap containing oats and almonds daily for 2 years before developing weals on her hands, then her body. Finally, 6 years after she started using the soap, she developed a serious food allergy to wheat. Although she stopped using the soap and eating wheat, she didn’t lose her sensitisation to either oats and wheat.

Sometimes, the results of testing can be surprising. A recent study was carried out in Germany to see whether people with WDEIA (aka WALDA) could tolerate spelt—a supposedly safer ‘ancient variety’ of wheat—better than a modern variety of wheat or barley. 40 people with challenge-confirmed wheat allergy submitted to skin and blood tests. 62.5% of them were found to be sensitised to barley and 85% to spelt. When the researchers comparing sensitization levels to barley and spelt, they found that people with WALDA had significantly higher sIgE levels in the blood and bigger skin test weals to spelt than to barley.

In order to see whether these results were clinically relevant—i.e. whether the people with positive tests to these grains would show symptoms—they carried out challenge tests on 3 of the people with a positive skin and blood tests to spelt and barley. All 3 reacted to spelt and all 3 tolerated barley.

In the end, although some tests have led some researchers to recommend rice and corn as an alternative for the wheat-allergic, rice, corn, oats, maize, millet and buckwheat have all demonstrated cross-reactive potential. The fact is, cereal-related allergy is complicated and everyone reacts differently.

Cross reactions between wheat and grass are also frequent, but this generally doesn’t cause problems. Research has identified several cross-reactive allergens in wheat and grass, meaning that people who are allergic to grass often show sensitisation to wheat and vice versa. People who are allergic to grass are also likely to become sensitised to wheat over time.

However, this kind of cross-sensitisation is generally clinically irrelevant—i.e. does not lead to actual symptoms of allergy. For example, in one study of 827 British children who had been followed from birth, a high level of cross-sensitization was noted between grass and wheat—however, although 36 children were sensitised to both wheat and grass, only 4 of them showed any symptoms. Of those, 3 were diagnosed with wheat intolerance and suffered from gastrointestinal symptoms. In the whole birth cohort, only one child was diagnosed with an actual IgE-mediated allergy to wheat.

Another study conducted on 72 grass pollen-allergic children found that 60% were sensitised to wheat, but all of those children were able to eat wheat. Many instead reported a current or past history of allergic reactions to milk, egg, wheat, soy or fish.

In 2011, Danish researchers tried to find out how many lab tests would result in false positive results—i.e. people allergic to grass pollen who would be found to be sensitised to wheat and thus told to avoid eating it. The researchers put out ads in local papers looking for adults who had a history of allergy to grass pollen but none to wheat. Their search and subsequent food challenges resulted in 65 grass-pollen allergic subjects who could happily eat wheat and 20 healthy subjects with no allergies. They then gave their test subjects a battery of lab tests looking for IgE antibodies to cereals including wheat, rye and barley.

They found that 29 of the grass-allergic 65 subjects were positive to at least one of the three cereals. 24 people were positive to two or more of wheat, rye or barley and 11 people were further sensitised to one or more of the other cereals tested (oat, maize or rice), 7 to two or more and 3 people to all 6 cereals. However, all of these people were able to tolerate all of the cereals in their diets.

What this means is that quite a few people who are allergic to grass but not actually allergic to wheat will get a false positive result when undergoing a skin or blood test because of cross-reactions with grass pollen.

This is less likely to be the case for bakers who tend to be exposed and sensitised to both wheat and grass. (Specifically, bakers are more likely to be sensitised to wheat grain allergens, and not pollen).

It’s also less likely to be the case for people who are strongly sensitised to grass pollens, as seen in a small Japanese study that showed that wheat-allergic people who have very high levels of IgE antibodies to grass may essentially go on to develop Pollen Food Syndrome, because the grass pollen proteins they are allergic to cross-react with water-soluble wheat proteins (namely peroxidase-1 and beta-glucosidase) and cause allergic reactions.

Image by Joshua Chekov on Unsplash

Symptoms of wheat allergy

Wheat allergy can be IgE-mediated, non-IgE-mediated or mixed; a combination of both. These variations generally present different types of symptoms.

Immediate reactions to wheat

Immediate allergic reactions are caused by IgE antibodies. These antibodies bind to certain immune system cells—mast cells and basophils—and trigger the release of histamine and other inflammatory chemicals that cause the characteristic symptoms of allergy.

Immediate reactions are the most common type of allergic reaction to wheat and they range from rashes to life-threatening anaphylaxis. Reactions are different for different people, and they can also be different for the same person, varying in severity from episode to episode.

There are three main routes to developing an IgE-mediated allergy to wheat, and the route taken affects the type of allergy that you get and the principal symptoms that go with it.

1. You can become allergic to wheat via gastrointestinal sensitisation—i.e. by eating it. This tends to produce the ‘classic’ signs of allergy.

These include:

• Skin symptoms: eczema (atopic dermatitis), hives (urticaria), swelling of the face (angio-oedema) and/or tongue and/or throat and/or hands, redness (erythema), itchy skin (pruritus), oral allergy syndrome (OAS, commonly manifesting as ‘itchy’ or ‘burning’ symptoms often limited to the mouth, sometimes also swollen lips and cheeks)
• Breathing symptoms: blocked nose (nasal congestion), runny nose (rhinorrhoea), wheezing, difficulty breathing/shortness of breath (dyspnoea), persistent cough, hoarse voice
• Digestive (GI) symptoms: nausea, diarrhoea, vomiting, stomach pain
• Cardiovascular symptoms: low blood pressure (hypotension), rapid heart rate (tachycardia), loss of consciousness (syncope)
• Neurological symptoms: headaches, dizziness, blurred vision, anxiety, confusion, seizures, fatigue and malaise (aka ‘a feeling of impending doom’, which can occur during anaphylactic reactions)

IgE-mediated reactions typically occur within 5 to 30 minutes of eating the trigger food, but they often take longer to appear when the trigger is wheat. A Japanese study in which 19 wheat-allergic children aged between around 2 and 5 years old were given oral food challenges noted that the symptoms appeared at a median time of 53 minutes after the children had eaten the wheat, with a range of 36 to 74 minutes.

Tests carried out on adults have also produced delayed symptoms in the form of shortness of breath (in a patient with mild asthma, 22 hours after an inhalation test with wheat flour) and migraine headaches, 12 to 15 hours after eating wheat.

Skin symptoms are by far the most common and often occur in conjunction with other types of symptoms. A review of children seen at an American hospital reported that, of the 61 who were symptomatic on their first visit (and who were, on average, 19 months old), most had suffered a rash as their initial symptom.

A retrospective review of wheat oral food challenges (OFCs) performed at a Swiss children’s hospital reported that, of 42 children aged between 1 and 12 (average age 4) with a positive challenge, 80% suffered from skin symptoms, 50% from respiratory symptoms and 26.7% from GI symptoms.

A review of challenges carried out in Finnish children aged between 7 months and 17 years reported that, of 57 children with a positive challenge (25% of whom had delayed symptoms), 47 (82%) had skin symptoms (mostly hives or redness), 28 (49%) had GI symptoms and 17 (20%) had respiratory symptoms.

A review of Japanese wheat-allergic children aged between 6 months and 14.6 years (average age 1.3 years) reported that 98% suffered from skin symptoms, 15% from lower respiratory (asthma-like) symptoms and 7% from anaphylaxis.

Headaches and wheat allergy are apparently no strangers to each other. In the late 1970s, tests were carried out to see whether migraines could be provoked by food allergens. Wheat was found to be the most common irritant, with 47 of 60 people reporting reduced symptoms when they eliminated it from their diets.

A more recent report describes the case of a 48-year-old woman who suddenly began to get headaches on a daily basis. They would start around lunchtime and last until late evening, sometimes accompanied by diarrhoea and stomach pain. After suffering from these headaches for about 13 months, they suddenly stopped for a few days before starting again. She later realised that, during the days without the headaches, she had not eaten her usual diet ‘digestive tasty wheat’ biscuits for breakfast because she had forgotten to buy them. So she stopped eating the biscuits and her headaches went away.

Symptoms tend to be age-dependent. Infants and young children are more likely to suffer from gastroenterological symptoms. Toddlers are more likely to suffer from skin symptoms, either alone or together with respiratory symptoms and/or digestive problems. Gastrointestinal symptoms tend to recede with age, therefore older children suffer mostly from skin symptoms accompanied by respiratory symptoms and, more rarely, anaphylaxis.

Teenagers and adults are more likely to have the most severe symptoms, including anaphylaxis, and mixed or non-IgE-mediated conditions and intolerances, such as irritable bowel syndrome (IBS) and eosinophilic oesophagitis (EoE). They are less likely to suffer from intestinal or respiratory symptoms.

A study of Danish and Italian adults with wheat allergy reported mostly skin symptoms as a result of failed food challenges, followed by GI symptoms then respiratory symptoms. Almost two thirds (62%) of the adults had symptoms involving 2 or more organ systems, thus fulfilling the criteria for anaphylaxis. Three of the adults ended up with migraines.

Don’t panic: To be clear, the official definition of anaphylaxis is probably not what you think it is.

This means that many of the cases of anaphylaxis reported in medical studies are not actually life-threatening—when dealing with an emergency, however, since it’s impossible to predict which reactions will become life-threatening, every case of anaphylaxis should be treated as if it is potentially deadly.

The frequency of wheat-induced anaphylaxis seems to vary according to geography. Anaphylaxis to wheat in Europe seems to be less frequent than it is elsewhere, although wheat has been reported as the most frequent cause of anaphylaxis in central European adults, generally in conjunction with cofactors and often partially delayed.

In the US, wheat has been reported as the 4^th most common food trigger of anaphylaxis in preschoolers and a risk factor for severe reactions requiring adrenaline, including to low doses of wheat, in children and young adults. In adults, almost half (42.6%) of the reactions are classified as severe (involving 2 or more organ systems).

Wheat seems to be a more important cause of anaphylaxis in young children in (Middle) Eastern countries. In Iran, a 2010 analysis of anaphylaxis registry data reported wheat as the second most common cause of anaphylaxis in children. Tests on children with suspected wheat allergy have reported anaphylaxis as the dominant symptom in those aged 12 or less, and one study of 19 infants referred to an allergy clinic after a severe reaction to a small amount of wheat noted that anaphylaxis occurred when the infants ate wheat for the first time and often consisted of skin and respiratory symptoms.

In another study of 21 Iranian children with severe wheat allergy, acute anaphylaxis was seen in over 90% within15 to 30 minutes of eating wheat. 19 (90.5%) had skin reactions including hives, flushing and itching, 18 (85.7%) had breathing problems including wheezing, cough, and shortness of breath and 10 (47.6%) had GI symptoms including nausea, vomiting and diarrhoea.

In China, an analysis of 14 years worth of medical records identified 907 people who had had anaphylaxis or severe allergic reactions and reported that wheat was the main trigger of food-induced anaphylaxis (37% of all episodes) in teenagers (20% of reactions) and adults (42% of reactions). 57% of the most severe anaphylactic episodes to food were triggered by wheat, in contrast to the other main trigger food category, fruits and vegetables, which caused mainly mild or moderate reactions. People allergic to wheat were also most likely to have several episodes of anaphylaxis before visiting a doctor.

In Korea, a 2016 analysis of anaphylaxis registry data reported that wheat was the fourth most common food trigger in children and the second most common in adults.

In Japan, parents have reported wheat as the third most common trigger of food-induced anaphylaxis in their children, whose first attack occurred between the ages of 3 and 6.

And in Thailand, a cross-sectional survey of 100 wheat-allergic children (aged between 6 months and 17 years old) reported that 49% had only skin reactions, while 51% had anaphylactic attacks. They revealed that eczema was less common among the children who suffered from anaphylaxis.

Wheat-dependent exercise-induced anaphylaxis (WDEIA)

The most common form of anaphylaxis to wheat, especially in older children and adults, is WDEIA.

Symptoms tend to vary depending on how long you’ve had the condition. In the beginning, you will often suffer milder symptoms, including:

• itchy skin (pruritus)
• diffuse warmth and/or flushing
• profuse sweating
• tingling in the extremities
• hives (urticaria, probably the most common symptom)
• swelling of the face (angio-oedema) and/or throat and/or extremities (often the hands)
• sudden fatigue
• headaches (rarely, but can last for hours or even days)

You may experience these milder symptoms for several months, sometimes years, before going through your first episode of anaphylaxis.

Research from China has revealed that around two-thirds of people who develop full-blown WDEIA experience recurrent hives after eating wheat in the run-up to their first anaphylactic attack. A 2019 study involving 193 people with wheat-induced anaphylaxis (104 with WDEIA) reported that 164 of them (84.9%) reported recurrent episodes of hives. Of these, 136 experienced recurrent hives before their first anaphylactic reaction (including 70.4% of the WDEIA group) and, of these, 63 (46.3%) experienced a worsening of their hives episodes before their first anaphylactic attack.

The average time between the beginning of the hives episodes and the first anaphylactic attack was around 3 years, with a wide range of 0.1 to 40 years. 54% of the cases fell within a range of 1 to 5 years.

More severe episodes of WDEIA also tend to start with these milder symptoms, so if you know you have WDEIA and you start to experience any of the above symptoms, stop what you’re doing. This generally stops the symptoms from getting worse.

If you don’t stop exercising or you have severe WDEIA, an episode can quickly progress to include more severe symptoms like:

• wheezing
• shortness of breath due to tightening of the air passages of the lung (bronchospasm)
• a feeling of tightness in the chest
• a swollen throat (laryngeal oedema) that makes swallowing difficult (dysphagia) and/or can make your voice hoarse
• nausea
• stomach cramps
• diarrhoea

Finally, you can experience cardiovascular symptoms, including:

• low blood pressure and feelings of dizziness or faintness
• anaphylactic shock, aka cardiovascular collapse—not enough blood gets to your brain and you lose consciousness

Severe anaphylaxis is relatively common in people with WDEIA, especially in East Asia, where up to three quarters of the reactions suffered are potentially life-threatening. An examination of the medical records of 197 WDEIA patients admitted to a hospital in Beijing, China, reported that the most common symptoms were hives (100%), loss of consciousness (82.7%), shortness of breath (50.8%), low blood pressure (47.2%), and blurred vision (39.1%). By contrast, an analysis of the reactions suffered by 30 British people with WDEIA reported that the most common manifestations were hives (77%), cardiovascular symptoms (70%), and breathing symptoms (30%).

One possible explanation for the reports of Asians experiencing more severe symptoms than Westerners may be genetic predisposition, but some experts think that another likely explanation is that Asians tend to have to experience more serious symptoms before being referred to an allergist for help in the first place.

In most cases of food-dependent exercise-induced anaphylaxis, the offending food is eaten within a few minutes to a couple of hours before exercise, but food eaten up to 5 or even 6 hours before exercising can still cause problems. There are also rare reports of people suffering from symptoms when eating their food trigger after exercise.

Symptoms generally occur within a half an hour of the onset of physical activity, but they can appear anywhere from 5 minutes after starting to exercise to 5 hours after the end of physical activity.

Sometimes they can be very delayed, as in the case of a 51-year-old man who experienced anaphylactic attacks 10 hours and 24 hours after eating wheat-containing meals and then exercising. The fact that he had a history of chronic gastroenteritis which was associated with intestinal blockage is thought to have exacerbated the delay.

Pro tip: The escalation of symptoms during an episode of WDEIA can often be prevented by simply stopping all activity, so it’s important to pay attention to the signs your body is sending you.

2. You can become allergic to wheat via inhalation—i.e. by breathing allergens in. This generally results in respiratory symptoms, although it can eventually lead to the ‘classic’ symptoms of food allergy.

Respiratory symptoms to wheat come in two flavours:

• allergic rhinoconjunctivitis, basically hay fever symptoms— itchy and/or watery eyes, a blocked or runny nose and sneezing
• asthma—wheezing, shortness of breath and a feeling of chest tightness

Most cases of respiratory allergy to wheat can be found among people who work with wheat. In fact, asthma caused by allergy to cereal grain proteins is the oldest occupational allergy. It was initially reported by Bernardino Ramazzini, aka the father of occupational medicine, who wrote the first scientific report about it in 1700. But he wasn’t the first person to mention it; there are several anecdotal references from antiquity about Roman slaves who worked in bakeries and mills covering their faces with cloths in an attempt to prevent breathing problems caused by inhaling flour.

This type of occupational asthma, which predominantly affects bakers, eventually became known as baker’s asthma. In 1929, Norwegian bacteriologist de Besche was the first to propose wheat allergy as its underlying cause.

These days, baker’s asthma is one of the most common types of occupational asthma worldwide. In Europe, cereal grains are the most important cause of occupational asthma in Finland, Sweden, France and Italy and the second most important cause in Norway and the UK.

Baker’s asthma is also the second most important cause of occupational asthma in New Zealand, a known cause of respiratory problems in biscuit factory workers in Singapore and mill workers in Iran, and has recently been demonstrated to affect a third of bakers in the Congo as well as other bakery personnel—salespeople, administrative staff and cleaners—in the Ivory Coast. In South Africa, it has been the cause of one reported death.

Baker’s asthma is mainly caused by exposure to wheat and rye flour, although enzymes also play an important role. (see Good to know section later).

People who work in bakeries and grain mills run the highest risk of developing baker’s asthma, with about 5% to 10% bakers suffering from asthma and 15% to 20% from rhinitis, but people working in pasta factories, pizza bakeries, cake and biscuit factories, restaurant kitchens, malt factories, animal feed plants and agriculture are also at risk of exposure to high levels of flour dust. In recent years, an increasing number of asthma cases has being reported among supermarket bakery workers.

It’s the intensity of exposure to cereal flour that ultimately determines whether or not you end up getting the disease, and this varies considerably depending on the type of job you have, the size of the bakery you work in and the type of baked goods you make; in the latter case, bread-making is much more likely to sensitise you to flour dust than pastry-making.

Research carried out in Belgium has found that people who work in small, traditional and craft bakeries are more likely to be affected than those who work in larger industrial ones, whereas research from the UK and South Africa (3) has reported the opposite. The fact is, bread-makers in all sizes of bakery have to contend with different types of exposure.

In both large and small bakeries the most high risk jobs are sieving, weighing and mixing but, whereas workers in small bakeries have to deal with high levels of airborne dust in the small spaces they’re working in, those in large bakeries also have to contend with the dust clouds that are formed when they receive and open large containers of flour. Dough-making and dusting during bread forming (to stop the dough from sticking to surfaces) also expose workers to high levels of flour dust.

However, although the risk of developing baker’s asthma tends to increase with exposure to flour dust, research suggests that the risk may actually level off or even decline at very high levels of exposure.

Other factors—such as a person’s genetic make-up or whether they have a personal history of allergies (i.e. are atopic)—also affect a person’s chances of developing the condition, and a person’s medical history, their job description and a simple skin test can theoretically be used to identify those at highest risk.

When a person gets baker’s asthma, it normally appears months or even years after they start their job. It generally start off as a runny nose (rhinitis) or as hay fever-type symptoms including itchy eyes before later progressing to asthma. Often, symptoms go away when that person takes a holiday, only to return when they get back to work. If a person continues to work with flour, over time, their symptoms may stop going away during their time off.

Most people who develop baker’s asthma can still eat wheat without symptoms. Why this is so continues to baffle scientists. It could have something to do with the different routes to sensitisation—inhalation versus eating—or it could be that, by regularly eating bread, they are able to maintain their oral tolerance to it, much in the same way that oral immunotherapy works.

Unfortunately, this is not the case for everyone, as demonstrated by a Turkish man who first developed a runny nose 10 years after starting work as a baker, and then asthma 10 years after that, and eventually was also unable to eat bread made from wheat flour without suffering from stomach pain and diarrhoea.

Baker’s asthma can be prevented by reducing the level of exposure to cereal allergens, although this may be easier said than done. There are legal limits governing exposure to flour dust in working environments, which can be achieved with a range of different methods, including better ventilation, the use of liquid dough improvers and low-dust flours, machinery shielding, protective equipment like respirators and facemasks, regular cleaning of workplaces and clothing, isolation of workstations and medical monitoring.

Of course, these methods can reduce the level of flour dust present in a worker’s environment, but they need to be properly implemented which is often not the case, meaning that a large proportion of workplaces fail to meet the legal standards set for air quality.

If you’re affected by baker’s asthma and you can’t come to a solution with your employer, you may be able to take legal action, either through your union, an advocacy group or lawyers (your options will differ depending on where you live) but, if your symptoms are serious, you should consider finding alternative employment if you can, because no amount of compensation will make up for losing your health.

It’s not just people who work with wheat who can develop respiratory symptoms to it. Research has shown that the families of bakers are also at risk of becoming sensitised to cereal flour allergens which are ‘taken home’ by the bakers on their skin, clothing and shoes. Research also suggests that the children of bakers are more likely to develop asthma in later childhood.

Simply visiting a relative at work in a bakery can be risky, as shown by the case report of a two-year-old boy who suffered from asthma, hives and eczema for a year because of the visits he made to his grandfather’s bakery where his mother worked. His symptoms improved once he started going to nursery school and was exposed less often to the flour dust at the bakery and on his mother’s clothes.

You don’t necessarily have to visit a bakery to develop problems with wheat. A study that tested the blood of random American blood donors for sensitisation to bakery-associated allergens revealed that, among the general population, 1% were sensitised to enzymes used in bakeries, 3.6% to wheat, and 5.8% to flour dust.

People who are very allergic to grass or tree pollen can also experience asthmatic symptoms if they inhale cereal flours because of cross-reactions, according to a small study of 25 mildly asthmatic Germans.

Finally, some people are allergic to wheat pollen which can provoke hay fever symptoms or asthma.

3. You can become allergic to wheat by touching it and developing a contact allergy. This generally results in rashes but can later lead to respiratory and ‘classic’ symptoms of allergy.

There are 2 main forms of contact allergy that you can get from touching wheat; contact urticaria (CU) and protein contact dermatitis (PCD).

Allergic contact urticaria basically looks like hives; an itchy, a weal and flare reaction that occurs within 10 to 60 minutes of touching the food and disappears within 24 hours.

Protein contact dermatitis describes allergic (or non-allergic) eczema-like reactions to food proteins. It can be chronic or recurrent and tends to occur on the hands, wrists and arms with periods of intensified reactions when you can feel of itching or tingling a few minutes after contact with the food you’re allergic to.

Sometimes symptoms of both contact urticaria or protein contact dermatitis extend to the face, either because someone touches their face with contaminated hands or because of airborne allergens.

Contact allergies are often experienced by professional food handlers because they are more likely to develop when a person is continuously exposed to allergens and to things that affect the integrity of their skin, such as wet working conditions.

As such, contact allergies to wheat are mostly reported in bakers, people who work in mills and flour factories and cooks. A person can work with wheat for years before developing a contact allergy and, unlike bakers who develop an allergy from breathing in wheat allergens, people who develop contact allergies to wheat also tend to go on to develop food allergies, too, although they are often allergic to the raw form of wheat, but not the cooked form; so they will have symptoms if they eat flour dusting on a loaf of bread, but not the loaf itself.

Contact allergies to wheat can also affect people who don’t work with wheat, such as mothers who regularly bake for their families, like the case of a working mother with a history of eczema on her hands who made chapatti bread for her family every day and ended up developing itchy wheals on her hands 20 minutes after handling wet (but not dry) chapatti flour (a mixture of wheat and rye). She was advised to wear gloves when handling the wet flour and her symptoms improved.

People who use cosmetics containing wheat can also develop contact allergies, especially if they have a skin condition like eczema. The symptoms can either be immediate or delayed.

It’s not just adults who have to be careful with wheat-containing cosmetics. One report describes the case of a 14-month-old boy who was admitted to hospital for treatment of his eczema. He was known to have symptoms after consuming milk and peas and had a bad case of eczema and his mother has been told to bathe him regularly in a wheat bran bath prescribed to reduce the itching. However, 4 months after beginning this treatment, he started getting weals and itching within a few minutes of being in the bath. Although the boy was able to eat wheat, his doctors put him on a wheat-free diet and his skin symptoms—including the eczema—disappeared.

The doctors were unsure whether he had become sensitised to wheat by breastfeeding, eating wheat or having the baths, but they still cautioned against giving bran baths over long periods of time to children with food allergies.

The wheat in cosmetics is often hydrolised so that it can properly dissolve in the product, and regular exposure to hydrolysed wheat protein (HWP) has caused more problems than exposure to whole wheat allergens. The first cases were reported about 2 decades ago in France, but the whole problem really came to light in Japan, after hundreds of women who had been using a certain type of HWP-containing soap ended up developing skin symptoms and, more alarmingly, anaphylactic attacks, either triggered by eating wheat or by exercise in combination with either HWP or wheat itself.

You can read more on hydrolysed wheat proteins in the Managing wheat allergy section.

Delayed reactions to wheat

Delayed allergic reactions can occur hours or even days after exposure to an allergen, unlike IgE-mediated reactions that often happen within minutes. These reactions either involve diseases that rely on cell-mediated mechanisms (immune responses that do not rely on the production of IgE antibodies but instead involve the activation of T cells and macrophages which leads to inflammation and tissue damage) or by ‘mixed’ diseases that rely on both IgE- and cell-mediated mechanisms.

The most common forms of delayed reactions to wheat are eczema (atopic dermatitis), eosinophilic oesophagitis, eosinophilic gastritis, food protein-induced enteropathy and food protein induced enterocolitis syndrome.

Eczemais a chronically relapsing inflammatory allergic condition that specifically affects the skin and look like this. It’s classified as a ‘mixed’ form of allergy that can produce either immediate or delayed reactions that can occur up to 48 hours after eating a trigger food.

Wheat allergy is more likely to produce a worsening of eczematous symptoms than other foods allergies (except for soy), according to a German retrospective review that examined the results of 1843 oral food challenges given to food-allergic children, 98 of whom were diagnosed as wheat allergic.

In an American study, a concomitant cereal (oats, wheat, rye and barley) allergy was detected in 66 of 90 milk-allergic children younger than 3 years old whose symptoms refused to disappear even though they were following a strict dairy-free diet. Roughly 1 in 5 were eventually diagnosed with an immediate form of eczema and the rest with a delayed form.

Eosinophilic oesophagitis (EoE) is an inflammation of the oesophagus caused by a food allergy, environmental allergens or acid reflux. It is characterised by symptoms including:

• food impaction; this is when food becoming stuck in the oesophagus which can lead to a sensation of squeezing in the chest, and can be accompanied by excessive salivation (unlike choking, a person can still breathe and talk, but they cannot eat or drink any more)
• difficulty swallowing (dysphagia)
• abdominal pain
• reflux (the flow of liquid back from the stomach into the oesophagus)
• vomiting
• heartburn (pyrosis)
• stomach pain
• food refusal

Symptoms are variable and often age-dependent. In infants, EoE tends to provoke general symptoms of oesophageal difficulties such as gagging, vomiting, feeding difficulties and weight loss, or so-called ‘failure to thrive’. Young and school-age children have symptoms that are indistinguishable from those associated with gastroesophageal reflux, such as abdominal pain, vomiting and an unpleasant taste in the back of the mouth that comes from regurgitating sour or bitter liquid. Older children and adults are more likely to have trouble swallowing and to get food lodged in their oesophagus (food impaction) and, less commonly, to suffer from heartburn.

Eosinophilic gastritis (EG) is a severe inflammation that is theoretically limited to the stomach but, in practice, can overflow into other areas. Symptoms depend on the degree and area of the gastrointestinal tract affected and include:

• nausea
• stomach pain
• bloating
• indigestion (dyspepsia)
• vomiting
• early satiety (feeling very full after eating just a small amount of food)
• weight loss (due to malnutrition)
• fatigue

EG can sometimes lead to the development of a gastric ulcer and it can co-exist with protein-losing enteropathy (PLE), which is a condition in which proteins are lost from the gastrointestinal tract, and eosinophilic oesophagitis.

Food Protein Induced Enterocolitis Syndrome (FPIES) is a delayed allergic reaction to food that affects the gastrointestinal (GI) tract. There are two main types of FPIES, chronic and acute.

Chronic FPIES is quite rare and occurs mostly in infants who eat the trigger food on a daily basis. It can be recognised by intermittent vomiting and diarrhoea and, occasionally, failure to thrive (which means that a child is not getting in enough calories to reach a similar weight and size to other children of the same age and sex). Cases of chronic FPIES in adults are vanishingly rare, but not unheard of.

Acute FPIES is by far the most common form. In children, symptoms often occur within 2 to 4 hours after eating the offending food and can include:

• vomiting
• pallor
• lethargy
• dehydration
• diarrhoea
• shock or hypotension (i.e. low blood pressure) which can manifest as dizziness, fainting or blurred vision (as well as pallor and lethargy)

Sometime children with chronic FPIES end up developing acute FPIES and this form of FPIES can, in turn, develop into an IgE-mediated form of allergy.

In adults, the typical symptoms of acute FPIES are not the same as those seen in children. They can also appear faster. They include:

• stomach pain and cramps
• diarrhoea
• vomiting
• dehydration
• transient weakness and shivering (possibly hypothermia)
• lethargy
• weight loss

People who experience severe symptoms of acute FPIES may have a longer-lasting form of the disease.

Food Protein-induced Enteropathy (FPE) affects the small intestine, resulting in digestive symptoms including:

• intermittent vomiting
• chronic diarrhoea
• malabsorption (steatorrhea) which can be accompanied by a ‘failure to thrive’ (FTT), that is, a failure to show proper growth
• rarely: bloody stools

Food protein-induced enteropathy (FPE) is a subset of protein-losing enteropathy (PLE); PLE is an umbrella term that encompasses a variety of diseases that lead to excessive protein loss in the gastrointestinal tract, while FPE is a specific type of PLE triggered by reactions to food proteins.

One team of scientists has proposed the catchy term ‘food-protein induced protein-losing enteropathy’ (FPIPLE) to refer to the condition, with the following signs to identify it:

• below-average weight gain (their current weight or rate of weight gain is significantly below what is expected for their age, sex and ethnicity)
• and/or swelling (oedema) brought on by abnormally low levels of protein in the body (hypoproteinemia)
• anaemia

Because symptoms can be severe, if you do suspect that you’re allergic to wheat, it’s important that you see your GP/family doctor and get a referral to an allergy clinic for further testing.

Threshold for reactions

Only a small amount of wheat is necessary to provoke a response in a sensitive wheat-allergic person.

VITAL®, the Australian initiative for voluntary incidental trace allergen labelling, put out recalculated threshold doses for the ‘Big 14’ allergenic foods in 2020. Using a database containing datasets from studies carried out worldwide that used double-blind, placebo-controlled food challenges (DBPCFC), they calculated that the lowest threshold dose of protein that was needed to produce a reaction in 1% of the population allergic to wheat is 0.7 mg. (Note: in this case, the ‘population allergic to wheat’ is 99 people who were given a DBPCFC)

15.4 mg was the dose needed to produce a response in 10% of the test subjects, and 174 mg was the dose needed to provoke a reaction in half of the test subjects.

Note: we’re talking about milligrams of wheat protein. There’s about 2.3 grams (2,300 mg) of wheat protein in a slice of white bread. The amount varies per type of bread but people with a particularly sensitive allergy clearly would not manage even a small nibble.

Ultimately, the threshold dose needed to provoke symptoms varies widely between people. Children tend to react to lower doses of bread than adults, but adults have more severe reactions. People who have respiratory allergies and react to inhaled wheat tend to have lower thresholds.

Reactions also vary per person, depending on the circumstances around the meal.

Your threshold can be lowered and your allergic reactions worsened by things called ‘cofactors’. Cofactors include things like how much you eat and whether those ingredients have been cooked or processed, as well as things like medications and alcohol (especially in older adults), infection and stress. A recent review of the European anaphylaxis registry singled out alcohol as being particularly likely to worsen reactions to wheat.

That said, exercise is by far the most common co-factor linked to severe reactions to wheat. Foods like bread and baked goods, pancakes, muesli, cereal bars, pizza, pasta, noodles, dumplings and beer have been implicated in so many cases of food-dependent exercise-induced anaphylaxis (FDEIA) that it has been given its own acronym, WDEIA.

Some people get exercise-induced reactions to other foods as well as wheat, and some need to eat other foods as well as wheat to have reactions.

Drugs are also a common cofactor in WDEIA, especially aspirin. Sometimes, there is no reaction without the combination of aspirin, wheat and exercise. In fact, aspirin is such a frequent offender that it’s routinely used in tests to diagnose WDEIA.

Although aspirin is the most commonly mentioned medication in cases of WDEIA (including cases that don’t actually involve exercise), naproxen has also been linked to the condition. And nonsteroidal anti-inflammatory drugs (NSAIDs) are not the only type of medication linked to WDEIA; angiotensin converting enzyme (ACE) inhibitors proton pump inhibitors, beta-blockers and antacids are frequently suspected as cofactors, as is the calcium channel blocker amlodipine (used to treat high blood pressure and certain heart problems).

Menstruation is also a cofactor that’s quite often associated with cases of WDEIA. Other cofactors that have specifically been implicated in cases of WDEIA include temperature (specifically, the cold) and cannabis. They, too, can worsen reactions without exercise.

Cofactors are thought to play a role in about 14% to 30% of all anaphylactic reactions.

A 2013 study carried out in Germany identified wheat as the most common cause of food-induced anaphylaxis in adults, including in situations involving cofactors.

Please note: the amount of wheat needed to provoke a reaction says nothing about how severe the reaction will be. And, even if your reactions have been mild in the past, it does not mean that they will continue to be mild.

Image by Ivan Samkov on Pexels

Diagnosing wheat allergy

A diagnosis of wheat allergy will primarily be based on your clinical history—a record of consistent symptoms following the consumption of wheat or wheat-containing foods. This will require you to provide your allergist with answers to questions about your general medical background (including any other allergies you may have and relevant illnesses in your family) and your dietary history (what you ate to provoke your symptoms, what those symptoms were, how long they lasted, whether you had exercised or taken painkillers and many other details).

If you have asthma or a contact allergy and suspect that the symptoms are a result of your job or using a cosmetic cream, you will need to note things like when you starting working with wheat (or using the cream), when you first started noticing symptoms, what the symptoms are exactly, what you are doing when you get them (e.g. mixing dough, using a certain face cream) and whether they ever go away, for instance, when you’re on holiday (or using a different cosmetic cream).

Your medical history determines what comes next; on the basis of your answers, the allergist will try to determine what type of allergy you have—a primary, immediate-type allergy, a cross-reactive allergy or a delayed-type allergy—or whether it could be something else, and this will determine the tests they ask for to come up with a diagnosis.

Diagnosing IgE-mediated reactions to wheat

Skin tests

An IgE-mediated sensitisation to wheat is typically confirmed by a skin prick test, which involves someone placing a small sample of wheat extract onto your skin (generally the forearm of an adult/older child or the upper back of a young child) and pushing it through the top layer of skin by pricking it with a lancet. It takes about 15 minutes to see a reaction (or not).

This test is often carried out first because it is quick and simple to perform and gives rapid results, but it is generally used to rule out an allergy rather than to confirm one, because it has excellent negative predictive value—if the skin weal is under a certain size, you are highly unlikely to have an allergy—but poor positive predictive value—the skin weal has to be very large before an allergist can say with any kind of confidence that you probably have an allergy.

Unfortunately, these tests are not always reliable. For example, in a study of 108 Finnish children, almost all of those with wheat allergy had a positive skin test. But so did about half of those who were tolerant to wheat. In this case, people could have been wrongly told that they were allergic to wheat. The processing of commercially-made allergen extracts can also destroy heat-sensitive allergens. In such cases, someone could get a false negative result and be wrongly told that they are not allergic to wheat.

One solution to this problem is the prick to prick test. This test is very similar to the skin prick test, except first the lancet is used to puncture fresh food—like fresh flour—and then it is used to prick your skin. When the food is in liquid form, the technique is actually the same as the one used for the skin prick test and, when the food is solid, it’s often ground down and put in some kind of solution.

The prick to prick test often produces superior results to commercial extracts because the fresh food used should contain all of the allergens that a person can react to. The lab used by the clinic can also prepare the extract in specific ways which may add to its efficacy.

Blood tests

Sometimes, the doctor may decide to order a blood test, aka an immunoassay. Perhaps the skin prick test was inconclusive, or the suspected allergen is not available for skin prick testing, or you’re unable to undergo the test for some reason.

A blood test involves having a small sample of blood drawn so that it can be sent to a lab where technicians will use allergen extracts to check whether there are IgE antibodies in your blood that react to them. It can take 1 or 2 weeks to get the results.

Blood tests can be less sensitive or specific than skin tests, but they have other advantages: they are perfect for people who cannot stop taking certain medications or have extensive skin disease or tattoos, and they can safely be used on infants, squirming toddlers and people who are at risk of suffering an anaphylactic reaction.

Blood test panels also typically include a whole range of potential allergen extracts including other foods or aeroallergens that the allergist may want to check your reaction to.

However, they’re not very reliable either. Although IgE cut-offs—levels of antibodies in the blood that can predict the result of a food challenge—have been found for other major allergens like peanut, egg, and milk, finding similarly meaningful values for wheat has, so far, proven difficult, although a few studies have reported that higher levels of specific IgE to wheat does increase the probability that someone will show symptoms, especially in children under 12 months old for whom specific cut-offs have been determined.

In Switzerland a review of the medical records of children given blood tests and food challenges at a hospital in Geneva between 2004 and 2019 found that there was a tendency for the children who failed food challenges to have higher levels of IgE antibodies in their blood, but even a high cut-off value would allow quite a few children who were actually asymptomatic to be diagnosed as allergic, emphasising the need for a challenge to be done to avoid children unnecessarily being put on a wheat-free diet.

A major problem is that the commercial wheat extracts used for skin and blood tests mainly contain water- and salt-soluble proteins and are poor in insoluble ones (the prolamins glutenin and gliadin). This makes it a particularly bad test for conditions like WDEIA (aka WALDA) which are mostly provoked by gluten allergens.

Different commercial wheat extracts also all vary widely in their content, and give widely different results (although they may give more reliable results for children under 12 months old). And, even though some allergists prepare their own wheat flour solutions using raw material, those aren’t very reliable either.

Another major problem is the cross reactivity between grass pollens and wheat, especially in adults, who can either be falsely labelled as allergic to wheat because of grass pollen cross-reactivity or falsely labelled as tolerant because of missing wheat allergens in commercial extracts.

For more specific information, a component blood test—aka Component Resolved Diagnosis (CRD)—can be carried out. Instead of using extracts of whole foods containing only (heat-stable, plentiful) allergens, the CRD tests the reaction of IgE antibodies in your blood to isolated, individual proteins. This improves the diagnostic sensitivity of the test as allergens that would otherwise be missing from the whole wheat extract or exist only in tiny amounts are present in concentrated form in the CRD test.

This type of test enables the doctor to see exactly which allergen(s) you react to, which allows them to determine whether you are sensitised to cross-reactive allergens that are unlikely to produce symptoms, and whether you are sensitised to certain allergens that could affect your management plan.

For example, a sensitisation to any of the gliadins would put you at of having more severe reactions and the higher the IgE levels, the more severe the reaction is likely to be. A sensitisation to Tri a 19, in particular, would suggest that your allergy is more likely to rely on cofactors (like alcohol and exercise).

Tri a 14 could help to differentiate wheat sensitisation from pollen allergy; people with a sensitisation to Tri a 14 are often asymptomatic, meaning that those who are sensitised to this wheat allergen alone could consider an oral food challenge to avoid unnecessarily restricting wheat from their diets.

Component blood tests are also made up of very large panels of allergens which include many other foods and aerollergens that the allergist may want to check your reaction to and can help to determine whether or not a sensitisation to a cross-reactive allergen will be symptomatic or not.

Unfortunately, although CRD could potentially reduce the need for oral food challenges and contribute to tailored management plans, it’s not yet considered a routine diagnostic method and it’s not comprehensive; the most widely used tests neither contain all of the identified allergens (which are also not all of the possible allergens), nor are they universally available. Testing for certain specific wheat allergens would require special preparation and is therefore only likely to be done for research purposes.

Additionally, as it is with skin and standard blood tests, CRD is better at confirming an allergy than at eliminating the possibility of one. And, because sensitisation patterns differ according to geography and populations, with different allergens being more important in different regions and in people of different ages, allergists need to understand their patient populations so that they interpret the results of the tests correctly.

In the end, blood blood tests alone will probably never be good enough for a definitive diagnosis, as demonstrated by a study of 106 children who had undergone wheat challenges and were either proven to be tolerant or still allergic; it found that both groups of children had similar patterns of IgE antibodies reacting to the same proteins.

So, it should come as no surprise to learn that a positive skin or blood test does not mean that you are allergic to something. While skin prick tests and blood tests help with diagnosis, positive results only show sensitisation to specific allergens. Being sensitised to a food doesn’t mean that you’re allergic to it and that you will develop any symptoms.

A positive result simply means that your immune system is specifically aware of an allergen or allergens in that food. Why some people later develop an allergy to that food, and some do not, is not yet known.

Neither can the results of your blood or skin test predict how severe your reaction to eating some wheat might be; a large skin wheal or high level of IgE in your blood does not mean that you will have a serious allergic reaction if you accidentally eat a wheat-containing sausage.

The only way to know for sure whether you’re allergic to wheat (and to have some idea of how severe your reactions may be and how much wheat is needed to provoke them) is to undergo a challenge. When it comes to wheat allergy, there are several types of possible challenge.

Food challenge

For those with a ‘classic’ IgE-mediated food allergy, there is the oral food challenge (OFC). This involves eating a very small amount of wheat (often in the form of wheat flakes in porridge, or bread, or noodles) waiting for a reaction, and then doing it again, gradually increasing the dose until an objective—visible—reaction occurs or a maximum dosage is reached. It can take around 4 hours, depending on the type of challenge undertaken and the length of observation time needed.

You can read more about oral food challenges here.

Oral food challenges are generally undertaken either when someone’s history and their test results disagree (i.e. they have negative tests results but their history strongly suggests an allergy, or vice versa) or to check whether someone has outgrown their allergy to make sure that they don’t unnecessarily avoid wheat in their diet.

Practically speaking, most people do not undergo this kind of test since it requires a lot of time and resources. And oral challenges are rarely, if ever, offered to people whose history includes severe reactions to a suspected food. Whenever possible, allergy diagnoses are based on a combination of medical history and lab tests.

However, lab tests for wheat often cannot be used to definitively predict whether or not someone will react to wheat, and they cannot predict whether or not a person is likely to outgrow their allergy. You can also have high levels of IgE antibodies in your blood to wheat and still outgrow it.

And, unlike many other food allergies, both children and adults who develop a tolerance to wheat often still have positive skin tests and the level of IgE in their blood can remain quite high (although lower than when their allergy was diagnosed).

So, the oral food challenge is the only way to know whether or not you can tolerate wheat in your diet. (It should be noted than even an oral food challenge is not 100% accurate; in this Swiss study, for example, one child who passed their supervised food challenge had an allergic reaction the next day when trying spaghetti, but these types of cases are vanishingly rare.)

Although food challenges help to diagnose food allergies and identify a suspect food, there are other reasons to undergo food challenges, namely:

• to identify culprit foods in cases of allergies to multiple unknown foods
• to determine a patient’s threshold—how much wheat they can eat without reacting—so that dietary advice based on the outcome of the challenge can be given
• to confirm the development of tolerance to wheat

Because of the risk of severe reactions, oral food challenges should only be done by an experienced consultant in a medical setting.

That said, the benefits that result from a negative food challenge tend to outweigh the risks, and those risks can be reduced by always carrying out the procedure under medical supervision and in settings equipped to deal with serious reactions.

People who are suspected of being at high risk of reacting to wheat can also undergo a more cautious challenge procedure, starting with a very low dose of wheat, then incorporating that dose (if they can tolerate it) into their diet for a few months before trying a larger dose. Even though they may not be able to tolerate the maximum dose, most people seem to be able to tolerate a small dose, meaning that they can avoid having to avoid wheat altogether. Eating a small amount of wheat on a regular basis will probably also help them to outgrow their allergy quicker.

Provocation challenge

People with WDEIA undergo a more complicated type of challenge. The steps they will have to take depend on their history of reactions and what seems to provoke them. The provocation challenge to test for WDEIA is often done over a period of 3 to 5 days, depending on how many potential cofactors needed to be investigated. It normally includes a standard food and/or aspirin challenge and some form of exercise done together wheat, and/or aspirin, and/or alcohol. In some cases, just a large amount of gluten (often using high gluten-flour, which has a protein content of 70%–80% compared to the 8%–15% in wheat flour) is all that’s needed to confirm WDEIA.

The conditions needed to provoke a reaction can be difficult to come up with, let alone reproduce—like this case in which symptoms only appeared when the person ate some wheat, exercised, and then lay down in a cold environment—and, as such, many of the WDEIA challenges end up producing (false) negative results.

Due to the nature of the condition, challenges also come with a high risk inducing anaphylactic reactions, although these can be mitigated by taking careful precautions.

However, because of the risk and effort involved in challenges, some people are understandably unwilling to go through (or watch their child be put through) such a challenge, and doctors also prefer not to carry them out. So most diagnoses of WDEIA are based on a person’s medical history of reactions and accompanying skin and blood tests. Challenges are necessary, however, when a person’s history clearly indicates some kind of food-dependent exercise-induced anaphylaxis, but tests have come back with negative results.

As there is no one reliable skin or blood test to confirm or exclude a diagnosis of WDEIA, testing tends to look for several things, such as the presence of IgE antibodies to different allergens—as a person can have negative test results to whole wheat extract but positive results with a specific allergen—or the presence of a wheat allergen in a person’s blood after exercise. Sometimes a wheat elimination diet is used to confirm a diagnosis.

The sheer variety of potential factors involved, as well as the large individual differences between the amount of exercise needed to provoke symptoms—from housework to mountaineering—means that WDEIA is often very difficult to diagnose and it can take months or even years to get a diagnosis. In fact, when people are admitted to hospital for cases of anaphylaxis with unknown causes—so-called ‘idiopathic analysis’—some doctors recommend testing their blood for antibodies to the major wheat allergen omega-5 gliadin, on the off-chance that they are suffering from WDEIA.

Once a diagnosis has been made, however, people with WDEIA who follow either a gluten-free diet or avoid wheat in combination with exercise tend to see a dramatic cut in the number of allergic reactions they have, suffering, on average, around two thirds fewer. Some people don’t have any more at all.

Inhalation challenge

Another type of challenge that someone with wheat allergy may have to undergo is an inhalation challenge test for baker’s asthma.

To diagnose this respiratory condition, first a person’s medical history is taken and, if there is a consistent history of work-related asthma symptoms, the usual skin and blood tests can be carried out with cereal proteins or other bakery allergens. In order to see whether exposure to inhaled allergens at work has affected that person’s lung function, a basic test called spirometry is normally done. This test measures how much air you can exhale in one forced breath. Then, to properly diagnose baker’s asthma, an inhalation challenge has to be carried out.

The gold standard is the specific inhalation challenge (SIC) which, in its realistic form, is designed to mimic the workplace environment. It can either be carried out in the lab (the person goes into a sealed chamber and is then exposed to the suspected allergen), or it can be done in the workplace itself.

However, this version of the test takes around 8 hours and the lab version can only be done in a few specialised centres around the world. Additionally, it’s not definitive because false negatives results can happen when someone is challenged with the incorrect allergen.

Instead, other less resource- and time-intensive tests can be carried out, the most reliable of which is the bronchial challenge test (BCT), which is designed to measure the sensitivity of your lungs.

The BCT can be non-specific (NSBP) and involve breathing in the chemical methacholine or the sugar alcohol mannitol, both of which will irritate your airways and cause them to narrow, like an asthma trigger. Low doses should cause the airways of asthmatic people to narrow (constrict) but only high doses will cause the same reaction in people without asthma. A decrease in lung function can be measured by spirometry.

Or it can be specific and involve breathing in a fine spray of (commercial) aqueous flour solution in increasing concentrations or inhaling wheat flour dust (either a standard, commercial sample or wheat obtained from the workplace). The specific test is considered the gold standard for establishing a definitive diagnosis of baker’s asthma.

The specific inhalation challenge is risky because it—ideally—requires that the person stop taking their usual asthma medications and it can provoke life-threatening asthmatic reactions.

Although skin and blood tests are generally not reliable enough to confirm a diagnosis on their own, people who are highly sensitised to wheat allergens and have strong positive skin test and blood test results, together with obvious symptoms, will get a provisional diagnosis of baker’s asthma and can avoid taking a challenge test.

Another test that can be carried out is a nasal lavage, in which a sterile saline solution is squirted in the nostrils and the fluid is re-collected and tested for inflammatory mediators like histamine. It can be used together with the positive results of a bronchial challenge to diagnose baker’s asthma.

In practice, many diagnoses of baker’s asthma are made based on a consistent medical history of work-related symptoms together with clearly positive skin and blood test results. In future, component resolved diagnosis identifying IgE antibodies to specific wheat allergens may make challenges even less necessary and common.

Diagnosing non IgE-mediated and mixed reactions to wheat

Non IgE-mediated diseases are difficult to diagnose for several reasons, not least of which is the fact that IgE testing is often of no use. This makes the clinical history especially important for the diagnosis of these types of conditions. Even then, the symptoms are not easy to connect to the actual meals because of the time delay, and the symptoms associated with digestive allergies lack the skin and respiratory signs that doctors usually associate with allergy.

Skin tests

Eczemais diagnosed based on personal and family history of allergy and a skin examination.. While there are no standard diagnostic criteria, there are certain features that a doctor can look for to diagnose it.

That said, these criteria are based on the characteristics of paediatric eczema, which is not the same as the manifestation of eczema is adolescents or adults, making diagnosis of eczema in older age groups more challenging. Sometimes people with eczema in these age groups will have to undergo additional tests to rule out other diseases first and a skin biopsy may be needed before a diagnosis of eczema is made. However, these differences is now being taken into account and guidelines are being updated.

Once the diagnosis of eczema is made, efforts will first be made to try and get the skin condition under control using topical skin creams and drugs before any further testing is done. Generally, only if the skin is not getting any better will tests be carried out to see whether allergens, like food, could be aggravating the condition.

The identification of potential food allergens is generally done by looking for specific IgE antibodies to a food using skin prick tests or blood tests (the latter is often used if the skin condition is too bad for a skin test, or medications are being taken that will interfere with the results or if the tests involve a young infant).

In cases of delayed allergy, doctors may use the atopy patch test (APT). It generally involves walking around with food (either fresh or in solution) contained in tiny aluminium capsules taped to your back for up to 3 days and having your skin checked for a reaction after 48 hours and 72 hours.

Patch testing has been used to diagnose eczema, with some success, proving itself to be a good test for wheat-allergic infants, young children under 2 years old and older children, especially when used in combination with other types of tests, but even without the need for other tests.

The atopy patch test has also been used to try and diagnose delayed digestive allergies, with mixed results; in the case of food protein–induced enterocolitis syndrome (FPIES), for example, it has proven itself to be both ‘a promising diagnostic tool for the diagnosis of FPIES’ and ‘not helpful in identifying the [trigger] foods’, while showing ‘poor utility in the follow-up prediction of outgrowing FPIES in children’. With food protein-induced enteropathy (FPE), it has shown low sensitivity and with eosinophilic oesophagitis (EoE), it has shown that it can ‘identify potential causative foods’. For these diseases, it is not the diagnostic instrument of choice.

Contact allergies can be tricky to diagnose because they can look very similar. Some like contact urticaria are immediate type allergies, which can be diagnosed by prick testing, and some are delayed-type allergies, which can be diagnosed using patch testing. (1)

A skin application food test (SAFT) may be used instead for children under the age of 4. It’s basically the same thing, but the capsule of food is only applied to the skin for 10 to 30 minutes. It’s had mixed results, having been described as reliable and child-friendly and also as not being as good as the APT in diagnosing certain food allergies.

Skin tests

While skin tests may provide an indication of sensitisation, they cannot diagnose a food allergy; that has to be done with a food challenge during which the doctor can see whether or not, in addition to the immediate reactions, the suspected food also produces a worsening of the skin symptoms within the next 48 hours (often within a day). If it does, the food can then be eliminated from a person’s diet and their skin condition will be monitored for the next few months to see if there is a persistent improvement. When more than one food is suspected, the next challenge will be done a few weeks after the first one.

The diagnosis of delayed digestive allergies generally starts with exclusion; first other possible causes of the symptoms are eliminated and only then will the suspected food(s) be excluded from a patient’s diet—and, if they are breastfeeding, from their mother’s diet, too.

If the symptoms disappear, the first step towards a diagnosis involves reintroducing the foods one by one into the diet and seeing if the symptoms return. If the symptoms don’t disappear, it could be that the diet has not been restricted enough or that other foods should (also) be considered for elimination. Or it could be that something other than an allergy is responsible, in which case, the allergist’s job ends and another specialist’s begins.

The diagnosis of food protein-induced enteropathy (FPE) relies on seeing how a patient responds to an elimination diet and then performing an endoscopy and biopsy to check on the state of the small intestine. If the right food is eliminated, the symptoms should disappear and the tissue samples should look normal within 1 to 4 weeks.

The diagnosis can be confirmed by an oral food challenge, which essentially involves reintroducing the food into the diet 1 or 2 months after it was eliminated (which can be done at home if previous reactions have not been severe). If the food produces vomiting and diarrhoea within 1.5 to 3 days after being eaten, the diagnosis is confirmed and it can be taken out of the diet. Most children outgrow the condition by the time they’re 2, sometimes 3 years old.

The diagnosis of food protein induced enterocolitis syndrome (FPIES) mainly relies on a person’s clinical history and symptoms appearing when the offending food is reintroduced after an elimination diet.

In the case of chronic FPIES, an elimination diet should result in the symptoms going away within 3 to 19 days. Reintroducing the trigger food should produce the symptoms of acute FPIES—i.e. projectile vomiting—which should be enough confirmation.

In the case of acute FPIES, eating the offending food should be followed by symptoms that should fit specific diagnostic criteria including copious vomiting within 4 hours. Although confirmation of the diagnosis officially requires an oral food challenge, because it often produces nasty symptoms that the patient quite rightly has no wish to suffer through, in practice, this is rarely done and challenges for the diagnosis of chronic FPIES are more common.

However, since FPIES symptoms tend to be different for adults with acute FPIES and there are no strict diagnosis guidelines for them, oral food challenges are often necessary.

There are other reasons to undergo food challenges in cases of FPIES, including:

• identifying a culprit food in cases of allergies to multiple foods
• confirming the development of tolerance to a trigger food, which is often done between 12 to 18 months after the most recent reaction

Many clinics will only carry out a food challenge in an infant to see whether they have outgrown their allergy.

Although the majority of people with FPIES will have negative skin or blood tests to their trigger food, in some cases people do have an IgE sensitisation too. This is called ‘atypical FPIES’ and it affects between 1 in 4 and 1 in 8 people with FPIES. According to American research, the foods most commonly associated with this type of FPIES are egg, milk and peanut, but this may just be because those are the foods most typically eaten by American children (who make up the bulk of these studies). A person can have atypical FPIES to several foods, and those foods can include anything, from shrimp to avocado.

Some children with atypical FPIES may take longer to outgrow their condition (if, indeed, this happens at all) or may develop a classic IgE-mediated food allergy with potentially more dangerous symptoms. As such, periodic testing for an IgE sensitisation is advised in children who also have an IgE-mediated food allergy to other foods or suspected food-induced eczema.

When diagnosing eosinophilic oesophagitis (EoE),other conditions that produce similar symptoms, like gastroesophageal reflux disease (GERD), are first eliminated as a possibility before any intrusive testing is done. Then, if eosinophilic oesophagitis is still suspected, an upper GI endoscopy (aka an oesophagogastroduodenoscopy) and biopsies are carried out to look for specific levels of eosinophils in the oesophageal tissue (15 or more eosinophils per high-powered field, to be precise).

Standard elimination diets for cases of EoE are often based on the most common causes of the disease, either ‘2 food diets’ (dairy and wheat), ‘4 food diets’ (dairy, wheat, egg, and legumes) or ‘6 food diets’ (dairy, wheat, egg, legumes peanuts/tree nuts and fish/shellfish). These are called ‘empiric’ diets, i.e. diets that are based on observation and experience. The diet can be made less cumbersome by starting small, first with one food (i.e. milk) or two foods and then eliminating more foods if the symptoms don’t disappear.

The empiric diet approach is not the only approach. Sometimes the foods to be eliminated are determined using lab tests—atopy patch test and SPT and/or blood test—first (a targetted approach). Both methods work equally well for both children and adults although the targetted approach has the advantage of often requiring the elimination of fewer foods. That said, a lot of people with EoE don’t have any measurable IgE antibodies to their trigger food, so the targetted approach can only help some.

The diet normally takes about 6 weeks. If the symptoms go away and the tissue samples look good, the trigger is assumed to be one or more of the foods that was eliminated. In order to pinpoint the trigger(s), each food is reintroduced back into the diet one by one. If a reintroduced food causes symptoms to return and/or biopsy specimens to look abnormal, then it is identified as a trigger food and must be eliminated from the diet indefinitely. (In the real world, children may balk at undergoing so many intrusive tests or there may not be the capacity to perform them, in which case, they will probably not be required for a diagnosis.)

If eosinophilic gastritis (EG) is suspected, a similar type of procedure is carried out, but there are no standard guidelines on how to diagnose the condition and no consensus on where to look and how many eosinophils to look for. This is further complicated by the fact that, unlike the oesophagus, a healthy stomach and intestine generally have a detectable complement of eosinophils floating around and the endoscopies often produce normal results. Ultimately, doctors have to follow ‘a diagnosis of exclusion’; first they rule out more common causes of eosinophilia before settling on EG. Unfortunately, there is a very long list of other, more common, causes, including but in no way limited to parasitic infections, drug allergy, adrenal disorders, vasculitis, hypereosinophilic syndrome, Crohn’s disease, IBS and lupus.

Elimination diets are best performed under expert guidance, because there is a risk that excluding a food from your diet because you think that you may be allergic to it or because it causes mild or delayed symptoms can lead to you developing an IgE-mediated allergy to that food, often with severe—sometimes fatal—reactions.

The good news is that, when a delayed digestive allergy is diagnosed, excluding offending food(s) from the diet leads to the resolution of symptoms and the repair of the underlying tissue damage in most children and adults, and improves quality of life, even though the diet may be difficult to stick to. When it comes to young children, if staple foods are being eliminated, dietary guidance may be needed to ensure normal growth and development.

Image by Mae Mu on Unsplash

Image by Jakub Żerdzicki on Unsplash

Good to know

‘Ancient’ varieties of wheat are not less allergenic than modern varieties.

There’s a widespread belief that so-called ‘traditional’ or ‘ancient’ varieties of wheat, such as spelt, einkorn and Khorasan, are less allergenic than modern varieties. That’s a myth, fake news spread by influencers on TikTok who are probably in the pocket of Big Ancient Wheat. You can read more about that here.

People who are allergic to wheat often have other allergies.

Multiple studies have found that the wheat-allergic are often atopic—prone to developing allergies—and atopy often runs in the family (although this is less likely among children and adults with WDEIA).

For example, a Polish study reported that 78% of the wheat-allergic children in their study suffered from eczema, 48% from asthma and 34% from hay fever. 80% also had an allergy to milk, 72% to eggs, 50% to peanuts, 28% to fish, 26% to nuts and 24% to soy. All of them had a family history of atopy; 82% had two atopic parents and 62% also had atopic siblings.

A study of American children revealed that 87% had eczema, 67% had asthma and 60% had hay fever. 90% were allergic to at least one other of the other major food allergens; 70% to milk, 56% to egg, 50% to soy, 29% to peanut and 15% to tree nuts. Three quarters had a recorded family history of atopy.

An Iranian study of 24 wheat-allergic children reported asthma and eczema in half of the children.

A Finnish study of wheat-allergic children found that they were at risk of developing asthma and, later, an allergy to birch pollen and hay fever.

Allergies to other foods are also very common, with the foods involved varying according to local dietary habits. Studies of Thai children with wheat allergy have found that around half are likely to suffer from another food allergy, including egg (36%), milk (27%), seafood (16%), soy 9% and peanuts 9%. A Danish study of 15 wheat-allergic children, most with eczema, reported allergies to rye, egg, milk, cashew, pistachio, hazelnut, poppy, peanut and melon.

Other food allergies are also common among adults with wheat allergy according to a study of Danish and Italian adults that reported that most of their subjects had adult-onset food allergies which included tomatoes, peach, hazelnut, chestnut, other cereals, grape, apple, melon, cherry, carrot, fennel and soy.

Atopy is also common among people with non-IgE-mediated wheat allergy. A Swiss study found that just over two thirds (68%) of their adult eosinophilic oesophagitis patients had other allergic diseases including hay fever, asthma and eczema. Up to 84% of them were sensitised to aeroallergens, food allergens or both.

Other allergies can masquerade as wheat allergy.

Oral mite anaphylaxis (OMA) aka ‘pancake syndrome’ is an allergic reaction that is provoked by eating flour-containing products contaminated with heat resistant dust or storage mites that remain allergenic during short cooking times. It was first reported after someone had a reaction to eating pancakes, hence the name. Cases have also been reported after eating other foods including beignets, pizza, polenta, battered fish, scones and grits.

OMA can—on very rare occasions—be fatal, as it was in the case of 56-year-old woman who died after eating a huge amount of mites in a pap made with milk and wheat flour.

Because the reactions often come after eating something made with wheat flour, OMA is often confused with wheat allergy. It also has the same kind of symptoms as wheat allergy, including exercise-induced anaphylaxis (EIA), in which a person only shows symptoms after exercise, like the case of a 29-year-old Thai woman who had EIA after eating some cake she made using mite-infested cooking flour, but otherwise tolerated the contaminated flour as long as she didn’t exercise.

A recent review highlights the fact that OMA is a potentially dangerous condition which affects both adults and children, presents many of the same symptoms as wheat allergy including EIA and acute asthma, can be worsened by cofactors like aspirin, and can also affect people eating oat and corn flour.

Things that are added to flour on purpose also cause allergic reactions, particularly in people who work with bread. The most problematic additives are enzymes. These are widely used in the baking industry to speed up the bread-making process by digesting starch and providing the yeast with sugar. They are also used to break down cell walls and weaken the gluten network when dough is too strong and are often added during the processing of fermented dough products.

The most widely used enzyme, alpha-amylase has been identified in a number of studies as a cause of bakers’ asthma, and allergic reactions to other enzymes such as cellulase, xylanase, beta-xylosidase and glucoamylase have also been reported.

These enzymes can also cause non-asthmatic eosinophilic bronchitis (an inflammation of the respiratory tract which manifests as a chronic cough) and provoke skin reactions including dermatitis, hives and delayed eczema.

You can develop different types of allergy to wheat, either at the same time or one after the other.

Sometimes two conditions can co-exist, as in the case of coeliac disease and wheat allergy. Cases of people with both the autoimmune condition and a concurrent allergy used to be vanishingly rare but, in the past decade, more cases have been reported of people suffering from both coeliac disease and wheat allergy at the same time. Cases have ranged in age from infants to the middle-aged and symptoms have ranged from hives, oral allergy syndrome, breathing problems and vomiting, to swelling, GI symptoms, weight loss and eczema, to several cases of anaphylaxis.

Because the symptoms of coeliac disease and wheat allergy are so similar, one condition can mask the other and lead to a delayed diagnosis.

No-one knows why these two conditions seem to co-exist so often in one person, but it’s possible that gluten-free diets are contributing to the growing problem. Diets that exclude certain foods have been shown to lead to a loss of tolerance to those foods in people who are sensitised to them but not showing symptoms. When a person eats a food again, they can have quite serious reactions to it.

In the case of people with coeliac disease, the accidental or occasional consumption of wheat-containing food after a long period of time without eating it may induce sensitisation to wheat allergens. Alternatively, trace amounts of cereals in the gluten-free food can induce sensitisation to wheat.

This tendency for exclusion diets to provoke new allergies means that the treatment of one condition can sometimes trigger a new one. This was the case for a 16-year-old boy who, having been diagnosed with coeliac disease at the age of 9 and put on a gluten-free diet, accidentally ate ice cream containing wheat while out for lunch in a restaurant and had a fatal anaphylactic attack.

The elimination of wheat in the diet of children with coeliac disease has also been shown to create new cases of FPIES. A study looking at adults with coeliac disease found that those who regularly ate oats were less likely to vomit or feel nauseous after being exposed to gluten, so that may help to increase tolerance to small amounts of gluten.

Sometimes you can outgrow one condition and develop a new one. For example, some children can outgrow their IgE-mediated allergy to wheat only to develop eosinophilic oesophagitis to the same food a couple of years later. And sometimes you can have both of those conditions at the same time.

You can develop an allergy to wheat after an organ transplant.

Although it can happen after different types of transplant, the liver is by far the organ most likely to come with a new food allergy. And, although it can happen to both adults and children, when it comes to acquiring a new wheat allergy after a liver transplant, case reports currently only describe it happening to young children. Wheat is the 6^th most common liver transplant-acquired food allergy (LTAFA) according to one large review.

Symptoms of liver transplant-acquired food allergies (LTAFA) generally appear within 18 months of the operation and typically involve the skin; facial swelling (angio-oedema) and hives (urticaria) occur in around 4 to 5 in 10 people. Gastrointestinal manifestations (diarrhoea, vomiting, stomach pain) also affect around half of people with LTAFA, while respiratory symptoms affect about 1 in 10. Anaphylaxis affects around 16 in 100 children with LTAFA, but no fatal cases have been reported so far. Although the majority (around 4 in 5) of the new food allergies are IgE-mediated, some people also get mixed or non-IgE-mediated allergies like Eosinophilic Gastrointestinal Disorders (EGIDs).

Children are much more likely to develop an allergy after a liver transplant than adults; in fact, there are case reports describing children and adults getting a liver from the same donor and the child developing a food allergy while the adult does not. Why this is so is not known; it could be something about the liver itself, or the fact that the child needs a liver transplant in the first place, or it could be because a child’s immune system is too immature to be able to suppress the expression of newly acquired food allergies.

Unfortunately, once you develop this type of allergy, you’re likely to keep it, with only about 1 in 4 people becoming tolerant to their food trigger(s). That said, the prognosis for outgrowing an allergy to wheat may be better than it is to most other foods; one study reported that children were most likely to outgrow a transplant-induced allergy to wheat and milk, with two thirds acquiring a tolerance to those triggers within 3 years.

Although the liver is far more likely to cause a new food allergy in paediatric transplant patients than any other organ, other types of transplant can also induce a new allergy to wheat, such as this case reported after a bone marrow transplant.

Delaying your child’s exposure to wheat may increase their risk of developing an allergy to wheat. Or it may not.

Some research has found that a later introduction to wheat is linked to a greater risk of developing wheat allergy. The most quoted study on this subject was carried out in 2006 by a team of American researchers who examined the data of a group of 1612 children whose parents regularly answered questions about their children’s diet and allergic status until around the age of 5. They found that children who were introduced to wheat after the age of 6 months were 4 times more likely to develop an allergy to wheat than children who’d had wheat introduced into their diets earlier.
.

Their finding influenced the subsequent statement made by the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) in 2008, which recommended avoiding both the early (less than 4 months) and the late (7 or more months) introduction of gluten into an infant’s diet.

2 years later, a team of Finnish researchers produced results that supported the recommendation, finding that sensitisation to wheat was linked to the late (after 6 months) introduction of wheat in a child’s diet. So did another study carried out more recently in Thailand. The early introduction of gluten in the diet has also been shown to lower the risk of getting coeliac disease.

But other research disagrees. A 2017 review of 7 studies found that the evidence was mixed, with some studies supporting the idea of early introduction and some not. The authors concluded that the ‘Early introduction of gluten might reduce the risk of sensitisation, but currently, no evidence exists that it affects the risk of wheat allergy.’

It may be that early introduction only benefits children with a parental history of asthma or allergy.

Breastfeeding has also been studied as a potential protective factor against developing wheat allergy. In fact, scientists have been examining the benefits of breastfeeding on the development of allergies since the 1930s and many studies have concluded that breastfeeding seems to protect infants from developing allergies, and the protective effect may be stronger in children with a familial history of atopy.

Some research has found that breastfeeding during the introduction of complementary foods is important for promoting tolerance to those foods. Some has not.

What’s more, according to some of the research that found a benefit to introducing wheat early into an infant’s diet, a longer period of breastfeeding may actually be associated with a higher risk of getting the allergy (an idea hotly disputed by a doctor in the comments section below the American paper’s summary).

A meta-analysis of meta-analyses published in 2016 found no evidence of an association between breastfeeding and protection against food allergies.

Current guidelines from the various official bodies are slightly different, but all recommend introducing wheat between the age of 4 months and 6 months and before the age of 1.

After it’s been introduced, it’s important to include it in the diet regularly, at least once a week, preferably more often. Research carried out to date on other allergenic foods like peanut and egg suggest that introducing a food less regularly than that may actually promote the development of food allergy. If you can’t make sure your infant eats wheat on a regular basis, it may be better to avoid introducing it until a later age, although more research needs to be done on this matter.

In the meantime, you might want to consider getting a cat which, according to this study, may reduce the risk of a child developing an allergy to wheat if they are exposed in utero (while the mother is pregnant) or during early infancy.

Image by Super Tseng on Unsplash