A food allergy epidemic… or just another case of overdiagnosis?

Food allergy is widely accepted to be increasing in many regions of the world—by the public, healthcare professionals and scientists. [1] This is based on high rates of self-reported food allergy, and clear increases in surrogate measures such as prescription of low-allergy formula or adrenaline (epinephrine) autoinjectors, or hospital admissions for severe allergic reactions. [2,3] The consequences of a diagnosis are significant: food allergy does not just mean dietary restrictions and increased food costs, but can also impact on social activities and cause anxiety due to fear of potential reactions. The unpredictable, but rare, possibility of a very sudden death from food anaphylaxis can understandably contribute to anxiety about food allergy.

The simplest approach to understanding food allergy prevalence is to evaluate rates of self-reported allergy, or frequency of positive diagnostic tests. Food allergy diagnostics are generally more sensitive than specific: IgE sensitisation is much more common than true clinical reactivity. Self-report is even less reliable, with studies consistently showing that many more people report a food hypersensitivity than are confirmed at a blinded food challenge. By relying on self-report or simple diagnostics, food allergy can appear to be much more common than it really is. The combination of diagnostic uncertainty and commercial or personal incentives provides all the ingredients needed for overdiagnosis. [4] Commercial pressures incentivise increased allergy testing, increased use of treatments such as low-allergy formula, adrenaline autoinjectors or desensitisation, and increased clinical service provision. Allergy charities are understandably keen to promote food allergy awareness, and may be supported by these same commercial interests. [5]

When we review prevalence data for food allergy, we see a familiar pattern—sharp increases in softer indicators of allergy such as self-report, prescription, and healthcare attendance rates; but no increase in markers of severe disease such as fatal reactions, or in objective markers such as allergic sensitisation, or challenge-proven food allergy. Few studies have reported changes in objective markers or fatality rates over time. In England, the Isle of Wight birth cohorts did not find any change in prevalence of challenge-proven food allergy or allergic sensitisation to foods in young children born between 1989 and 2001. [6] Similarly, in Melbourne, Australia, there were almost identical rates of sensitisation to milk, egg, and peanut in a 1990-94 birth cohort compared with a similar population from 2006-10. [7] In the United States National Health and Nutrition Examination Surveys, there was no change in IgE-sensitisation to peanut, milk, egg, or shrimp in young people aged 6 to 19 years between 1988-94 and 2005-06. [8] Finally, as we report in a new research paper in The BMJ, there has been no increase in fatal food anaphylaxis in the United Kingdom between 1992 and 2018, despite increasing hospitalisations—data which are consistent with those from USA and Australia. [9] So at least for the past 30 years, in these countries, the measures of food allergy prevalence, which are least susceptible to behavioural influences, do not appear to be changing.

One can propose alternative hypotheses to explain these findings—that food allergy has become more clinically manifest than in the past, so that food anaphylaxis is truly increasing, but we have become much better at treating reactions. However, Ockham’s razor suggests we should favour a simpler explanation for the data presented today: that we live in an era of increasing concern and awareness about food allergy, but we are not living in the midst of a food allergy epidemic. Clearly we must continue to do all we can to alleviate the burden of living with food allergy—by developing more reliable diagnostics, providing safer food choices and through more effective approaches to prevention and treatment—but overdiagnosis of food allergy or anaphylaxis does not usefully contribute to this effort and places an inappropriate burden on those who are mislabelled.

Robert J Boyle reader in paediatric allergy, National Heart and Lung Institute, Imperial College London and Centre of Evidence Based Dermatology, University of Nottingham.

Paul J Turner reader in paediatric allergy, National Heart and Lung Institute, Imperial College London.

Competing interests: We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: RJB has received payment for participating in advisory boards for DBV technologies and Prota therapeutics and has received payment for providing expert testimony in cases of food anaphylaxis and a class action related to an infant formula allergy prevention claim. PJT reports grants from JM Charitable Foundation, NIHR/Imperial Biomedical Research Centre and End Allergies Together, outside the submitted work; personal fees from UK Food Standards Agency, DBV Technologies, Aimmune Therapeutics, Allergenis and ILSI Europe outside the submitted work.


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