Food allergy overview

Anxiety triggers in food allergy

Our patient-focused animation highlights several triggers that may exacerbate the anxiety of both parents, and their children with food allergies. Triggers include social events and the potential of having to use an autoinjector, should accidental exposure occur. The animation also highlights several resources for autoinjector use, along with other useful links aimed at helping improve the overall mental health of individuals concerned with food allergies, in part by alleviating such anxiety and stress.

Download all of the resource links from the animation video, as vetted and recommended by Dr Sharon Chinthrajah

How does food allergy impact children and adolescents?

In a study of 150 children (0–12 years) and 24 teenagers (13–17 years), food allergies were found to have a greater impact in adolescents than younger children in terms of emotional, dietary, and social quality of life².

Specifically, the median Food Allergy Quality of Life Questionnaire (FAQLQ) score was shown to be significantly higher in adolescents compared with children (4.7 vs 3.5, P=0.007), highlighting a lower quality of life (Figure 1)².

Figure 3. Food Allergy Quality of Life Questionnaire (FAQLQ), Emotional Impact (EI), Food Anxiety, and Social and Dietary Limitations (SDL) scores from childhood to adolescence (Adapted²).

Adolescents also had a higher median social and dietary limitations (SDL) score (5.2 vs 4.0, P=0.002) and median emotional impact (EI) score (3.8 vs 3.1, P=0.02) than children. Food anxieties in children were also seen to be rising, with a median Food Allergy Quality of Life Questionnaire (FAQLQ) score increase of 0.18 points (95% CI, 0.12–0.26) per year².

The study also found that the impact on family activities due to food allergy also lowers the quality of life and well-being of all family members².

However, studies have found that oral immunotherapy (OIT) and the oral food challenge (OFC) are associated with improvements in health-related quality of life³. In a meta-analysis of 13 publications, a mean change of –1.25 (P<0.001) and –0.78 (P=0.052) was observed in health-related quality of life scores following OIT and OFC, respectively³.

Moreover, five OIT studies demonstrated significant health-related quality of life improvements with OIT compared to placebo, with an overall standardized mean difference of –0.56 (P=0.007)³.

Bullying and food anxiety

Food anxieties and bullying can have a large impact on the quality of life of children and adults living with food allergies.

Bullying

In a survey of 353 food-allergic children and adults, 24% stated they were harassed because of their food allergy⁴. The most common site of bullying was at school, with 82.4% facing bullying, teasing, or harassment from classmates. Moreover, 21.4% of students reported that teachers and school staff were also perpetrators of bullying⁴.

In a study of school teachers, only 4% (N=203) claimed to have personally witnessed or known about bullying towards food-allergic school children, and 99% underestimated the frequency of bullying directed against food-allergic students⁵.

Food anxiety

Excessive anxiety of children or parents can result from a persistence of unnecessary and unhelpful avoidance of certain foods as a coping strategy to alleviate the distress associated with food allergies⁶. While avoidance of low-risk situations can lead to temporary  symptom relief, it can inadvertently drive an increase in anxiety via negative reinforcement (Figure 4)⁶.

Figure 4. Escalating avoidance-anxiety cycle in children with food allergy and caregivers (Adapted⁶).

This negative reinforcement can be further compounded by a perception of effectiveness due to the avoidance of an anaphylactic reaction, even to the detriment of daily functioning. This flawed risk assessment grows increasingly burdensome, requiring a high level of vigilance to maintain this level of avoidance⁶.

What is the burden of food allergy on caregivers and families?

Food allergies can cause emotional distress among families and caregivers, even prior to receiving a definitive diagnosis, due to limited guidance, lack of access to an allergist, and avoiding multiple suspected allergens¹.

Accurate diagnosis is essential, as false positives can lead to unnecessary elimination of safe food, unjustified nutritional deficiencies, and impact on quality of life⁷

In a quantitative cross-sectional study, 150 parents completed validated questionnaires measuring quality of life, anxiety, depression, and stress. Parents of children with food allergies were shown to have higher stress, anxiety, and depression compared to healthy controls (all P<0.05). This is regardless of whether the food allergy was a medically diagnosed allergy (MA) or parent-diagnosed allergy (PA)⁸.

Increased levels of anxiety may have been due to uncertainty about the medical diagnosis or lack of suitable information from healthcare professionals. Greater levels of depression among parents of children could be a result of internalising the life-threatening risks of food allergies, for which there is currently no cure⁸.

Global prevalence of food allergies

Current estimates of food allergy prevalence vary due to differences in age, geographic location, study methodologies, and awareness of food allergies^9,10. However, food allergies are widely considered to be common and are continually increasing in prevalence².

International population-based estimates of paediatric food allergy prevalence (Figure 1) can provide valuable insights into the disease burden⁹.

Figure 1. Population-based estimates of current paediatric food allergy prevalence in various countries around the world (Adapted⁹).

In Europe, it is estimated that approximately 11–26 million people have food allergies¹¹. If this were projected onto the global population, it would translate into an approximate global prevalence of 240–550 million food-allergic people¹¹. A particular concern is also the incidence of food allergy in young children, which is estimated to be greater in toddlers (5–8%) than adults (1–2%)¹¹.

The United States shows similar rates of food allergies. In a population-based cross-sectional prevalence study of over 50,000 households, 10% of the US population was shown to be affected by at least one immunoglobulin E (IgE)-mediated food allergy¹².

However, cross-sectional prevalence surveys may overestimate food allergy prevalence¹³. Epidemiological studies that provide clinical confirmation through oral food challenges are more accurate, although these can be expensive and logistically challenging. Moreover, while such studies exist, they can lack consistent or standardised criteria for defining outcomes¹⁴.

Why is the natural history of food allergy important?

Not all allergies are the same in terms of their likelihood to resolve. Food allergies can differ in being either persistent or transient with the loss of the same food allergy over time.

Join Professor Alexandra Santos and find out why it is essential to understand the differences in natural history and how this can impact the management of food allergies in children.

Are there racial differences in food allergy burden?

Racial and socioeconomic disparities have been observed in the prevalence of food allergies⁹. An understanding of the aetiology of these disparities may help identify ways to reduce the inequalities and potentially eliminate them.

In a US population-based cross-sectional prevalence survey, significant differences in food allergy prevalence were observed in ethnic groups: asian (11.4%), black (11.2%), hispanic (11.6%) and other non-white people (15.9%) all had a higher prevalence than white non-hispanic (10.1%) people (P<0.001)¹².

Infants of Black race (predominantly UK Afro-Caribbean or African) are associated with a higher risk of peanut-specific IgE sensitisation than White infants¹⁵

The Learning Early About Peanut Allergy (LEAP) screening study, a large randomised controlled trial in the United Kingdom, highlighted racial differences in the prevalence of food allergy. With the original aim to characterise the population and screen for the risk of peanut allergy, the LEAP screen study showed that infants of black race (predominantly UK Afro-Caribbean or African) were associated with a significantly higher risk of peanut-specific IgE sensitisation than white infants (OR, 5.30 [95% CI, 2.85–9.86])¹⁵.

The HealthNuts study demonstrated that Asian infants born in Australia had a higher rate of peanut allergy with one (6.7%) or both (7.7%) parents born in East Asia, compared to infants with both parents born in Australia (2.3%, P<0.001)¹⁶. This was also observed in a later Australian study that found Australian-born Asian children to have higher rates of food allergy and anaphylaxis¹⁷.

How does the environment impact food allergy risk?

There is currently no clear evidence that genes drive racial and ethnic health disparities¹⁸. However, there are clear racial and ethnic differences in socioeconomic and environmental factors, such as poverty, education, healthcare access, and pollutant exposure¹⁸.

These environmental influences may be more important in determining the risk of atopy than ethnicity. In a high-quality unselected cohort study from South Africa, food sensitisation and allergy among urban South Africans of white (3.5%), mixed (4.2%), and black race (3.6%) were seen to have similar rates¹⁹. However, only 0.5% (95% CI, 0.1–1.8%) of rural black African children had a food allergy, compared to 2.5% of the overall urban cohort and 2.9% of urban black Africans (95% CI, 1.5–4.3%; P=0.006)¹⁹.

How are food allergies defined?

Guidelines broadly divide adverse reactions to food into immune mediated and non-immune mediated (Figure 2). Immune mediated adverse reactions are further subdivided into IgE-mediated, non-IgE-mediated, or mixed IgE- and non-IgE-mediated^21,22.

Figure 2. Classification of adverse food reactions: Immune-mediated and non-immune-mediated mechanisms (Adapted²¹).

When consuming foods, antigens present on food normally induce an antigen-specific immune unresponsiveness known as oral tolerance²³. Food allergies occur when oral tolerance to one or more dietary antigens does not develop²³. Adverse reactions to foods or food components that do not utilise known immunologic mechanisms are considered food intolerances²¹.

What are the most common food allergens?

In IgE-mediated food allergies, exposure to a specific antigen in a trigger food will induce immediate and reproducible effects in the gastrointestinal tract, skin and/or respiratory system²⁴. This requires prior food allergen sensitisation, and the development of a serum-specific IgE antibody to the food allergen.

While any protein can theoretically cause this sensitisation, according to the United States Food and Drug Administration (USFDA), 90% of allergic reactions are attributable to nine major food groups²⁵:

• Milk
• Eggs
• Fish
• Crustacean shellfish
• Tree nuts
• Peanuts
• Wheat
• Soybeans
• Sesame (to be included in 2023)

However, the most common food allergens differ around the world, possibly due to varying cultural dietary practices²⁶. For example, peanut allergy is very uncommon in Asia (excluding Japan)²⁷ while a predominate allergy in the United Kingdom, United States, and Australia, particularly in children less than 5 years of age¹³.

In Thailand, Japan, and Korea, wheat, egg, and milk are becoming the most common food allergens in childhood²⁸. In other parts of Asia, shellfish is a leading cause of food allergy in adolescents and adults²⁹.

Differences in prevalence across the globe may be attributed to variances in cultural dietary habits, such as early food introduction, as well as differences in food processing, skin care, and other cultural practices^29,30. More research is ongoing to understand the factors that are critical in the development of food allergy³⁰.

What are the symptoms of food allergy?

Following exposure to a trigger food, the symptoms of food allergy normally begin within minutes. This triggering of symptoms most often occurs within two hours of exposure in an an IgE-mediated response²⁴. However, the timing of this reaction may be influenced by various co-factors, including alcohol consumption, physical exercise, and the specific medications³¹.

α-Gal syndrome is also an exception. The sensitisation associated with this condition is initially triggered through tick bites, such as the lone star tick. Reactions can then occur within 2–6 hours after eating meat of mammalian origin³².

While symptoms vary between different instances of exposure, there can be any combination of oral dermatological, gastrointestinal, and respiratory symptoms (Table 1)²⁴.

Table 1. Clinical features of IgE-mediated food allergy (Adapted²⁴).

The most common effects are cutaneous, which are found in 80% of food allergy cases²⁴. Gastrointestinal symptoms can occur through immediate gastrointestinal hypersensitivity; respiratory symptoms normally occur as part of a generalised reaction. While isolated respiratory symptoms within the period of food ingestion of a known allergen can be suggestive of food allergy, isolated respiratory symptoms outside of this period may prompt a reconsideration of the food allergy diagnosis²⁴. In more severe reactions, the systemic effects of food allergy can lead to fatal anaphylaxis²⁴.

There are also various specific clinical syndromes associated with food allergy. These include:

Food-induced anaphylaxis: In more severe reactions, food allergy can lead to fatal anaphylaxis. Typically, IgE-mediated food-induced anaphylaxis involves systemic mediator release from sensitised mast cells and basophils²¹.

Eosinophilic esophagitis: Food allergy can also cause a chronic, immune/antigen-mediated oesophageal disease characterised by eosinophil-predominant inflammation and oesophageal dysfunction²².

How do genetics affect food allergy?

Two notable twin studies examined heritability in families and have shown a genetic component to food allergy^35,36.

The first study of 14 monozygotic and 44 dizygotic twins demonstrated a significantly higher concordance for peanut allergy among monozygotic (64.3%) twins compared to dizygotic (6.8%) twins (P<0.0001)³⁵. The overall heritability of peanut allergy was found to be 81.6% (95% CI; 41.6–99.7%) in a study where food allergy was assessed with a clinical history and a positive skin prick test (SPT) and/or peanut-specific IgE³⁵.

Extensive studies have identified an association between a heterogeneous and complex set of genetic mechanisms and the development of food allergy³³

A further study with 472 monozygotic and 354 dizygotic twins examined the rates of sensitisation³⁶. Concordance rates for sensitisation were similarly shown to be much higher in monozygotic (52.1%) than in dizygotic twins (39.2%), with concordance rates higher among monozygotic twins sensitised to peanut (53% vs. 29%, P=0.002) and shellfish (58% vs. 45%, P=0.08) than dizygotic twins³⁶. Estimated heritability to allergen sensitization ranged from 51% (95% CI, 0.34–0.66) to 68% (95% CI, 0.58–0.76)²⁸.

However, there was discordance in the data between numerous twin pairs, suggesting that environmental factors, in addition to genetics, play a significant role in the development of food allergy³⁶.

How does the environment in early life impact the risk of food allergy?

Mothers not only provide 50% of their genes to their baby, but they also provide a specific environment in which the baby lives for the first nine months. Following birth, mothers continue to have a major influence on the environment of the baby, especially while breastfeeding³⁷.

Research has shown that early food introduction of potentially allergenic foods may decrease the risk of developing food allergies, and that protein transfer via breast milk is an important method of initial exposure to food³⁸

Different factors in breast milk can confer a passive immunity to a new-born infant. The processing of various proteins in the gastrointestinal tract from the maternal diet will determine the specific proteins and/or peptides that are in the mother’s milk³⁹. In addition to other immunomodulatory components, such as oligosaccharides or immunoglobulins, these proteins and/or peptides influence whether an allergic response will develop in the breastfed infant³⁹.

Currently recommendations from the World Health Organisation (WHO) and the American Academy of Paediatrics (AAP) recommend initiating breasting feeding within the first hour of birth and exclusively breastfeeding infants for the first 6 months of life^40,41.