What GPs can do to help manage food allergies

8 minute read

Diagnosis of allergic reactions can be a complex process and requires a thorough clinical history

Food allergy is a growing problem in Australia with 4 to 8% of children aged zero to five years and 2 to 4% of adults affected. The incidence of food allergy-induced anaphylaxis has doubled in the last decade in Australia, US and UK.1

In Australia, admissions for anaphylaxis due to food allergy in children aged zero to four years are even higher, having increased five-fold over the same period. Deaths caused by anaphylaxis have increased by 7% per year.1

As food allergy continues to affect an ever-growing proportion of our population, general practitioners will be required to play a greater role in helping to manage this problem.

When talking about food allergy, it is essential to understand the terminology used in this area.

A food allergy refers to an immunological hypersensitivity reaction that develops after exposure to a culprit food. Most of these allergies are immediate type 1 IgE-mediated hypersensitivity reactions, which can be divided into mild-to-moderate reactions or anaphylactic reactions.

Mild-to-moderate reactions manifest as non airway-threatening angioedema, urticaria, oral pruritus, abdominal pain and vomiting.

Anaphylactic reactions require life-threatening features such as airway threatening angioedema, bronchospasm or hypotension. This type of food allergy is mediated by IgE antibodies directed against specific food proteins that can activated mast cells and basophils.

There are also cell-mediated hypersensitivity reactions, such as food protein-induced enterocolitis syndrome, food protein-induced enteropathy and food protein-induced proctocolitis. These types of hypersensitivity reactions are less common that IgE-mediated food allergies and will not be discussed any further in this article. 

The term sensitisation refers to the presence of IgE antibodies directed against an antigen, as determined by skin prick testing or specific IgE blood tests.

It is very important to understand that sensitisation is not synonymous with allergy, as it is possible to be sensitised to a food without being allergic to it. In an Australian birth cohort, the prevalence of sensitisation to peanut, egg, and sesame during the first year of life was 8.9%, 16.5%, and 2.5%, respectively, whereas the prevalence of challenge-proven allergy to these same foods was 3.0%, 8.9%, and 0.8%, respectively.2

It is not known why food allergy has increased so rapidly in recent years. One explanation is the hygiene hypothesis, which proposes that less exposure to infections in early childhood is associated with an increased risk of allergy.

Other explanations include delayed introduction of allergenic foods and the use of skin products, such as moisturisers, that contain animal or plant proteins.

Food allergies can develop at any age, but occur most commonly in children aged less than five years.

Almost any food can cause an allergic reaction, but cow’s milk, egg, peanut, tree nuts, sesame, soy, fish, shellfish and wheat are responsible 90% of food related allergic reactions. Peanut, tree nuts, shellfish, fish, sesame and egg are the most common food allergens in older children and adults.1

The severity of an allergic reaction can be influenced by a number of factors, including the amount of food eaten, how well it is cooked (baked, lightly cooked or raw), intake of alcohol, exercise around the same time as the meal, use of non-steroidal anti-inflammatory drugs or ACE inhibitors and the presence of unstable asthma.

To prevent the development of allergies, parents should be encouraged to introduce their babies to common allergy-causing foods within their first 12 months. This directly contradicts advice previously provided by health professionals.

A randomised trial of peanut consumption in infants at risk for peanut allergy established that the early introduction of peanuts significantly decreased the frequency of the development of peanut allergy among children at high risk for this allergy and modulated immune responses to peanuts.3

Diagnosing food allergy can be a complex process and so all patients with a suspected food allergy should be referred to an allergist/immunologist for further assessment.

Diagnosing food allergy requires a very thorough clinical history. Without a good clinical history it is very difficult to determine the clinical relevance of skin prick or specific IgE test results.

The important details include the manifestations of the allergic reaction, what was consumed prior to the onset of the reaction and the duration inbetween.

Other important clinical details include the presence of potential co-factors, such as exercise, infections and use of non-steroidal anti-inflammatory drugs and alcohol.

Most IgE-mediated food allergies develop rapidly, typically beginning within minutes to two hours from the time of ingestion. One exception is IgE-mediated reactions to carbohydrate (alpha-gal) allergens in patients with tick bite-induced red meat allergy. These reactions can developed two to 12 hours after exposure.4

If a person develops an allergic reaction after consuming a meal containing a number of ingredients they should be advised to record this list of ingredients.

Where processed foods are used photographs of the ingredient lists should be taken.

Once this list is acquired, the next step should be to determine which of these ingredients have been consumed without problems since the index reaction. In most cases, these foods can be ruled out as the cause of the reaction. Skin prick and specific IgE testing should then be used to help identify which of the remaining ingredients caused the reaction.

These tests must be targeted. Too often doctors test foods indiscriminatingly and without clear purpose. Specific IgE testing should be used for individual foods.

Testing food mixes is unhelpful and should be avoided.

Do not order specific IgE testing for staple food mixes.

Do not test foods that your patient is currently consuming without any problems, as positive results are not clinically significant and will also serve to encourage unnecessary food avoidance.

When skin prick and specific IgE testing is targeted it can help to identify the foods a patient is allergic to. Results demonstrating large wheal sizes and high specific IgE levels are more likely to be clinically relevant.

The size of the wheal and the level of specific IgE do not predict the severity of a reaction.

A positive result for skin prick testing is a wheal size that is 3mm larger than the negative control. A positive result for specific IgE testing will be determined by the laboratory performing the test.

A common scenario encountered is borderline positive results to foods a patient has not been exposed to since their index reaction.

The safest way to clarify if a patient is allergic to these foods is to perform a clinically supervised food challenge.

This is best performed by an allergist/immunologist with expertise in managing anaphylaxis.

Sometimes skin prick and specific IgE tests can be falsely negative in patients with a very high pre-test probability for having food allergy. These patients should also have a supervised food challenge.

Most childhood food allergies are lost over time, although this varies among different foods and individual patients.

The mechanisms by which food allergy resolves are not fully understood.

Food-specific IgE levels tend to fall over time in most patients and is the best known predictor of clinical tolerance.5-7

However, some patients can become tolerant even with persistently elevated food-specific IgE levels.

Most children allergic to cow’s milk, soy, wheat or egg will outgrow their food allergy.1

By contrast, allergic reactions to peanut, tree nuts, sesame and seafood persist in approximately 75% of children affected. When food allergy develops for the first time in adults, it usually persists.1

When a food allergy diagnosis is established, strict avoidance is mandatory in most cases. Some foods, such as egg and milk, may be consumed in more cooked forms. For example, a child who is allergic to lightly cooked egg (boiled, fried) may be able to tolerate baked egg (cakes, muffins) and should be encouraged to eat baked egg regularly to accelerate tolerance.

All patients with a food allergy should be referred to an allergist/immunologist for consideration of an adrenalin auto-injector and be provided with an allergy plan or anaphylaxis action plan.

Specific IgE and skin prick testing can be repeated at one to two yearly intervals to monitor a child’s food allergies.

Based on these results, an allergist/immunologist can determine if the child can safely perform a supervised food challenge to establish whether tolerance has been achieved.

Food desensitisation or immunotherapy is not currently established clinical practice in Australia, but there are a number of trials under way looking at its utility in the treatment of food allergy.

Dr Ari Murad is a consultant immunologist and allergist practising in Castle Hill, Sydney 


1.  Australasian Society of Clinical Immunology and Allergy (ASCIA). https://www.allergy.org.au

2.  Osborne NJ, Koplin JJ, Martin PE, et al. Prevalence of challenge-proven IgE-mediated food allergy using population-based sampling and predetermined challenge criteria in infants. J Allergy Clin Immunol 2011; 127:668.

3. Du Toit G, Roberts G, Sayre PH, Bahnson HT, Radulovic S, Santos AF, Brough HA, Phippard D, Basting M, Feeney M, Turcanu V, Sever ML, Gomez Lorenzo M, Plaut M, Lack G. Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy. N Engl J Med. 2015 Feb 26;372(9):803-13.

4. Van Nunen, S. Tick-induced allergies: mammalian meat allergy and tick anaphylaxis. Med J Aust. 2018 Apr 16;208(7):316-321.

5. Wood RA, Sicherer SH, Vickery BP, et al. The natural history of milk allergy in an observational cohort. J Allergy Clin Immunol 2013; 131:805.

6. Sicherer SH, Wood RA, Vickery BP, et al. The natural history of egg allergy in an observational cohort. J Allergy Clin Immunol 2014; 133:492.

7. Peters RL, Allen KJ, Dharmage SC, et al. Natural history of peanut allergy and predictors of resolution in the first 4 years of life: A population-based assessment. J Allergy Clin Immunol 2015; 135:1257.

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