What happens when somebody is allergic to mustard?
The immune system has an extraordinarily difficult job.
Every day it encounters huge numbers of substances and has to distinguish genuine threats — such as some viruses, bacteria and parasites — from the harmless material that surrounds us and passes through us.
Food presents a particularly interesting challenge. We deliberately introduce foreign material into our bodies several times a day, yet the immune system normally learns to tolerate it.
In a food allergy, that tolerance has gone wrong.
With a typical IgE-mediated mustard allergy, the immune system identifies particular mustard proteins as though they represent a threat.
IgE stands for immunoglobulin E, a type of antibody.
The easiest way to understand an antibody is to imagine a highly specialised recognition molecule. Different antibodies can recognise particular molecular shapes. In an allergic person, IgE antibodies have been produced that recognise particular structures on an otherwise harmless allergen.
Those IgE antibodies can sit on the surface of immune cells including mast cells and basophils.
Think of these cells as containing packets of powerful chemical messengers, with allergen-specific IgE acting rather like sensors on their surface.
When the relevant mustard proteins arrive and connect with those IgE antibodies in the right way, the cells can rapidly release chemicals including histamine.
And histamine is not merely the substance that gives somebody a runny nose during hay fever.
It can contribute to blood vessels widening and becoming leaky, skin becoming red, swollen and itchy, the airways narrowing, the gut reacting and blood pressure changing. Other inflammatory chemicals are released as well.
This is why an allergic reaction can seemingly involve completely unrelated parts of the body at the same time. Hives on the skin, swelling around the lips, vomiting and difficulty breathing may look like four separate problems. They can actually be different consequences of the same immune alarm.
In a severe systemic reaction — anaphylaxis — the effects can involve the airway, breathing and/or circulation and become life-threatening.
The mustard itself has not poisoned the person.
The immune response to it is causing the danger.
Your immune system reads shapes, not food labels
Imagine you have a key cut for one lock.
Now imagine encountering another lock made by a different manufacturer whose internal shape happens to be sufficiently similar that the same key can interact with it.
Something conceptually similar can happen in allergy.
An IgE antibody that recognises part of a protein from one source may sometimes also recognise a sufficiently similar protein from another source. The foods do not have to look alike, taste alike or even be things that an ordinary person would ever associate with one another.
What matters is molecular similarity.
This helps explain why allergy specialists are interested not simply in which foods somebody reacts to, but sometimes in which proteins within those foods their immune system recognises.
And mustard provides an excellent example.
Sin a 3 belongs to the non-specific lipid transfer protein, or nsLTP, family. Related LTP allergens occur in many plant foods. Research has demonstrated IgE cross-reactivity involving mustard Sin a 3 and peach LTP.
Sin a 4 is a profilin. Profilins are proteins found throughout the plant world and are involved in the internal machinery of plant cells. Because similar profilins occur in pollens and numerous plant foods, sensitisation to profilin can help create seemingly strange patterns of pollen and food reactions.
This does not mean that somebody with mustard allergy should automatically stop eating peaches, melon, broccoli, cabbage or every related plant.
That would be precisely the wrong conclusion.
A laboratory finding of sensitisation — evidence that someone's IgE recognises something — is not automatically the same thing as a clinical allergy, where eating the food actually produces symptoms.
That distinction is so important that it deserves a section of its own.
Sensitised is not the same as allergic
An allergy test can be enormously useful, but it does not operate like a simple yes/no detector.
A skin-prick test or blood test for specific IgE can provide evidence that the immune system has become sensitised to an allergen.
But sensitisation and clinical allergy are not identical.
A person can have detectable specific IgE and yet eat the food without symptoms.
This is not merely theoretical. In an early prospective mustard study involving people already sensitised to mustard, only a proportion reacted when challenged with a normal quantity under controlled conditions. The researchers found that positive skin tests and mustard-specific IgE alone did not reliably predict who would actually react.
That is why allergy diagnosis begins with something decidedly less technological than a blood test:
the story of what actually happened.
What was eaten? How much? How quickly did symptoms begin? What were the symptoms? Has it happened more than once? Can the food normally be eaten without a problem? Was exercise involved? Were there other possible ingredients? What do appropriately interpreted tests show?
Sometimes, where the specialist considers it appropriate and safe, a supervised oral food challenge can be used to answer a question that testing alone cannot settle.
During a food challenge, carefully controlled amounts of the suspected food are given under medical supervision while the patient is observed for symptoms. Depending on the circumstances, this can help establish whether somebody is genuinely allergic or can actually tolerate the food.
It is emphatically not something to reproduce at home if a significant food allergy is suspected.
This distinction between sensitisation and actual clinical allergy becomes especially important with mustard because of its botanical relatives and its connections with pollen allergies.
And one of those connections has a wonderfully peculiar name:
mugwort–mustard allergy syndrome.