Antibodies to α-gliadin have been significantly increased in non-celiacs individuals with oral ulceration. Anti-α-gliadin antibodies are frequently found in celiac disease (CD), to a lesser degree CD, but are also found in a subset who do not have the disease. Of people with pseudo-exfoliation syndrome, 25% showed increased levels of anti-gliadin IgA. Other patients that are also at risk are those taking gluten despite having the disorder, or whose family members with CD. In addition patients with autoimmune conditions are also at risk for CD. It has just been found that there is a risk of death in CD. Therefore gluten intake should be limited before or even after the diagnosis. One fourth of people with Sjögren's syndrome had responses to gluten, of 5 that had positive response to gluten, only one could be confirmed as CD and another was potentially , the remaining 3 appear to be gluten-sensitive. All were HLA-DQ2 and/or DQ8-positive.

In the United States, fewer cases of CD have been found compared to other countries. The incidence of celiac disease and of wheat allergy is estimated each to lie at around 1% of the population. There has been a 6.4 increase in the case reports of celiac disease between 1990 and 2009. The incidence of NCGS is unknown; some estimates range from 0.6% to 6%, and a systematic review of 2015 reported on studies with NCGS prevalence rates between 0.5% and 13%.

In Europe, the average consumption of gluten is 10g to 20g per day, with parts of the population reaching 50g or more per day.

Approximately one third of presumed NGCS patients continue to have symptoms, despite gluten withdrawal. Apart from a possible diagnostic error, there are multiple possible explanations.

One reason is poor compliance with gluten withdrawal, whether voluntary and/or involuntary. There may be ingestion of gluten, in the form of cross contamination or food containing hidden sources. In some cases, the amelioration of gastrointestinal symptoms with a gluten-free diet is only partial, and these patients could significantly improve with the addition of a low-FODMAPs diet.

A subgroup may not improve when eating commercially available gluten-free products, as these can be rich in preservatives and additives such as sulfites, glutamates, nitrates and benzoates, which can also have a role in triggering functional gastrointestinal symptoms. Furthermore, people with NCGS may often present with IgE-mediated allergies to one or more foods. It has been estimated that around 35% suffer other food intolerances, mainly lactose intolerance.

There are various theories as to what determines whether a genetically susceptible individual will go on to develop coeliac disease. Major theories include surgery, pregnancy, infection and emotional stress.

The eating of gluten early in a baby's life does not appear to increase the risk of CD but later introduction after 6 months may increase it. There is uncertainty whether breastfeeding reduces risk. Prolonging breastfeeding until the introduction of gluten-containing grains into the diet appears to be associated with a 50% reduced risk of developing coeliac disease in infancy; whether this persists into adulthood is not clear. These factors may just influence the timing of onset.

Other cereals such as corn, millet, sorghum, teff, rice, and wild rice are safe for people with coeliac to consume, as well as noncereals such as amaranth, quinoa, and buckwheat. Noncereal carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms.

FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) that are present in gluten-containing grains have recently been identified as a possible cause of gastrointestinal symptoms in people with NCGS, in place of, or in addition to, gluten. FODMAPs cause mild wheat intolerance mainly limited to gastrointestinal symptoms.

There is a great deal of conflicting information regarding the inclusion of oats in a gluten-free diet. Although cross-contamination in the field and during processing partially explains the different reactions that celiacs can have to oats, a recent study indicates that there are also different amounts of avenin present in different cultivars of oat. The G12 antibody used in the study is currently the only one that can reliably distinguish between varieties of oat. Previous studies have indicated both children and adult coeliacs are largely tolerant of oats. Other studies have followed both children and adults for one, two, and five years on the "uncontaminated" oat containing gluten-free diet. These studies failed to show significant changes in intestinal morphology indicative of a relapse of celiac disease. Anti-gliadin and reticulin antibodies as well as numbers of intraepithelial lymphocytes (IELs) did not differ significantly between oat-eating celiacs and non-oat-eating controls in remission. Invitro tests that are sensitive to wheat gluten found that tryptic peptides of avenin could not induce EMA production in supernatant fluid from cultured duodenal mucosa specimen from celiac patients.

Algorithms that successfully predict T cell stimulatory peptides in gluten identified many similar peptides in hordeins and secalins, but not in oat avenins.

The Canadian Celiac Association suggests that adults can consume up to 70g of oats per day, and children up to 25g. However, two studies indicated that celiac adults could consume 93 grams (3.3 ounces) of oats per day. There is no evidence that oats can trigger GSE, only that in a small number of celiacs disease can be sustained or reinitiated by oats once triggered by wheat. A recent paper examining the IEL levels of celiac patients in remission showed a significantly higher number of IELs in oat-eating celiacs. In addition, antibodies to avenin remain low as long as the diet is gluten-free, but higher anti-avenin antibodies can increase with a diet containing wheat.

Some coeliacs respond adversely to oats. Estimates range from 0.5 to 20% of the GSE population. With coeliac disease, non-compliance in attempting to achieve normal intestinal morphology is a risk factor for refractory disease and cancer.

Gluten-sensitive enteropathy and its common and more severe form, coeliac disease, results in the increased inflammation of the tissues of the small bowel, eventually leading to villus atrophy. The disease progresses from increased lymphocyte counts to eventual flattening of the villi, and crypt hyperplasia. Originally, oats were believed to cause coeliac disease. However, this confusion was largely due to significant contamination of oats with wheat, barley, or rye. A recent review of controlled oat tolerance studies indicated only one documented avenin-sensitive enteropathy (ASE) in 165, placing the risk of ASE at 0.6% of the coeliac disease population. However, during the controlled studies, 17 candidates dropped out due to symptoms after ingestion of gluten-free oats and were not tested at the completion of their respective studies. As a result, the actual risk of ASE in the coelic disease population may be slightly higher.

There appears to be an association of autoimmune rheumatoid arthritis (ARA) both with GSE and gluten allergies. ARA in GSE/CD may be secondary to tTG autoimmunity. In a recent study in Turkey, 8 of 20 ARA patients had wheat reactivities on the RAST tests. When this allergic food and all other patient specific RAST+ foods were removed half of the patients had improved ARA by serological markers. In patients with wheat allergies, rye was effectively substituted. This may indicate that some proportion of RA in GSE/CD is due to downstream effects of allergic responses. In addition, cross-reactive anti-beef-collagen antibodies (IgG) may explain some "rheumatoid arthritis" (RA) incidences.

Contact sensitivity, atopic dermatitis, eczema, and urticaria appear to be related phenomena, the cause of which is generally believed to be the hydrophobic prolamin components of certain Triticeae, Aveneae cultivars. In wheat one of these proteins is ω-gliadin (Gli-B1 gene product). A study of mothers and infants on an allergen-free diet demonstrated that these conditions can be avoided if wheat sensitive cohort in the population avoid wheat in the first year of life. As with exercise induced anaphylaxis aspirin (also: tartrazine, sodium benzoate, sodium glutamate (MSG), sodium metabisulfite, tyramine) may be sensitizing factors for reactivity. Studies of the wheat-dependent exercise induced anaphylaxis demonstrate that atopy and EIA can be triggered from the ingestion of that aspirin and probably NSAIDs allow the entry of wheat proteins into the blood, where IgE reacts within allergens in the dermal tissues. Some individuals may be so sensitive that low dose aspirin therapy can increase risk for both atopy and WDEIA.

Wheat allergies were also common with contact dermatitis. A primary cause was the donning agent used for latex gloves prior to the 1990s, however most gloves now use protein free starch as donning agents.

GSE can result in high risk pregnancies and infertility. Some infertile women have GSE and iron deficiency anemia others have zinc deficiency and birth defects may be attributed to folic acid deficiencies.

It has also been found to be a rare cause of amenorrhea.

The prognosis of children diagnosed with intolerance to milk is good: patients respond to diet which excludes cow's milk protein and the majority of patients succeed in forming tolerance. Children with non-IgE-mediated cows milk intolerance have a good prognosis, whereas children with IgE-mediated cows milk allergy in early childhood have a significantly increased risk for persistent allergy, development of other food allergies, asthma and rhinoconjunctivitis.

A study has demonstrated that identifying and appropriately addressing food sensitivity in IBS patients not previously responding to standard therapy results in a sustained clinical improvement and increased overall well being and quality of life.

Fibromyalgia was found in 9% of adult patients relative to 0.03% in the general population with a link common to IBD. Concurrent IBS is found in 30% to 70%. Small intestinal bacterial overgrowth is associated is common with a transient response to antimicrobial therapy.

Food intolerance are all other adverse reactions to food. Subgroups include enzymatic (e.g. lactose intolerance due to lactase deficiency), pharmacological (e.g. reactions against biogenic amines, histamine intolerance), and undefined food intolerance (e.g. against some food additives).

Food intolerances can be caused by enzymatic defects in the digestive system, can also result from pharmacological effects of vasoactive amines present in foods (e.g. Histamine), among other metabolic, pharmacological and digestive abnormalities.

Allergies and intolerances to a food group may coexist with separate pathologies; for example, cow's milk allergy (CMA) and lactose intolerance are two distinct pathologies.

The most common food allergens account for about 90% of all allergic reactions; in adults they include shellfish, peanuts, tree nuts, fish, and egg. In children, they include milk, eggs, peanuts, and tree nuts. Six to 8% of children under the age of three have food allergies and nearly 4% of adults have food allergies.

For reasons not entirely understood, the diagnosis of food allergies has apparently become more common in Western nations recently. In the United States, food allergy affects as many as 5% of infants less than three years of age and 3% to 4% of adults. A similar prevalence is found in Canada.

About 75% of children who have allergies to milk protein are able to tolerate baked-in milk products, i.e., muffins, cookies, cake, and hydrolyzed formulas.

About 50% of children with allergies to milk, egg, soy, peanuts, tree nuts, and wheat will outgrow their allergy by the age of 6. Those who are still allergic by the age of 12 or so have less than an 8% chance of outgrowing the allergy.

Peanut and tree nut allergies are less likely to be outgrown, although evidence now shows that about 20% of those with peanut allergies and 9% of those with tree nut allergies will outgrow them.

In Japan, allergy to buckwheat flour, used for soba noodles, is more common than peanuts, tree nuts or foods made from soy beans.

Corn allergy may also be prevalent in many populations, although it may be difficult to recognize in areas such as the United States and Canada where corn derivatives are common in the food supply.

Food allergies develop more easily in people with the atopic syndrome, a very common combination of diseases: allergic rhinitis and conjunctivitis, eczema, and asthma. The syndrome has a strong inherited component; a family history of allergic diseases can be indicative of the atopic syndrome.

A 2008 literature review concluded that, "From the evidence-based perspective, there is conflicting evidence whether there is or is not an association between coeliac disease or auto-antibodies and epilepsy. As yet there is no compelling evidence that there is a causal relation. There probably is a specific syndrome—coeliac disease with epilepsy and calcifications—which is rare and perhaps geographically specific."

While the causes of IBS are still unknown, it is believed that the entire gut–brain axis is affected.

The risk of developing IBS increases six-fold after acute gastrointestinal infection. Postinfection, further risk factors are young age, prolonged fever, anxiety, and depression. Psychological factors, such as depression or anxiety, have not been shown to cause or influence the onset of IBS, but may play a role in the persistence and perceived severity of symptoms. Nevertheless, they may worsen IBS symptoms and the patient quality of life. Antibiotic use also appears to increase the risk of developing IBS. Research has found that genetic defects in innate immunity and epithelial homeostasis increase the risk of developing both post-infectious as well as other forms of IBS.

Approximately 10 percent of IBS cases are triggered by an acute gastroenteritis infection. Genetic defects relating to the innate immune system and epithelial barrier as well as high stress and anxiety levels appear to increase the risk of developing post-infectious IBS. Post-infectious IBS usually manifests itself as the diarrhea-predominant subtype. Evidence has demonstrated that the release of high levels of proinflammatory cytokines during acute enteric infection causes increased gut permeability leading to translocation of the commensal bacteria across the epithelial barrier resulting in significant damage to local tissues, which can result in chronic gut abnormalities in sensitive individuals. However, increased gut permeability is strongly associated with IBS regardless of whether IBS was initiated by an infection or not. A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the aetiology of post-infectious IBS.

Treatment is primarily through diet. Dietary fiber and fat can be increased and fluid intake, especially fruit juice intake, decreased. With these considerations, the patient should consume a normal balanced diet to avoid malnutrition or growth restriction. Medications such as loperamide should not be used. Studies have shown that certain probiotic preparations such as "Lactobacillus rhamnosus" (a bacterium) and "Saccharomyces boulardii" (a yeast) may be effective at reducing symptoms.