Adverse Food Reactions (click to enlarge the image).
Up to 20% of people develop gastrointestinal (GI) symptoms following a meal. Millions of people have chronic symptoms labeled as functional gastrointestinal pain or irritable bowel syndrome (IBS), with no clearly identifiable cause.
The gut–brain axis theory is an attempt to explain IBS symptoms. Overly sensitive nerves in the GI tract react to normal functions, such as stretching and motility, that now feel painful. During periods of stress (e.g., anxiety or GI infection), symptoms may flare up.
Mast cells and mediators (neurotropic substances) may be involved in visceral hypersensitivity.
A new hypothesis is that GI mast cells stimulated by food-induced local IgE may be the cause of IBS symptoms. It is possible that a GI bacterial infection can break tolerance to a food antigen. The immune response toward that antigen can lead to increased GI permeability and pain when exposure to the antigen happens again.
In a study of 12 patients with IBS there was no evidence of systemic IgE against common foods. However, when the same common allergens were injected into the rectal mucosa, every patient with IBS had a localized reaction to at least one of the antigens.
This test is not applicable to real-life patients yet. No one will be injecting antigens into the rectal mucosa in an allergy clinic near you anytime soon. Examination of mast cells in GI biopsy specimens is not routinely performed.
Prolonged and high doses of a histamine H1 receptor antagonist (antihistamines) may reduce visceral hypersensitivity, symptoms, and abdominal pain in patients with IBS.
This recent NEJM commentary (see references below) attempts to expand the term “food allergy” beyond only systemic IgE-mediated reactions. Adverse food reaction is the more appropriate term in my opinion. Adverse food reactions can be IgE-mediated, cell mediated, mixed, not mediated by the immune system, etc. This gastrointestinal tissue–IgE-specific allergic response, if mast cell mediated, is more accurately described as a mixed IgE-/cell-mediated reaction. Eosinophilic esophagitis (EoE) may be in the same category.
The ovalbumin-specific IgE antibodies identified by Aguilera-Lizarraga et al. were detectable only in colonic tissue. This is very similar to the previously described “local allergic rhinitis”: local application of the allergen induces local sIgE and mediators.
It is too soon to jump to the conclusion that IBS is a food-induced “allergic” disorder. It may still be food induced as many patients will verify. However, the application of the term “food allergy” to IBS in this case may not be helpful, especially for the same patients that need nothing more than a relief of the GI symptoms that may severely affect their quality of life. A follow-up with a gastroenterologist is recommended for patients with IBS.