What is food allergy?

Food allergies are adverse health effects arising from a specific immune response that occurs reproducibly on exposure to a given food allergen(1). ASCIA provides details on how to recognise an allergic reaction to foods https://www.allergy.org.au/patients/food-allergy/food-allergy. Symptoms can be mild to moderate including swelling of face or lips, hives on the skin or abdominal pain or vomiting, or can be more severe and indicative of anaphylaxis. Signs of anaphylaxis include difficulty breathing, swelling of the tongue and/or throat, hoarse voice, wheeze or cough, dizziness and/or collapse or being pale and floppy. The prevalence of anaphylaxis in Australia is increasing, particularly to foods (Figure 1)(2).

Figure 1: Anaphylaxis prevalence in Australia, by food and non-food causes(2).

Common Food Allergens

The most common food allergens are egg, peanut, tree nut, soy, sesame, shellfish and cow’s milk. Some of the highest rates of food allergy are noted in Australia. This data comes from the population-based HealthNuts study, where suspected allergy was investigated in a cohort of 5,276 children aged 1 year. Food allergen sensitivity based on skin prick tests was evident in 14% of the children for egg, 8.1% for peanut and 1.9% for sesame. For formal food allergy diagnosis, skin prick sensitivity should be combined with challenge-proven outcomes to the food allergen, which when conducted in the HealthNuts study, found lower true food allergy prevalence; 11% overall, with peanut (3%), raw egg (8.9%) and sesame (0.8%). Follow up at 4 years saw the prevalence further decline to 3.8% overall, with specific food allergy prevalence reducing considerably for egg (down to 1.2%) and sesame (0.4%), but less so for peanut (1.9%)(3).

Milk Allergy

Historical data on cow’s milk allergy shows a prevalence of 7.5% in 1-3 year old children(4). More recent meta-analysis data demonstrates 6.0% of children have self-reported cow’s milk allergy, but only 0.6% have challenge-proven cow’s milk allergy. Food intolerance rather than food allergy may explain the large discrepancy, with cow’s milk foods such as cheese being rich in amines, which may cause food intolerance responses(5).

Diagnosing Food Allergy

Clinical assessment by an allergist is required to confirm food allergy. A combination of clinical parameters, symptoms and investigation needs to be considered to make a diagnosis. A history of atopic disease, first time exposure to the food, acute symptoms, which may be relieved by antihistamines, may indicate food allergy. Follow up skin prick testing may be useful, but in general the incidence of positive skin prick testing is much higher than true challenge-proven allergy outcomes(3). Many children can grow out of food allergies over time, although it is well established that signs of this are generally shown at a younger age(6). If the food allergy continues past the age of 4, the likelihood that the food allergy will remain is high.

Managing Food Allergy

Management of food allergy involves avoidance of the allergen containing food. Allergy or anaphylaxis action plans should be prepared and are a requirement for childcare centres, kindergartens and schools. A copy of the relevant plans are available via ASCIA. (See Link https://www.allergy.org.au/hp/ascia-plans-action-and-treatment) In the event that an EpiPen is required, the family, care facility or school must have an EpiPen on hand for the child at all times. Details on the prescription of EpiPens and guidelines on anaphylaxis management can be found at ASCIA. (See Link https://www.allergy.org.au/hp/anaphylaxis )

Allergy Prevention

For many new parents, the increasing prevalence of food allergies has lead to increasing fear and an overall excessive restriction of common food allergens during pregnancy and in the diet of young infants. Evidence is mounting to suggest that this may in fact be a contributing factor in increasing prevalence of food allergies and that early exposure to common food allergens may be one of the keys to preventing allergies(7).

Earlier introduction of peanut in high-risk infants (eczema and/or egg allergy) has been demonstrated to reduce the risk of peanut allergy. Six hundred and forty infants were randomised to consume or avoid peanut from age 4-11 months up to 5 years. The latter had peanut allergy prevalence of 35.3% compared to 10.6% for those consuming peanut from an early age(8). For other common food allergens, the data supporting early introduction to prevent allergy is inconclusive, however recommendations remain to not avoid egg and milk during early infancy(9).

In terms of infant formula and food allergy prevention, meta-analysis reveal no consistent evidence to support that partially or extensively hydrolysed formulas reduce the risk of allergic or autoimmune outcomes in infants at high pre-existing risk of these outcomes.

Probiotics have received much attention, particularly Lactobacillus rhamnosus which is showing promising results in food allergy prevention. Canani and colleagues reported a randomised trial of hypoallergenic infant formula with or without added Lactobacillus rhamnosus in infant’s with cow’s milk allergy, which demonstrated a risk reduction when receiving the probiotic for the development of additional atopic disease (e.g. asthma, eczema and other food allergies)(10). Oral immunotherapy (OIT) (i.e. giving small doses of a known food allergen and achieving desensitisation) has been demonstrated to work as long as the OIT is ongoing(9). An exciting area of research involves achieving tolerance to the food allergen, where desensitisation is ongoing despite ceasing OIT(11). This has been observed when Lactobacillus rhamnosus is added to OIT for peanut allergy, with 89.7% of those receiving the probiotic achieving desensitisation and positive changes in skin prick testing and immune markers(11). Follow up studies are needed to confirm these results.

Vitamin D is involved in immune regulation and there is some evidence linking vitamin D insufficiency with food allergy prevalence. Some research suggests that vitamin D insufficiency increases the risk of IgE-mediated food allergy(12, 13). On the other hand, vitamin D excess in pregnancy and at birth has been associated with increased risk of food allergy(14). Follow up studies have failed to confirm a relationship between vitamin D status at birth or six months and food allergy prevalence at one year(15). Vitamin D bioavailability may be more of the key to food allergy. It is enhanced by a reduction in vitamin D binding proteins, the level of which is determined by genetic polymorphisms. Food allergy prevalence is increased with genetic polymorphisms that increase vitamin D binding proteins, thereby reducing vitamin D bioavailability(16).

The hygiene hypothesis has also been proposed as an explanation for the increased incidence of allergic disease, with cofactors including the number of siblings, antibiotic use, infection history, pet exposure and child care exposure. Higher rates of viral illnesses, infections and eczema are associated with a higher prevalence of food allergies, whereas there is a protective benefit observed with lower rates of food allergy and asthma where there is a greater number of siblings(17). Natural childbirth, breast feeding, increased outdoor activities, diet and limited and appropriate antibiotic use may also lead to improved microbiota outcomes, which could in turn reduce the risk of allergic disease(18).

ASCIA, Australia’s peak body on allergy, provides useful guidelines for healthcare professionals on infant feeding and allergy prevention. See link https://www.allergy.org.au/hp/papers/infant-feeding-allergy-prevention

What is food intolerance?

Food intolerance is very different to food allergy, the former affecting approximately 20% of the population, including both adults and children. Intolerance responses involve non-immune reactions that include metabolic, toxic, pharmacologic and undefined mechanisms(1). Common food intolerance symptoms include headaches, bloating and abdominal pain and diarrhoea. Common food intolerance triggers include lactose, amines, salicylates and fermentable carbohydrates (FODMAPs) in those with irritable bowel syndrome. A patient experiencing known food intolerance responses will need to avoid the associated foods, to manage symptoms but complete avoidance is not imperative, which differentiates food intolerance from food allergy and the risk of anaphylaxis, where complete avoidance is required.  

Food allergy prevalence is on the rise, but there is much research being undertaken in this space and there is hope for more data to help us understand how to prevent and treat food allergies. Diagnosis of food allergy is paramount and distinguishing between allergy and intolerance is vital, as this determines the level of food avoidance and treatment requirements.

Article provided by:

Dr Jaci Barrett and Dr Sonja Kukuljan
Accredited Practising Dietitians

References

  1. Boyce JA, et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAID-Sponsored Expert Panel Report. J Allergy Clin Immunol. 2010;126(6):1105-18. Access Link. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249938/)
  2. Laemmle-Ruff I, et al. Anaphylaxis Identification, management and prevention. Australian Family Physician. 2013;42(1):38-42. Access Link. (https://www.racgp.org.au/afp/2013/januaryfebruary/anaphylaxis/)
  3. Peters RL, et al. The prevalence of food allergy and other allergic diseases in early childhood in a population-based study: HealthNuts age 4-year follow-up. J Allergy Clin Immunol. 2017;140(1):145-53 e8. Access Link. (https://www.ncbi.nlm.nih.gov/pubmed/28514997)
  4. Gerrard JW, et al. Cow’s milk allergy: prevalence and manifestations in an unselected series of newborns. Acta Paediatrica. 1973;62(S234):3-21. Access Link. (https://www.ncbi.nlm.nih.gov/pubmed/4517311)
  5. Wagner N, et al. A Popular myth – low-histamine diet improves chronic spontaneous urticaria – fact or fiction? J European Academy of Dermatology and Venereology. 2017;31(4):650-5. Access Link. (https://onlinelibrary.wiley.com/doi/abs/10.1111/jdv.13966)
  6. Savage J, et al. The Natural History of Food Allergy. J Allergy Clin Immunol Pract. 2016;4(2):196-203. Access Link. (https://www.ncbi.nlm.nih.gov/pubmed/12777603)
  7. Allen KJ & Koplin JJ. Prospects for Prevention of Food Allergy. J Allergy Clin Immunol Pract. 2016;4(2):215-20. Access Link. (https://www.sciencedirect.com/science/article/pii/S2213219815005747)
  8. Du Toit G, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med. 2015;372(9):803-13. Access Link. (https://www.nejm.org/doi/full/10.1056/nejmoa1414850)
  9. Sicherer SH & Sampson HA. Food allergy: A review and update on epidemiology, pathogenesis, diagnosis, prevention, and management. J Allergy Clin Immunol. 2018;141(1):41-58. Access Link. (https://www.sciencedirect.com/science/article/pii/S0091674917317943)
  10. Berni Canani R, et al. Extensively hydrolyzed casein formula containing Lactobacillus rhamnosus GG reduces the occurrence of other allergic manifestations in children with cow’s milk allergy: 3-year randomized controlled trial. J Allergy Clin Immunol. 2017;139(6):1906-13 e4. Access Link. (https://www.sciencedirect.com/science/article/pii/S0091674916324873)
  11. Tang ML, et al. Administration of a probiotic with peanut oral immunotherapy: A randomized trial. J Allergy Clin Immunol. 2015;135(3):737-44 e8. Access Link. (https://www.sciencedirect.com/science/article/pii/S0091674914017370)
  12. Allen KJ, et al. Vitamin D insufficiency is associated with challenge-proven food allergy in infants. J Allergy Clin Immunol. 2013;131(4):1109-16, 16.e1-6. Access Link. (https://www.sciencedirect.com/science/article/pii/S0091674913001541)
  13. Baek JH, et al. The link between serum vitamin D level, sensitization to food allergens, and the severity of atopic dermatitis in infancy. J of Pediatrics. 2014;165(4):849-54.e1. Access Link. (https://www.sciencedirect.com/science/article/pii/S0022347614006039)
  14. Weisse K, et al. Maternal and newborn vitamin D status and its impact on food allergy development in the German LINA cohort study. Allergy. 2013;68(2):220-8. Access Link. (https://onlinelibrary.wiley.com/doi/abs/10.1111/all.12081)
  15. Molloy J, et al. Vitamin D insufficiency in the `first 6 months of infancy and challenge-proven IgE-mediated food allergy at 1 year of age: a case-cohort study. Allergy. 2017;72(8):1222-31. Access Link. ( https://onlinelibrary.wiley.com/doi/abs/10.1111/all.13122 )
  16. Koplin JJ, et al. Polymorphisms affecting vitamin D–binding protein modify the relationship between serum vitamin D (25[OH]D3) and food allergy. J Allergy Clin Immunol. 2016;137(2):500-6.e4. Access Link. (https://www.sciencedirect.com/science/article/pii/S0091674915009112)
  17. Gupta RS, et al. Hygiene factors associated with childhood food allergy and asthma. Allergy and Asthma Proceedings. 2016;37(6):e140-e6. Access Link. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5080537/)
  18. Bloomfield SF, et al. Time to abandon the hygiene hypothesis: new perspectives on allergic disease, the human microbiome, infectious disease prevention and the role of targeted hygiene. Perspectives in Public Health. 2016;136(4):213-24. Access Link. (https://journals.sagepub.com/doi/full/10.1177/1757913916650225)