Most people with a peanut allergy know it can be serious. Fewer understand why. That gap — between knowing a fact and understanding what is behind it matters. When you understand the mechanism, you ask better questions, you make better decisions, and you can explain your condition more clearly to the people who need to hear it.
This is the first in a three-part series on allergen biology. No science background needed. By the end of it, you will understand not just what food allergies are, but how they work, and why that changes the way you think about eating out.
A defence system that makes a mistake
Your body has a defence system — the immune system — whose job is to spot and destroy harmful invaders. Bacteria, viruses, parasites: the immune system detects these threats and mounts a targeted response. Most of the time, it does this without you noticing.
Food allergy is what happens when that system gets it wrong. It identifies a harmless food protein as a threat and launches a full defensive response against it.
If you have a peanut allergy, your immune system treats proteins found in peanuts as dangerous. The first time this happened — the sensitisation phase — your immune system produced a specific type of antibody called IgE (immunoglobulin E), shaped to recognise those peanut proteins. If you did biology at school, you may remember that antibodies are Y-shaped proteins made by white blood cells, each designed to lock onto a specific target. IgE works the same way, but it is aimed at the wrong target: a food protein that poses no real threat.
This IgE then attaches to specialised immune cells called mast cells, found in tissues throughout your body — in the gut lining, the airways, the skin, and around blood vessels. Your mast cells are now armed and waiting. You may have had no idea anything happened.
The trigger
When you eat peanut again, the peanut proteins bind to the IgE already sitting on the surface of your mast cells. This binding — called cross-linking — is the trigger. Mast cells line the gastrointestinal tract and are the main cells involved in IgE-mediated allergic reactions to food. When the allergen cross-links IgE on their surface, they release chemicals that set off a rapid response across multiple parts of the body at once [1].
Those chemicals include histamine, which makes blood vessels widen and leak fluid into surrounding tissues, and substances that tighten the airways. This happens fast and it happens everywhere. The result is anaphylaxis: a severe, whole-body reaction that can go from first symptom to life-threatening collapse within minutes [2]. It is not the peanut causing harm directly. It is your immune system's own disproportionate response to it.
The only effective treatment is an injection of adrenaline (epinephrine), given straight away. Antihistamines on their own are not enough to reverse anaphylaxis.
It can come back
Something that catches many people off guard is that anaphylaxis can have a second wave hours after the first. You might have been treated with adrenaline and feel fine, then deteriorate again. This is called a biphasic reaction, and it has been documented in between 1% and 20% of anaphylaxis cases in the clinical literature [3].
This is why anyone who has had anaphylaxis needs to be monitored afterwards, even when the first response to treatment looks good. "I felt better" is not the same as "I am safe."
How common is this?
In the UK, roughly 6% of adults — around 2.4 million people — live with a clinically confirmed food allergy. More than 30% report some form of adverse reaction to a particular food [4]. That larger group includes people with intolerances and sensitivities, which we cover in Part 2. But the 6% with confirmed IgE-mediated allergies are the people for whom accurate allergen information is a genuine safety matter.
Why this matters when you eat out
Once you understand the mechanism, you understand why verbal allergen information at a restaurant is not good enough.
Your mast cells do not respond to good intentions. They do not care whether the kitchen was briefed before service, whether the server usually remembers, or whether an ingredient changed last Tuesday and nobody updated the allergen record. They respond to protein. If the protein is present, the cascade begins.
Verbal information passes through too many steps where accuracy can be lost. A server mishears. A temporary staff member was not fully briefed. A supplier changed an ingredient. A dish was updated on the specials board but not in the allergen record. Every one of those is a point where something can go wrong.
Written allergen information — specific, current, built into the menu, available to you before you order — removes the relay. You get the information directly from the source. That is not just a nice-to-have. The biology of how anaphylaxis works is the reason you need it.
When you are deciding where to eat, look for restaurants that put their allergen information in writing, on their website, before you even walk in. When you are at the table, ask specific questions about specific dishes. And when the answer is vague or uncertain, trust that feeling. You know more about what your body needs than the server does.
Coming in Part 2: the difference between IgE and IgG — two antibodies that are often confused, and why understanding the distinction matters for how you think about your own diagnosis.
References
Oettgen HC. Mast cells in food allergy: inducing immediate reactions and shaping long-term immunity. J Allergy Clin Immunol. 2023;151(1):21–25. DOI: 10.1016/j.jaci.2022.10.003
Reber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol. 2017;140(2):335–348. DOI: 10.1016/j.jaci.2017.06.003
Lieberman P. Biphasic anaphylactic reactions. Ann Allergy Asthma Immunol. 2005;95(3):217–226. DOI: 10.1016/S1081-1206(10)61217-3
University of Manchester, Manchester University NHS Foundation Trust, University of Southampton, Amsterdam University Medical Centre, Isle of Wight NHS Trust. Patterns and Prevalence of Adult Food Allergy (PAFA). London: UK Food Standards Agency; 2024. DOI: 10.46756/sci.fsa.ehu454
