Prevention of Food Allergy: Harmonizing Perspectives from the East and West Open Access

Food allergy is an increasingly common condition and typically develops during childhood. It is defined as an adverse health effect arising from a specific immune response that occurs reproducibly upon exposure to a given food [1]. Food allergies are characterized by an aberrant immune response and are distinct from food intolerances, which are nonimmune reactions resulting from various mechanisms such as metabolic, toxic, pharmacological, and undefined causes [2]. A typical example of food intolerance is lactose intolerance, which is due to lactase deficiency and results in lactose malabsorption. The significance of primary prevention of food allergy lies in its potential to reduce the burden of this protracted condition, which often persists into adulthood and requires lifelong management. Moreover, food allergies carry the risk of life-threatening reactions, such as anaphylaxis, which pose significant challenges to affected individuals, their families, and healthcare systems. Effective prevention strategies can help mitigate these risks and improve quality of life.

Food allergies can be classified as IgE-mediated and non-IgE-mediated conditions [3]. In IgE-mediated allergies, foods trigger reactions through immunoglobulin E (IgE) antibodies. Initially, individuals become sensitized without symptoms, but subsequent exposure can lead to rapid reactions due to the release of histamine and inflammatory mediators from mast cells and basophils. Symptoms can affect multiple organs, including skin reactions (pruritus, urticaria), gastrointestinal manifestations (abdominal pain, vomiting), and respiratory involvement (wheezing, stridor). Importantly, individual tolerance levels vary; a small amount that triggers symptoms in one person may not have the same effect on another. Severe cases can result in anaphylaxis, a potentially fatal multisystemic reaction [4]. In contrast, non-IgE-mediated food allergies occur without the involvement of IgE antibodies. The reactions are typically delayed and manifest with gastrointestinal symptoms like bloating, diarrhea, and vomiting. The exact mechanism of non-IgE reactions is unknown.

In Westernized English-speaking countries such as the USA and Britain, the rise in food allergy was first noticeable in 1995 [5]. Since then, evidence has shown a rising trend of food allergies between 1995 and 2000. In the recent decade, the prevalence of food allergies in the West appeared to have steadied over time. Specifically, in the Isle of Wight, UK, the food allergy prevalence was recorded at 2.3% (95% CI: 1.7–3.3%) in the cohort started in 1989 and remained at 3.6% (95% CI: 2.5–5.2%) in the FAIR cohort in 2001–2002 [6]. Between 1993 and 1998, peanut allergies in 3- to 4-year-old children increased significantly from 1.3% to 3.3%. However, between 1998 and 2005, the prevalence of peanut allergy showed a nonsignificant decline to 2.0% [7]. In Australia, a population-based study in Melbourne conducted between 2007 and 2011 showed that up to 1 in 10 one-year-old children had food allergies [8]. Among these children, 3.1% (95% CI: 2.7–3.6%) suffered from peanut allergies. Children who were recruited underwent skin prick tests (SPTs) and then oral food challenges for those who had positive results. Follow-up studies conducted in 2018–2019, using the same sampling frame and methods in Melbourne, showed that the prevalence of peanut allergies was 2.6% (95% CI: 1.9–3.4%), suggesting that the prevalence of food allergies has steadied in Australia [9]. In the USA, food prevalence based on parent-reported food allergy symptoms was 8% (95% CI: 7.6–0.9%) in 2009–2010 [10]. Follow-up studies using a similar sampling frame and methodology were 7.6% (95% CI: 7.1–8.1%) in 2015–2016 [11]. Moreover, in other Westernized but non-English-speaking countries, the food-allergic population is still steadily increasing, from 0.85% to 2.8% between 2002 and 2018 in Israel [12], and from 0.325% to 0.797% between 2010 and 2019 in Japan [13]. Although these rates are rising, they remain significantly lower than those observed in the Western world, highlighting potential regional differences in environmental exposures, dietary practices, and prevention strategies.

Despite a steady prevalence of food allergy in Western countries, the rate of anaphylaxis has continued to rise since 2000. A study by Motosue et al. [14] found a 214% increase in emergency department visits for food-induced anaphylaxis (FIA) among US children from 2005 to 2014, particularly in infants and toddlers. Similarly, Mullins et al. [15] reported a 1.5-fold increase in hospital admissions for anaphylaxis in Australia between 2005–2006 and 2011–2012, especially in children under 4 years, with the most significant rise among 5–14 years old. Recent trends indicate continued increases in Australia, and the rise is most significant in children younger than 1 year old, highlighting that food allergy is still a major issue in the West [16].

Data on the prevalence of food allergies over time in the East are limited. In the Chongqing province of China, a city with a rapidly developing economy, the prevalence of food allergies increased significantly from 3.5% in 1999 to 7.7% in 2009. Follow-up studies showed a nonsignificant increase to 11.1% in 2019 [17]. However, in the more rural parts of Asia, food allergies remain uncommon. In the Chiang Mai province of Thailand, two cross-sectional studies using similar methodology revealed that the prevalence of food allergy remained at 1% in both 2010 and 2019 [18, 19]. Overall, there remain a lack of data assessing the time-trend prevalence of food allergies in Asia and the incidence of anaphylaxis in developing regions [5].

The estimation of food allergy prevalence varies widely between studies, influenced significantly by differences in methodologies. These methodological disparities can hinder direct comparisons of food allergy burden between the East and West. In Australia, a population-based cohort study found that 10% of 1-year-old infants had challenge-confirmed IgE-mediated food allergies to common allergenic foods of infancy [8]. In contrast, cross-sectional surveys in Canada and the USA reported a prevalence of approximately 7% for food allergies among children [20]. However, in the EuroPrevall-INCO cross-sectional survey of children aged 6–11 years in Asia, the prevalence of probable food allergy, defined by the presence of allergic symptoms and food-specific IgE ≥0.7 kUA/L, indicated a significantly lower food allergy burden. The prevalence was higher in Hong Kong (1.50%; 95% CI: 1.23–1.84), compared to other Chinese centers including Guangzhou (0.21%, 95% CI: 0.12–0.38), Shaoguan (0.69%, 95% CI: 0.50–0.95), Russia (0.87%, 95% CI: 0.73–1.05), and India (0.14%, 95% CI: 0.07–0.27) [21]. Compared to children born in mainland China who immigrated to Hong Kong, children born in Hong Kong had a fourfold higher risk of developing food allergies than children born in mainland China who later migrated to Hong Kong, with probable food allergy rates of 1.68% versus 0.48%, respectively. Interestingly, peanut sensitization was low across Chinese centers, ranging from 0% in Guangzhou to 2.7% in Hong Kong, while shrimp sensitization was highest in rural Shaoguan (13.1%) and India (10.3%). Similarly, findings from the GUSTO [22] study indicate that peanut allergy prevalence in Singaporean infants remains low, ranging from 0.1% to 0.3% between ages 12 and 48 months, despite the delayed introduction of peanuts in the majority of infants (88.7% introduced after 10 months) [23]. Le et al. [24] revealed that the prevalence of food allergies in Vietnam was higher in the modernized Hue City (8.4%) compared to the more rural Tien Giang province (4.96%). The South African Food Allergy research similarly reveals that urban children (2.5%) have higher food sensitization and allergy rates compared with rural children (0.5%), with livestock exposure potentially protective in rural areas [25]. These findings underscore the interplay between urbanization, environmental factors, and dietary habits in shaping the prevalence and patterns of food allergies in different regions. The relationship between genetics and the environment and their combined impact on the development of allergic diseases is a complex and rapidly evolving area of research. As some countries undergo continuous economic development, concerns arise that this rapid growth could lead to a parallel increase in the global prevalence of food allergies. Identifying and deploying effective prevention strategies are important in preparation for the rise of food allergies.

Table 1 highlights the predominant allergen triggers, illustrating notable differences between Eastern and Western regions, influenced by dietary habits and regional exposures. In Western countries, cow’s milk, peanuts, and tree nuts are the most common allergens. In contrast, Eastern regions report higher rates of seafood allergies, such as shrimp and crab, alongside common allergens like hen’s eggs, cow’s milk, and region-specific items like mango, buckwheat, and sesame. Patterns of FIA are another valuable indicator of food allergy, providing insight into which food allergens impact allergic individuals the most. In the USA, peanuts and tree nuts were the most common elicitors of FIA, leading to emergency department attendance [14]. The European Anaphylaxis Registry found that food is the major trigger of anaphylaxis [26, 27]. Cow’s milk and eggs are the most common triggers in the first 2 years of life, while tree nuts (such as cashews and hazelnuts) become more predominant in preschool-aged children. There is also a significant level of peanut-induced anaphylaxis at all ages.

This contrasts with the pattern of FIA experienced in other parts of the world. The Asia-Pacific Research Network for Anaphylaxis (APRA) highlighted the significant variation in the elicitors of FIA across regions of Asia [49]. Eggs and milk are common triggers for FIA among infants. As children grow older, shellfish become the major overall trigger of FIA in Asia. Wheat allergies were common in Thailand and Japan but relatively uncommon in other regions. Peanut and tree nut allergies were more common in Westernized cities like Singapore and Hong Kong but less prevalent in Bangkok and Qingdao (China). Shellfish-induced anaphylaxis was relatively more common in Thailand compared to other Asian regions. Bird’s nest-induced anaphylaxis, which was common in Singapore, was not evident in the latest study [50].

Peanut-induced anaphylaxis is prevalent in Europe and the USA, but data from the Latin American Anaphylaxis registry show that peanuts are not the major triggers in 12 Latin American countries and Spain [51]. Instead, milk and eggs are common significant elicitors, alongside shellfish, fresh fruits, and fish. In Portugal, cow’s milk, tree nuts, and shellfish are major FIA triggers, with peanuts accounting for only a small percentage of cases [52]. This highlights the need for tailored food allergy prevention strategies that consider regional dietary patterns and allergen variations, particularly in Asia and the Latin America.

Food allergies not only pose health risks but also create a significant economic burden at individual and household levels. A systematic review indicated that lost opportunity costs, such as missed work or activities, represent the largest financial impact averaging USD 4,881 [53]. Additionally, food allergies adversely affect the health-related quality of life across various domains, including social and psychological aspects [54]. Oral food challenges to determine the eliciting dose in children with food allergies have been shown to improve the health-related quality of life of parents [55], while oral immunotherapy has improved management strategies despite the risk of anaphylaxis [56]. Psychological interventions, such as self-regulation training and dedicated educational interventions, have also been shown to benefit the quality of life for parents with food-allergic children [57, 58].

The “dual allergen exposure hypothesis” is a concept in allergy research that proposes two critical channels of allergen exposure that influence the development of food allergies in children [59, 60]. Exposure to food allergens through the oral route (e.g., ingestion) during infancy may promote the development of oral tolerance and reduce the risk of food allergy (Fig. 1). Exposure to food allergens through the skin (e.g., in ointments, creams) during infancy, before oral exposure, may lead to sensitization and increase the risk of developing a food allergy. According to this hypothesis, the timing and route of allergen exposure in early life play a crucial role in shaping the immune system’s response, in which early oral exposure promotes tolerance, while delayed skin exposure before oral exposure may prime the immune system to overreact and develop an allergy. This hypothesis has implications for allergy prevention strategies, such as the timing of food introduction and avoidance of skin exposure to food allergens in infants. The dual allergen hypothesis is an active area of research, with ongoing studies examining the mechanisms and validity of this proposed model of food allergy development.

The Learning Early About Peanut Allergy (LEAP) study was a landmark clinical trial that explored the impact of early peanut introduction on peanut allergy development [61]. Du Toi et al. [61] recruited infants at high risk of peanut allergy and randomly assigned them to either consume peanut products regularly between 4 and 11 months of age or avoid peanuts until 5 years old. The results showed that among infants with initially negative SPTs, early peanut consumption led to an 81% relative reduction in the development of peanut allergy compared to avoidance. Among infants with initially positive SPTs, early peanut consumption led to a 70% relative reduction in the development of peanut allergy compared to avoidance. LEAP provided strong evidence that early and sustained exposure to peanuts during infancy can prevent the development of peanut allergy in high-risk children. The LEAP-On (Learning Early About Peanut Allergy – On) [62] and LEAP-Adol (Learning Early About Peanut Allergy – Adolescence) [63] studies provide additional insights into the long-term effects of early peanut introduction. After the initial LEAP study, all participants stopped consuming peanuts for 12 months. Despite this pause in peanut consumption, the protective effect against peanut allergy was maintained in the group that had been instructed to consume peanuts early, and only three children developed peanut allergy after 12 months of peanut avoidance. Children in the early peanut consumption group had consistently higher levels of peanut-specific IgG4 antibodies, which are linked to immune tolerance, and lower levels of peanut-specific IgE antibodies, which are associated with allergic responses.

Based on the same underlying principle, the prevention of egg allergy in high-risk infants with eczema (PETIT) study focused specifically on the early introduction of heated egg powder between 4 and 6 months of age in high-risk infants [64]. Natsume et al. [64] demonstrated that this early egg introduction significantly reduced the risk of developing egg allergy compared to delayed introduction. This provides further evidence that exposing infants to potential food allergens, like egg, during a critical window of immune system development can promote oral tolerance and prevent allergy. The Enquiring About Tolerance (EAT) study further examined the impact of early introduction of multiple allergenic foods, including peanut, egg, sesame, fish, cow’s milk, and wheat [65]. Infants were randomized to either introduce these foods between 3 and 6 months of age or follow standard advice to exclusively breastfeed for around 6 months. The results were mixed, with per-protocol analyses suggesting potential benefits of early, high-dose introduction of certain allergenic foods (2.4% standard vs 7.3% early), but the overall intention-to-treat analysis did not demonstrate efficacy 7.1% vs 5.6%). Early introduction of multiple allergenic foods was not easily achieved but was safe, and its effect on the prevention of food allergy may be dose-dependent.

Recent studies have investigated the relationship between breastfeeding duration, the timing of cow’s milk formula (CMF) introduction and the development of cow’s milk allergy (CMA) in infants. A retrospective evaluation of a nationwide population-based cohort in Japan found that exclusive or extended breastfeeding was linked to a higher risk of food allergies in children without eczema [66], and may reduce breastfeeding’s protective benefits, even for some with eczema. However, parental reports on food allergy and breastfeeding could introduce bias. Consistent findings from other studies indicated that infants exclusively breastfed or receiving a combination of breastfeeding and CMF had a higher rate of IgE-mediated food allergy compared to those fed only CMF [67]. This may be due to components in mature breast milk or to behavioral habits, such as delays in introducing allergenic foods due to exclusive or extended breastfeeding. Research by Katz et al. [68] showed that introducing cow’s milk protein within the first 14 days significantly lowered (0.05%) the cumulative incidence of CMA compared to those introduced between 105 and 194 days (1.75%). Infants exposed to cow’s milk protein at 15 days or later faced a 19.3 times higher risk of developing CMA. Early exposure to CMF is associated with a lower risk of cow’s milk sensitization, parent-reported reactions, and allergy at 12 months [69, 70]. These observations collectively suggest that the timing of breastfeeding and CMF introduction plays a crucial role in the development of CMA, highlighting the need for careful dietary management in infants.

Sakihara et al. [71], involving 491 infants in an RCT, demonstrated that those receiving ≥10 mL/day of CMF intake, in addition to breastfeeding between 1 and 2 months of age, had a CMA rate of 0.8%, compared to 6.8% in the avoidance group. A recent trial involving 1,992 Israeli newborns found that early, consistent exposure to CMF from birth significantly reduces the risk of developing IgE-mediated CMA, with no cases observed in infants receiving daily CMF [72]. In contrast, the relative risk of developing CMA was 29.98 (p < 0.001) for infants exclusively breastfed, with a prevalence of 1.58% compared to 0% in the CMF-exposed group, and occasional CMF exposure increased the risk of CMA. On the other hand, Urashima et al. [73] examined the risk of cow’s milk sensitization and allergic disease in high-risk infants (defined as having a family history of atopic disease) who were supplemented with either CMF or an amino-acid-based formula (AAF) during the first 3 days of life, without ongoing exposure. Sensitization to cow’s milk, indicated by IgE levels of 0.35 allergen units/mL or higher, was found in 16.8% of the AAF group compared to 32.3% in the CMF group. Additionally, the prevalence of food allergies by the second birthday was significantly lower in the AAF group (2.6%) versus the CMF group (13.2%). The findings highlighted that consistent daily CMF exposure is essential for prevention, as intermittent exposure may increase the risk of IgE-mediated CMA.

In murine models, early immune education from diet and commensals has also been shown to be critical for establishing durable immune tolerance later in life [74]. Microbial colonization occurs in the immediate postnatal period, with dynamic changes in diversity reaching equilibrium by the first few years. This triggers a “weaning reaction” involving a surge in Clostridiales species that induces RORγt+ Treg cells, conferring protection against gut pathologies. Disruption of this critical neonatal window, such as by antibiotics or dysbiosis, can lead to pathological imprinting of the immune system. The infant gut microbiome gradually transits from a Bifidobacteria/Lactobacillus-dominated phase to a Clostridiales/Bacteroidales-dominated “weaning reaction” with a transient proinflammatory wave. Analyses from the EAT study found that infants in the early introduction group showed greater microbial diversity at 6 months and exhibited distinct shifts in their microbiota, including increased levels of Prevotella, Escherichia/Shigella, and certain Firmicutes genera like Paraprevotella [75]. These changes were transient, as both groups eventually converged toward Bacteroides-rich communities by 12 months, suggesting that early allergenic food exposure leads to short-term alterations in the gut microbiota, including within Firmicutes, which may influence immune development. Overall, the research suggests that exposing infants to potential food allergens in a timely manner, rather than delaying introduction, can induce beneficial changes in the infant gut microbiome, promote oral tolerance, and reduce the risk of food allergy later in childhood.

Through the EAT study, investigators explored whether regular moisturizer use in infancy could increase the risk of developing food allergy, based on the hypothesis that this could promote transcutaneous allergen sensitization [76]. The study found a statistically significant dose-response relationship between the frequency of parent-reported moisturizer use at 3 months of age and the subsequent development of food allergy by 36 months. Specifically, each additional moisturizer application per week, predominantly food-derived oils, was associated with a 20% increase in the adjusted odds of developing food allergy. This association was observed in both infants with no visible eczema and those with eczema at enrollment.

The Barrier Enhancement for Eczema Prevention (BEEP) RCT was conducted in the UK to determine if daily emollient application in the first year of life could prevent eczema and other atopic diseases in high-risk infants [77]. A total of 1,394 infants at high risk of developing eczema were randomized to either apply emollient daily for the first year (plus standard skin care advice) or receive standard skin care advice only. At 2 years, there was no significant difference in eczema rates between the emollient and control groups, while the compliance was fair (74% at 12 months). Additionally, there was some indication that emollient use may be associated with an increase in skin infections.

On the other hand, a protective effect was observed when a specific emollient was used. In 2014, two RCTs discovered that daily full-body emollient use in newborn infants at high risk for atopic dermatitis (AD) significantly reduced the incidence of AD by 50% [78] and 32% [79]. In the trial by Horimukai et al. [79], a higher percentage of infants with AD at 32 weeks showed allergic sensitization, indicated by egg white-specific IgE levels, compared to those without AD (p = 0.043) in the post hoc analysis. The odds ratio for sensitization in infants with AD was 2.86 (95% CI: 2.22–6.73). Using a ceremide-based emollient, the Prevention of Eczema By a Barrier Lipid Equilibrium Strategy (PEBBLES) study showed a nonsignificant trend toward reduced AD and food sensitization at 6 and 12 months [80]. However, in the per-protocol analysis, infants who applied emollient at least 5 days per week showed a significant reduction in food sensitization at 12 months in the treatment group. In an Irish study, high-risk newborns were randomly assigned to receive either twice-daily whole-body emollient application for the first 8 weeks of life or standard skin care [81]. Among 321 infants, the cumulative incidence of AD at 12 months was 32.8% in the intervention group vs. 46.4% in the control group (p = 0.036), indicating a 29.3% relative risk reduction. There was no significant difference in skin infection between the groups, but the study was not designed to assess food allergy risk reduction.

This evidence supports that early and regular skin care, particularly through the application of specialized emollients, can significantly reduce the incidence of AD and potentially mitigate the risk of developing food allergies. By prioritizing skin health from infancy, we can take a proactive step in protecting our children from the burdens of food allergies.

Evidence suggests that skin inflammation plays an important role in the development of further allergic disease. A retrospective study showed that early aggressive topical corticosteroid (TCS) treatment with proactive maintenance reduced food allergy development in AD infants compared to delayed treatment [82]. In a subgroup analysis, 84% of egg white-sensitized infants in the early treatment group, compared with 60% in the delayed treatment group, did not develop an egg allergy. A subsequent multicenter randomized controlled trial of 650 infants (7–13 weeks old) with AD demonstrated enhanced early TCS treatment significantly reduced hen’s egg allergy compared to conventional treatment (31.4% vs 41.9%, p = 0.0028) [83]. However, the enhanced treatment protocol was associated with reduced infant growth. Alternative maintenance approaches using lower potency TCS or other topical treatments, such as topical calcineurin inhibitors, could be considered instead [84, 85].

Food allergies pose a significant lifelong burden, as they often persist throughout an individual’s lifetime and currently lack effective curative treatments. With the high risks associated with interventions like oral immunotherapy, primary prevention of food allergy development emerges as a crucial strategy. Preventing food allergies can mitigate the growing prevalence of food allergies, avoid the constant threat of life-threatening reactions, enhance the quality of life, and reduce the substantial healthcare costs involved in managing these chronic conditions. Investing in evidence-based primary prevention should be a top priority to address this pressing health challenge.

Clinical practice guidelines (CPGs) provide evidence-based recommendations to standardize and optimize clinical practice, leading to more consistent, high-quality care [86]. However, the evidence base for many allergy prevention recommendations is heterogeneous, with some being specific to certain populations or evolving as new data emerge. A systematic review assessed the quality and consistency of recommendations in CPGs, as well as the implementability of these guidelines across various geographical settings, for the primary prevention of food allergy and AD [87]. Of the 30 CPGs, only 8 (27%) met the predefined quality criteria based on the AGREE II instrument, while the rest lacked clarity in scope and rigor in development (online suppl. Table 2; for all online suppl. material, see https://doi.org/10.1159/000543617). Notably, even among the high-quality CPGs, the overall quality did not strongly align with global applicability.

Allergy prevention guidelines need to be carefully adapted to the local context, taking into account the regional patterns of food allergy prevalence, cultural norms, and dietary preferences. Online supplementary Table 1 highlights the differences in prevention guidance between the East and West. The differences in food allergy prevention guidance between the East and West primarily stem from the varying prevalence of food allergies in infants. In the West, where food allergies are more common, there is often no clear distinction between “normal risk” and “high-risk” infants. As a result, prevention strategies are applied more universally, regardless of an infant’s risk level. In contrast, in the East, where the prevalence of food allergies is lower, the distinction between normal and high-risk infants is more pronounced. This leads to tailored prevention strategies that are more focused on high-risk infants. The recommendations for the early peanuts introduction from the USA and Canada may not be well suited or directly applicable to countries in Asia and Latin America, where peanuts are less common triggers for allergies [88]. The prevalence and specific allergens vary greatly by region, and early peanut introduction may not fit traditional feeding practices in these areas. A one-size-fits-all approach, based on one region’s guidelines, may not be effective elsewhere. Figure 2 summarizes the current recommendations for primary prevention of food allergy.

The evidence supporting many allergy prevention recommendations is continually evolving as new data become available, so healthcare professionals must stay informed and up to date. Early studies suggested the benefits of partially hydrolyzed formulas, but later trials and meta-analyses did not support this, leading many CPGs to remove this recommendation. Findings on probiotics, vitamin D, and emollient use for allergy prevention have been mixed, leading to heterogeneous recommendations in CPGs. Only recommendations on maternal diet and complementary feeding were fairly consistent across CPGs, but there come the issues with global applicability. In areas with a high prevalence of food allergies, peanuts and eggs, in an age-appropriate form, should be introduced around 6 months of age, but not before 4 months. [88‒90]. Other allergens should also be introduced around the same time. In regions with a more diverse food allergy profile, such as Asia, recommendations suggest non-delayed introduction of allergens as part of complementary feeding in at-risk infants [91]. There is currently low certainty of evidence, suggesting the avoidance of CMF supplementation in breastfed infants during the first week of life [89]. Recently, the Canadian Paediatric Society (CPS) recommended early and regular consumption of CMF to prevent CMA [92]. While the CPS suggests a daily intake of just 10 mL of CMF based on RCTs, this poses practical issues such as formula wastage, costs, and the effects on breastfeeding, particularly for low-risk infants. To address these concerns, three alternative strategies are put forward: exclusive breastfeeding, using extensively hydrolyzed formula for occasional supplementation (but not partially hydrolyzed formula), and ensuring regular servings of CMF (such as “one bottle per day”) once CMF has been introduced in an infant’s diet. Table 2 summarizes a streamlined version of the more universally accepted recommendations for food allergy prevention, with target and timing references, offering a practical guide for front-line healthcare providers.

In Western countries, despite the stabilizing food allergy prevalence after 2020, the incidence of anaphylaxis continues to rise steadily. The situation in the developing regions is more heterogeneous, as there are generally a lack of reliable data on the time-trend prevalence of food allergies and the incidence of anaphylaxis worldwide. The variation in regional food allergens and dietary patterns across the globe necessitates that food allergy prevention measures be tailored and modified according to the specific needs and characteristics of individual regions.

The prevention of food allergies currently focuses on the timing and route of allergen exposure in early life, which is crucial in children’s allergy development. Current guidelines recommend early oral exposure to food allergens in high-prevalence areas to promote oral tolerance, while non-delayed introduction of allergenic solids is advised in regions with lower prevalence. Early skin exposure may increase allergy risk, but early use of specialized emollients may reduce AD incidence in high-risk infants. Further evidence is needed to determine if this approach reduces food sensitization and allergy development. Overall, guidelines should be robust, adaptable to different contexts, and continuously updated to reflect the latest available evidence. Importantly, prevention approaches should be personalized based on individual and population-level factors, and a multifaceted approach combining various strategies may be most effective in preventing the development of food allergies.

The authors thank Ms. Vanessa Tang and Ms. Ann Au for their assistance in the preparation of the figures included in this review.

ASYL received funding from the Research Grants Council (Ref. Nos. GRF 14111223 and ECS 24109922), Health and Medical Research Fund (Ref. No. 11220346), Direct Grants for Research (2024.123), SKLMP Seed Collaborative Research Fund (2023), and Hong Kong HOPE Seed Funding (2023); and received honorarium as an associate editor of Pediatric Allergy & Immunology, consultancy fee as PCV20 Paediatric Advisory Board member, and speakers’ fee from Danone. GWKW received funding from the T.S. Lo Foundation.

This article was not supported by any sponsor or funder.

A.S.Y.L. and G.W.K.W. were responsible for the concept of this article. All authors were responsible for drafting and revision of the final paper.