Allergies and Intolerances

TL;DR. An allergy is an immune reaction that can kill from a trace; an intolerance is a digestive or pharmacological problem that is unpleasant and dose-dependent. Conflating them is the source of most of the confusion in this area, and it has consequences in both directions: people with genuine anaphylaxis are taken less seriously, and people avoid foods they do not need to. The advice on preventing food allergy reversed completely after 2015: introducing peanut early in infancy reduces allergy by around 80 percent, where avoidance was previously recommended. And adrenaline, given early into the outer thigh, is the only treatment for anaphylaxis.

1. The distinction that matters

Prevalence: genuine food allergy affects roughly 2 to 4 percent of adults and 5 to 8 percent of children in Western countries. Self-reported food allergy is around 20 percent, so most self-diagnosis is wrong, and much of it is intolerance.

2. Food allergy

The main allergens, which are legally required to be declared in the EU and UK (the "big 14") and the US (the "big 9"):

Oral allergy syndrome (pollen-food syndrome) is a distinct and far more common thing: proteins in raw fruit and vegetables cross-react with pollen allergens, causing itching and tingling of the mouth and lips within minutes. It is usually mild and confined to the mouth, and because the proteins are heat-labile, cooked versions are usually tolerated, which is a useful diagnostic clue.

Latex-fruit syndrome: banana, avocado, kiwi, chestnut, and sometimes papaya and fig, in people allergic to natural rubber latex. These reactions can be systemic and serious, unlike most oral allergy syndrome.

Lipid transfer protein (LTP) allergy is the important exception to "cooking helps": LTPs are heat- and digestion-stable, concentrated in the skin of fruit (peach is the classic), and cause systemic reactions. It is more common in Mediterranean populations (Chapter 25).

Alpha-gal syndrome deserves mention as the strangest entry on the list: a tick bite sensitises a person to galactose-alpha-1,3-galactose, a sugar in mammalian meat, producing delayed anaphylaxis 3 to 6 hours after eating red meat. The delay means it is frequently missed for years. Cases are rising in the US, Australia, and Europe.

Exercise-induced anaphylaxis, sometimes food-dependent (wheat is the classic co-factor), occurs only when the food is followed by exercise, which makes it baffling until identified. Alcohol and NSAIDs are also co-factors.

3. Anaphylaxis

This is the emergency. Learn it before you need it.

Recognise it by the ABC:

• Airway: swelling of tongue or throat, hoarseness, difficulty swallowing, stridor
• Breathing: wheeze, shortness of breath, persistent cough
• Circulation: dizziness, collapse, pale and clammy, feeling of impending doom

Plus, usually but not always, skin symptoms (hives, flushing, swelling). Around 10 to 20 percent of anaphylaxis presents without any skin signs, which is a common reason it is missed.

What to do:

1. Give adrenaline immediately, intramuscularly into the outer mid-thigh, through clothing if necessary. Do not wait to see if it worsens.
2. Call an ambulance and say the word "anaphylaxis."
3. Lie the person flat with legs raised. Sit them up only if breathing is the dominant problem; put them on their side if vomiting or unconscious.

   Do not let them stand or walk. Sudden standing during anaphylaxis has caused deaths from cardiovascular collapse. This is one of the most important and least known facts about it.

4. Second dose after 5 minutes if no improvement. This is why two auto-injectors are prescribed.
5. Go to hospital regardless of improvement, because of biphasic reactions hours later.

Adrenaline is safe. There is no situation where giving it for suspected anaphylaxis causes more harm than withholding it. Delay in administration is the factor most consistently associated with death. Antihistamines and steroids do not treat anaphylaxis (Chapter 70).

Practical: carry two auto-injectors at all times, check expiry dates, know the specific device (EpiPen, Jext, Emerade, and Auvi-Q all work differently), teach family and colleagues, and do not store them in a car, where heat and cold both destroy them.

Risk factors for fatal reactions: asthma, particularly poorly controlled asthma; adolescence and young adulthood; delayed adrenaline; and peanut and tree nut allergy.

4. Coeliac disease

Autoimmune, not an allergy or an intolerance. Gluten triggers an immune attack on the small intestine, flattening the villi and causing malabsorption. Affects roughly 1 percent of people, and a large proportion are undiagnosed.

Presentations are varied and frequently not gastrointestinal: iron-deficiency anaemia, osteoporosis, fatigue, mouth ulcers, infertility, neurological symptoms, raised liver enzymes, and dermatitis herpetiformis, an intensely itchy blistering rash.

You must be eating gluten for the tests to work. Serology (tTG-IgA) and biopsy both require current gluten exposure. Cutting out gluten before testing makes diagnosis impossible without months of reintroduction, and self-imposed avoidance before testing is a genuine and common clinical problem.

Treatment is complete, lifelong gluten avoidance, including trace cross-contamination. It is not a preference and it is not a fashion. Untreated coeliac disease carries increased risks of osteoporosis, infertility, and small bowel lymphoma.

Non-coeliac gluten sensitivity exists as a symptom description with a contested cause. Blinded crossover trials, notably Biesiekierski and colleagues, found that people reporting gluten sensitivity did not reliably react to blinded gluten and did improve on a low-FODMAP diet, pointing at fructans in wheat rather than gluten (Chapter 51).

5. Lactose intolerance

The global norm, not a disorder. Roughly two thirds of adults worldwide lose lactase production after weaning; lactase persistence is the mutation (Chapter 54).

Dose-dependent: most people tolerate around 12 g of lactose (a glass of milk), especially with a meal, and tolerance improves with regular small exposures as colonic bacteria adapt.

Hard cheese and yoghurt are naturally low in lactose, and yoghurt's live bacteria supply their own lactase.

Secondary lactose intolerance after gastroenteritis, coeliac disease, or Crohn's is common and usually temporary.

Diagnosis: hydrogen breath test, or simply elimination and rechallenge.

6. Other intolerances

FODMAP sensitivity and IBS. Fermentable carbohydrates draw water in and are rapidly fermented, causing pain and bloating in a hypersensitive gut. The low-FODMAP diet improves symptoms in 50 to 75 percent of people with IBS and is a diagnostic protocol, not a permanent diet: strict elimination for 2 to 6 weeks, systematic reintroduction to identify personal triggers, then the least restrictive long-term diet. Staying on it permanently reduces fibre and beneficial bacteria (Chapter 14). Do it with a dietitian.

Histamine intolerance. Reduced diamine oxidase activity, so histamine-rich foods (aged cheese, cured meat, wine, fermented foods, tomatoes, spinach) cause headaches, flushing, itching, and gut symptoms. Real, dose-dependent, and poorly served by testing.

Sulphite sensitivity. Affects around 3 to 10 percent of asthmatics, causing wheeze (Chapter 90).

Salicylate sensitivity. Uncommon and real, overlapping with aspirin-exacerbated respiratory disease (Chapter 66).

Caffeine sensitivity. Largely genetic, via CYP1A2 and ADORA2A (Chapter 88).

Alcohol flush. ALDH2 deficiency, and a genuine cancer risk signal, not a curiosity (Chapter 61).

7. Tests that do not work

This section exists because these tests are widely sold, expensive, and cause real harm by prompting unnecessary elimination diets.

The harms are real: unnecessary restriction, nutritional deficiency, disordered eating, cost, and delayed diagnosis of the actual problem, which is frequently IBS, coeliac disease, or something unrelated to food.

The tests that do work: skin prick testing, specific IgE blood tests (both interpreted alongside clinical history, because sensitisation without clinical allergy is common), component testing, supervised oral food challenge (the gold standard), coeliac serology plus biopsy, and hydrogen breath testing for lactose and fructose.

8. Prevention: the reversal

The advice changed completely, and this is the most consequential item in this chapter.

For years, guidance was to delay introducing allergenic foods. Allergy rates rose anyway.

The LEAP trial (Du Toit and colleagues, NEJM, 2015) randomised 640 infants at high risk to early peanut introduction or avoidance until age five. Early introduction reduced peanut allergy by around 80 percent. LEAP-On showed the protection persisted after a year of avoidance.

The EAT study found similar directional evidence for multiple allergens, though adherence to early introduction was difficult.

Current guidance in the UK, US, Australia, and elsewhere:

• Introduce allergenic foods from around 4 to 6 months, alongside other solids, once the infant is developmentally ready.
• Peanut as smooth peanut butter thinned with milk or water, or peanut puffs. Never whole nuts, a choking hazard until about five.
• Keep them in the diet regularly, at least weekly. Introducing once and stopping does not maintain tolerance.
• Infants with severe eczema or existing egg allergy should be assessed first, because they are the highest-risk group and the ones LEAP specifically studied.
• Do not delay introduction of egg, dairy, fish, wheat, or sesame either.

Other prevention factors with reasonable evidence: treating eczema aggressively (the "dual allergen exposure hypothesis" holds that sensitisation happens through broken skin while tolerance develops through the gut, so intact skin plus early oral exposure is the goal), vitamin D sufficiency, and vaginal birth and breastfeeding, both with weaker evidence.

Maternal avoidance during pregnancy or breastfeeding does not prevent allergy and is not recommended.

9. Treatment beyond avoidance

Oral immunotherapy (OIT) gives gradually increasing doses under supervision to raise the threshold that triggers a reaction. Palforzia, a standardised peanut OIT product, is licensed in the US and Europe for children.

What it does: raises the reaction threshold, so accidental exposure is far less likely to cause a serious reaction. What it does not do: cure the allergy. Most people must continue daily dosing to maintain protection, and reactions during treatment are common.

Other approaches: sublingual and epicutaneous (patch) immunotherapy, and omalizumab, an anti-IgE monoclonal antibody, which was approved in the US in 2024 for reducing reactions to multiple food allergens.

10. Living with it

• Read every label, every time. Formulations change without notice.
• "May contain" is voluntary and inconsistently applied. It is a risk judgement you have to make.
• Restaurants: in the EU and UK, businesses must provide allergen information. Natasha's Law in the UK, following the death of Natasha Ednan-Laperouse from sesame in a baguette, requires full ingredient labelling on food prepacked for direct sale.
• Carry two auto-injectors, always, and replace them before expiry.
• Wear a medical alert bracelet.
• Teach the people around you. Most fatal reactions occur away from home, and bystanders who know where the auto-injector is and how to use it save lives.
• Treat asthma properly. It is the strongest predictor of a fatal food reaction.
• Get a written allergy action plan from an allergy service.
• Re-test periodically in children. Milk, egg, wheat, and soy allergies are frequently outgrown, and unnecessary lifelong avoidance has nutritional and social costs.

11. The bottom line

• Allergy is immune and not dose-dependent; intolerance is dose-dependent and not life-threatening. Most self-reported food allergy is intolerance or nothing.
• Anaphylaxis: adrenaline into the outer thigh immediately, call an ambulance, keep them lying down. Do not let them stand up. Antihistamines do not treat it, and delay is what kills.
• Coeliac disease is autoimmune, affects 1 percent, and requires testing while still eating gluten. Most self-reported gluten sensitivity appears in blinded trials to be a fructan problem.
• IgG food intolerance testing does not work. It measures exposure, every major allergy body advises against it, and it drives harmful unnecessary restriction.
• The prevention advice reversed: introduce peanut and other allergens from around 4 to 6 months and keep them in the diet. LEAP reduced peanut allergy by around 80 percent.
• Oral immunotherapy raises the threshold for accidental exposure; it does not cure allergy.

Sources and notes

Allergy versus intolerance definitions and prevalence follow the EAACI and BSACI guidelines and the EuroPrevall population studies, which document the gap between self-reported and confirmed food allergy. Named allergen labelling follows EU Regulation 1169/2011 and the US FALCPA plus the 2023 FASTER Act adding sesame. Oral allergy syndrome and pollen cross-reactivity patterns follow Ballmer-Weber and Vieths' work. Lipid transfer protein allergy and its heat stability follow Fernandez-Rivas' Mediterranean cohort work. Latex-fruit syndrome follows Blanco's reviews. Alpha-gal syndrome follows Commins and Platts-Mills, Journal of Allergy and Clinical Immunology, 2009. Anaphylaxis recognition, intramuscular adrenaline, and the danger of standing the patient up follow Resuscitation Council UK guidance and Pumphrey's fatal reaction series; delayed adrenaline as the factor most associated with death follows the same source. Coeliac disease diagnosis, including the requirement to remain on gluten, follows NICE NG20 and ACG guidance. Non-coeliac gluten sensitivity blinded rechallenge is Biesiekierski et al., Gastroenterology, 2013. Lactose tolerance thresholds follow Suarez, Savaiano, and Levitt. Low-FODMAP efficacy and the requirement for structured reintroduction follow the Monash programme and BDA guidance. IgG food antibody testing is advised against by the EAACI (Stapel et al., Allergy, 2008), the AAAAI Choosing Wisely list, and BSACI. Peanut allergy prevention is LEAP, Du Toit et al., NEJM, 2015, and LEAP-On; EAT is Perkin et al., NEJM, 2016. The dual allergen exposure hypothesis follows Lack's work. Oral immunotherapy and Palforzia follow the PALISADE trial and EMA and FDA approvals; omalizumab for food allergy follows the OUtMATCH trial and the 2024 FDA approval. Natasha's Law follows the UK Food Information Amendment 2019.

Open questions. Whether oral immunotherapy improves quality of life enough to justify its treatment burden and reaction rate is debated. Non-coeliac gluten sensitivity's existence as a distinct entity remains unresolved.

👉 Next: eating for your situation.