Category Archives: Allergy

Food allergy diagnosis

Getting it right is important because otherwise people end up scared of foods, cut out different foods and risk nutritional/growth problems as well as aversion in the child. Having unproven food allergies also causes huge problems for schools and nurseries, and may lead to the public becoming sceptical of true allergy, with potentially disastrous consequences.

Getting it right can identify other potential allergies; it can help estimate risk of anaphylaxis; it can help with predicting whether the allergy is going to go away or not.

Allergy focused history

EATERS method –

  • Exposure – did they actually eat it!? Or was there clear skin contact? Perhaps from surface contamination?
  • Allergen (suspected) – one of the common ones? Although you can be allergic to pretty much anything, it is really rare to have an isolated rare food allergy.
  • Timing – type 1 is immediate (within 15 minutes, rarely up to 1hr after) and then settles even without treatment within 24 hours. Rare to fluctuate.
  • Environment – home (usually during weaning)? Outside home? Co-factors (infection, medicines, exercise, sleep deprivation) come in here.
  • Reproducible – consistent reactions with exposure? May have had before with type 1 allergy but often on trying for the first time, and won’t have had recently. Milk/egg different, of course…
  • Symptoms – type 1 vs non type 1. Some overlap of course.
[Mich Erlewyn-Lajeunesse, ADC 2019]

Other issues are age (adolescents with hay fever more likely to develop secondary pollen food syndrome type allergies), alpha-gal allergy can be delayed up to 3 hours; raw vs cooked food sometimes makes a difference; usually you already have eczema and family history of atopy.


At the end of history taking, you should have be able to assess probability of type 1 allergy. If low, you may wish to proceed straight to challenge (unless reactions sound severe). Otherwise testing may help confirm or refute.

If negative/equivocal on initial skin prick or specific IgE testing, do another test! Skin prick if negative/equivocal IgE, and vice versa.

IgE Component testing may give added information, esp where potential pollen co-sensitisation – best evidence (mostly in US population, however) for Peanut, Hazelnut, Cashew (respectively Ara h 2, Cor a 14, Ana o 3 – other components may give extra information in some cases). Jug r 1 v specific (walnut) but not v sensitive.


Challenge will be useful where results still equivocal – viz

  • Results positive but never eaten or history inconsistent
  • Results positive but possibly co-sensitivity without allergy
  • Food in alternative form might be OK eg baked

Allergy testing

Gold standard is double blind challenge, but who has time for that?

Mostly based on history – combination of characteristic features without other, more likely, explanation.

NICE has list of type 1 vs non type 1 allergy signs/symptoms – some overlap, eg vomiting, diarrhoea, itch.

EAACI guidance 2023 says where type 1 allergy suspected (signs/symptoms but also timing and consistency of reaction):

  • Do skin prick testing and/or specific IgE testing as first line
  • For peanut, hazelnut or cashew, if in doubt do component tests Ara h 2, Cor a 14, Ana o 3 respectively as well (if available) – otherwise do skin prick or IgE if not done already.
  • Where peanut or sesame allergy still in doubt, do basophil activation test (BAT – if available)
  • “Reassessment of food allergic children, at regular intervals, depending on age, food and patient’s history, is suggested for possible development of spontaneous tolerance”

Ara h 2 (cut off 0.44) has 82% sensitivity and 92% specificity cf 84 and 86% for SPT of 4mm. Cor a 14 (cut off 0.64%) has 73 and 95%, Ana o 3 (cut off 0.4) 96 and 94%.

Common hidden allergens (!): celery, mustard, cochineal, lupin, soy, fenugreek, other legumes such as pea/bean/lentil protein, insects/mealworm, pink peppercorns).

Allergies and School/Nursery

First do no harm – parents tend to overestimate risk of anaphylaxis, whereas there are clear consequences to restricting the child’s ability to sit with other children at snack/meal times, or restricting the food choices of other children.

Probably better to increase allergy awareness (which varies widely) than rely on classroom or school-wide bans [Dave Stukus editorial]

George Raptis has shown how allergy training can improve allergy awareness, not just confidence in managing an allergic emergency.

Onion and garlic allergy

Alliums, as are leeks, shallots and chives. Part of same bigger family as asparagus but probably not co-sensitivity.

The main issue with onion is the chemicals released from cut surfaces, which can trigger eye/nose reactions and potentially asthma. But there’s actually some evidence that onion has an anti-allergy action.

With garlic, there is a well recognised contact dermatitis relating to chopping it.

Otherwise, allergy is very rare. Potentially part of celery-spice-mugwort syndrome.

As with that syndrome, the problem for the allergic person is that not only is it not one of the 14 UK recognised allergens for food labelling and restaurants, but it can be included under “spices” if less than 2% of the overall product, without further detail.

Food allergy

Different from intolerance and sensitivity, which are not immune mediated problems. Sometimes hard to tell the difference.

2 basic types of food allergy, you can have both at the same time – type 1 (IgE mediated), and non-type 1 (non-IgE mediated – possibly type 4 hypersensitivity).

Most commonly (in Scotland – but varies across UK, especially with different ethnic groups), and varies widely across the world):

  • Milk
  • Egg
  • Peanut
  • Tree nuts
  • Legumes/Pulses
  • Sesame
  • Wheat
  • Crustaceans/molluscs
  • Various fruits

Birch pollen sensitization in Northern Europe changes the kinds of allergies you get – cross sensitivity with fruit and nuts (pollen food syndrome) – whereas in the rest of Western Europe you get more fruit and seed allergies based on LPS.

Hospital admissions for food allergy in the UK have been increasing for some time. If you ask people about their children’s allergies, up to 28% of infants will report allergies – real figure is probably between 1 and 4%. Lifetime and point prevalence of self-reported food allergy 20% and 13%, respectively – point prevalence of sensitization as assessed by sIgE stands at 17%, skin prick test 6%, and food challenge positivity 1%. Based on clinical history or positive food challenge, food allergies have increased from 2.6% in 2000–2012 to 3.5% in 2012–2021. Point prevalence for under 16s for self reported but physician diagnosed food allergy is 3.75%. Patterns vary across European regions but not in a consistent way. [Spolidoro and Venter 2022]

Having a child with a food allergy has a significant effect on the quality of life for the whole family. One study suggested that having a peanut allergic child had a worse effect on a family than having a child with diabetes, even though with diabetes you also have restrictions on eating and the potential for serious adverse events. A similar study found the same comparing food allergic families with families where a child had a rheumatological diagnosis. The main domains affected were social. Patient/parent feedback pretty consistent across the world however (although most studies done in Europe and English speaking countries), and across time:

  • Parents lived in fear after the first reaction, often perceiving it as traumatic, and often feeling guilt too
  • They tried to live an ordinary family life and had to learn how to be one-step ahead and understand early signs.
  • The family’s social life was also influenced.
  • Parents asked for support and information from health professionals
  • More knowledge and skills increased parents’ confidence (and by implication quality of life – Knibb 2015)

Mothers tend to report greater impact on the child’s quality of life and experience more anxiety and stress than fathers. Mothers tend to shelter the child, whereas fathers more often express a desire to expand their child’s life, and these differences are often greater where parents are separated.

The concern for the child’s safety affected eating outside the home, with birthday parties and visits to peers’ homes particularly threatening. School and nursery are a major source of concern and often led to more parental work, preparing safe lunches.

Parents often felt they had to teach themselves about allergies, due to the lack of early information provided by health care, and then ended up having to teach family, friends and educational institutions too.

Adolescence is a particularly stressful time, as parents recognize the need for the child to become more independent, at the same time that the adolescent can see the parents as excessively controlling (at least with respect to peanut allergy). Supportive friends particularly important for adolescents.

[Larsen Moen, J Ped Nursing 2019]


Initial studies did not show any relationship between moulds/damp and health, as there was major confounding with socioeconomic status, and because it is hard to quantify mould exposure (with many different mould species).

Then there is the effect of climate, and the built environment – heating, ventilation, insulation, materials etc.

More recently systemic reviews have made it clear there is a link particularly with development of asthma, particularly in older children, and where there is already a family history of atopy.

Coroner ruled death of 2yr old Awaab Ishak in 2020 from granulomatous tracheobronchitis was due to environmental mould exposure from poor housing.

Longitudinal studies have suggested that there may be protective effects but data is limited.

Similarly there is evidence that higher exposure to moulds leads to more asthma exacerbations.

There are genetic polymorphisms that affect ability to break down the fungal protein chitin, and these have been linked to urgent medical care visits, which suggests a non-immune mechanism may be important.

Dampness is linked to mould growth but also to house dust mite, microbial volatile compounds, mycotoxins and endotoxin.

The most studied mould species are AspergillusPenicilliumAlternaria and Cladosporium.

Limited evidence that interventions to reduce mould make any difference.

[European respiratory review 2018]

Allergen families

Hundreds of different allergens have been identified, and can be classified by similarities in structure/genetics, usually based on the plants being related to each other in evolutionary terms.

This is useful because cross reactivity is more common, the more closely different proteins are related. Not all are allergenic however, and not all cross react.

You can also predict how heat stable these proteins are by how cross linked their structure is. Linear proteins are more easily disrupted by heat, so the allergy is likely to only be an issue with raw (or frozen from raw).

Most allergens belong to one of a small number of groups:

  • PR-10 eg Bet v 1, Ara h 8, Cor a 1, Pru p 1, Mal d 1. Heat labile, homologous. Most pollen food syndrome cases (birch pollen).
  • Profilin eg Bet v 2, Cor a 2. About 20% of pollen food syndrome cases. More common in Southern Europe – birch and oak too, but also olive tree, London plane, grasses, ragweed. More common in high grass pollen intensity areas? Can be associated with severe food reactions (esp melon, watermelon, banana, tomato).
  • Prolamin – includes nonspecific lipid transfer proteins (nsLTP) which are heat stable but very cross reactive, and are found in fruit, vegetables, nuts, legumes, seeds and cereals, as well as plane trees and mugwort. Best known is Pru p 3, which is a good surrogate marker for any nsLTP sensitisation, even if cherry (prunus) isn’t a known issue. Ara h 9, Cor a 8, Mal d 3.
  • Cupin – includes legumins. Heat stable. Ara h 1 and 3, lentil, cor a 9/11 (hazelnut), some soya.
  • Thaumatin – named after W African shrub! Various fruit including apple, kiwi, plus cedar pollen.
  • 2S albumin eg Ara h 6.

Glasgow lab offers only hz, peanut, peach/cherry, egg (Gal d 1), alpha galactose and bee/wasp. Dundee offers those plus milk and cashew.

Private testing available for Bos d 8 (milk casein) and soya.

Sesame allergy

An emerging food allergy over the last few decades in the UK.

Sometimes isolated, but 25% of peanut allergic are also sesame allergic.

Black, white, red varieties are found – in allergy terms identical.

Other co-sensitivities are pine nut (!), brazil nut and macadamia [Helen Brough, JACI 2020].

Sesame often used in bakery products, also in Far Eastern (gomashio, furikake are sprinkled over Japanese food) and Middle eastern food. Typical white seeds are obvious (and stick to everything, which makes cross contamination a big problem) but black sesame seeds found in Japanese cooking, and tahini (sesame paste, used in hummus and dressings), are not recognisably sesame seeds at all.

Sesame oil is generally unrefined, which is to say that it is likely to contain significant amounts of sesame protein and therefore trigger reactions. With many other kinds of oil, this isn’t the case because they are refined and lack proteins.

Evidence exists that ingested whole seeds can pass through digestive tract of allergic person without causing a reaction – which can confuse diagnosis and/or suggest tolerance when it isn’t. Or delayed rupture of seed case may cause delayed but severe reactions (90 mins plus after ingestion)

Some sesame allergic appear to be sensitized to oleosins, which are not water soluble so are not found in standard skin prick and IgE test solutions, potentially giving a false negative result.

The Farm effect in allergy

Children growing up on farms are less likely to develop allergies and asthma. Farming has been part of human culture for probably 7000 years.

It is widely accepted now that a symbiotic relationship with a diverse population of microbes in the environment, on the skin, in the gut and in the lung is necessary for a healthy immune system (“microbiome“). These microbes influence the balance between inflammation and immune tolerance. That relationship needs to be developed in early life, and nutrition is a major part.

Big European cross sectional studies – PARSIFAL and GABRIEL. Amish and Hutterites in US are genetically similar but Hutterites use industrial rather than traditional farming techniques (and have 4-6x the rate of hay fever and atopic sensitization).

Prenatal maternal exposure to farm animals is protective against eczema in the first 2 years of life, and against asthma symptoms pre-school.

Farm milk consumption in the first year of life is protective against respiratory allergies. Not clear what it is about it – more whey? Higher levels of cytokines or polyunsaturated fatty acids?

In children, exposure to cows and hay was protective against asthma. Some evidence for pigs, but risk seems to go up for sheep.

Mediators thought to potentially be N-gylcolylneuraminic acid (animals/pets) and arabinogalactan (plants).

Lipopolysaccharide (endotoxin) is widespread in the farm environment. Levels in mattresses inversely associated with hay fever, atopic sensitisation and asthma.

Lack of gut microbial diversity in first month of life predicts school age asthma.

Dietary diversity in first 2 years of life protects against asthma and allergic rhinitis. The link between gut microbes and lung health is thought to be short chain fatty acids, such as acetate and butyrate.

[Ped Allergy and Imm 2022]

In a study of 589 children, 1-year microbiota maturation (based on metagenomics – genetic material of a community of micro-organisms – and metabolomics – metabolites in environment) closely related to eczema, asthma, food allergy and allergic rhinitis at age 5 years. Found a core set of “functional and metabolic imbalances” characterized by compromised mucous integrity, elevated oxidative activity, decreased secondary fermentation, and elevated trace amines. [Hoskinson, BC, Canada – Nature communications . 14(1):4785, 2023 08 29.]