ABSTRACT
Food allergies are increasing globally, particularly in Asia; however, the etiologies of allergic diseases remain poorly understood despite comprehensive studies conducted across a variety of populations. Epidemiological research demonstrates that food allergy is more prevalent in Westernized or urbanized societies than in rural or developing ones. As such, comparing the distribution and patterns of food allergies as well as the environmental exposures between regions may provide insight into potential causal and protective factors of food allergy. Diet is an important exposome that has been shown to modulate the immune system both directly and indirectly via pathways involving the microbiota. Changes in dietary patterns, especially the shift to a Westernized diet with reduced dietary fiber and an abundance of processed foods, impact the gut and skin epithelial barrier and contribute to the development of chronic inflammatory diseases, such as food allergy. Although dietary intervention is believed to have tremendous potential as a strategy to promote immunological health, it is essential to recognize that diet is only one of many factors that have changed in urbanized societies. Other factors, such as pollution, microplastics, the use of medications like antibiotics, and exposure to biodiversity and animals, may also play significant roles, and further research is needed to determine which exposures are most critical for the development of food allergies.
Keywords: emulsifier, epithelial barrier, fiber, food allergy, modernization, nutritional transition, SCFA, ultra‐processed foods
Abbreviations
- AGEs
advanced glycation end products
- ALADDIN
Assessment of Lifestyle and Allergic Disease During Infancy
- aOR
adjusted odds ratio
- APRA
Asia‐Pacific Research Network for Anaphylaxis
- CAGR
compounded annual growth rate
- COCOA
COhort for Childhood Origin of Asthma and allergic diseases
- EAACI
European Academy of Allergy & Clinical Immunology
- FA
food allergy
- FPIES
food protein–induced enterocolitis syndrome
- HDACs
histone deacetylase
- HK
Hong Kong
- LMIC
low‐ or middle‐income country
- n‐3 LC‐PUFA
n‐3 long‐chain polyunsaturated fatty acid
- ORs
odds ratios
- OVA
ovalbumin
- PARSIFAL
Prevention of Allergy Risk factors for Sensitization In children related to Farming and Anthroposophic Lifestyle
- PIFA
prevalence of infant food allergy
- SCFAs
short‐chain fatty acids
- SDS
sodium dodecyl sulfate
- TCD
traditional Chinese diets
- UK
United Kingdom
- UPFs
ultra‐processed foods
- US
United States
1. Introduction
The prevalence of food allergy (FA) has been steadily increasing in many parts of the world, including Asia [1]. As we enter the Anthropocene Epoch—a geological period defined by the transformative impact of human activities such as industrialization, pollution, deforestation, and species extinction—key environmental factors such as diet, allergens, and microbiota are also being reshaped, altering the host–environment interaction [2]. Notable markers such as elevated carbon dioxide levels and synthetic materials embedded in geological records further highlight the distinctions of this era [3]. One key gap in our understanding of FA pathophysiology is the complex interplay between genetic and environmental factors. Although certain genetic variants may confer increased susceptibility to developing FA, the specific gene–environment interactions that trigger the onset and progression of these conditions are not fully elucidated. This lack of knowledge hinders the development of targeted preventive strategies and personalized treatment approaches.
The process of modernization leads to the loss of protective factors that are commonly associated with traditional rural settings. Conversely, it brings about the emergence of risk factors that are correlated with modern urbanized living. Asia, as an incredibly diverse continent with significant economic disparities, has led to varied lifestyles and dietary patterns across the region, resulting in diverse patterns of FA and anaphylaxis in Asia. Approximately 2500 years ago, Hippocrates introduced the idea that “food is medicine,” declaring “Let food be thy medicine and medicine be thy food.” It is crucial for researchers to investigate the complex relationship between diet and the prevalence of food allergies in the region.
This review aims to dissect the epidemiological link between dietary patterns and FA prevalence, contrasting the trends observed in the West versus the East. It provides background on the global nutritional transition and how the processes of modernization in the East have impacted local dietary habits and the corresponding FA landscapes. The review will delve into the relationship between diets and the epidemiology of FA, highlighting the protective role of dietary fiber and the potential risks associated with processed foods, and discuss how changes in the epithelial barrier function related to emulsifiers in ultra‐processed foods (UPFs) may contribute to increased FA risk.
Understanding the dynamic interplay between dietary patterns and the emergence of food allergies in Asia can provide valuable insights for developing targeted prevention and management strategies. Collaborative research efforts, involving epidemiological studies and mechanistic investigations, are necessary to elucidate the complex relationship between diet, the gut microbiome, and the immune responses underlying food allergies in this diverse and rapidly evolving region.
2. Heterogeneity of FA and Anaphylaxis in Asia
Between 1990 and 2000, food allergies significantly increased in Western countries but have remained stable over the past two decades [4]. In the Isle of Wight, United Kingdom, peanut allergy prevalence increased from 1.3% to 3.3% between 1993 and 1998, but remained at 2% in 2005 [5, 6].
In Australia, two cohort studies indicated that the prevalence of peanut allergy remained stable at around 3% between 2007–2011 and 2018–2019 [7, 8]. This stability contrasts with earlier increases in peanut allergy prevalence observed in other regions and suggests that the rates may have plateaued rather than continued to rise. In contrast, the prevalence of FA in China appears to be rising in the past decade [9]. The rise was, however, not homogeneous across Asia. In rural parts of Thailand, FA remains uncommon over time [10]. Figure 1 illustrates the changing prevalence of FA between Eastern [11] and Western [12, 13, 14] regions over time.
FIGURE 1.

The changing prevalence of food allergies in eastern and western regions over time. In Japan, the overall prevalence of food allergies increased from 0.325% in 2010 (95% CI, 0.311–0.339) to 0.797% in 2019 (95% CI, 0.790–0.804) [11]. For peanut and tree nut allergies among children under 18 years, the prevalence rose from 0.6% in 1997 to 1.2% in 2002, reaching 2.1% in 2008 in the United States [12]. Additionally, studies by Gupta et al. indicated that the prevalence of peanut allergies was 2.0% in 2011 (95% CI, 1.8–2.2) and increased to 2.2% in 2018 (95% CI, 2.0–2.5) [13, 14].
The incidence of anaphylaxis serves as a useful marker of FA burden. A systematic review of 59 pediatric studies found that food‐induced anaphylaxis rates ranged from 1 to 77 per 100,000 person‐years globally, with 19 studies indicating an upward trend over time [15]. The incidence varied significantly by study and region, with Asia reporting lower rates of both total and food‐induced anaphylaxis compared to other areas. However, the review's findings were limited by underrepresentation of studies from developing countries, differing methodologies, and high heterogeneity among the studies. Recent data from the Asia‐Pacific Research Network for Anaphylaxis (APRA) shed light on food anaphylaxis patterns across Asia [16]. A pediatric anaphylaxis registry established between 2019 and 2022 captured 721 episodes from locations including Hong Kong (HK), Qingdao, Singapore, Bangkok, and Nakhon Nayok. Food was the most common trigger, accounting for 62% of cases among children under 18. Specific triggers varied by country: eggs and cow's milk were predominant for children under three, whereas shellfish was most common for those aged seven and older. Nut allergies were more common in HK and Singapore, whereas wheat allergies were more prevalent in Bangkok. Although peanut allergies were less prevalent in HK and Singapore [17, 18], peanuts were the leading cause of food‐induced anaphylaxis in older children, likely due to their potential for severe reactions and their presence in various Asian dishes [19]. In Japan, early onset tree nut allergies, particularly to walnuts, are on the rise [20, 21]. Current limitations include the reliance on self‐reported data for most prevalence studies on FA in Asia. Few studies are based on challenge‐proven outcomes, and even fewer are time‐trend studies.
Since the 2017 international consensus guidelines for food protein–induced enterocolitis syndrome (FPIES) [22], cases have increased in Europe, the United States, Australia, Israel, Japan, and Korea [23]. The first cases of milk‐induced FPIES were documented in 1967, followed by rice‐induced cases in 1963 and egg‐induced cases in 1984. Common triggers now include milk, soy, egg, rice, and fish [24]. Although FPIES remains rare, with a prevalence of 0.015%–0.7% [24], there is preliminary evidence of a rising trend [25], particularly in egg‐induced cases in Japan and emerging peanut‐induced cases in the United States [26, 27, 28]. The epidemiology of FPIES and other non‐IgE–mediated gastrointestinal allergies in Asia, however, remains unclear.
Overall, the global prevalence and pattern of FA, whether IgE or non‐IgE mediated, are constantly evolving. Recent evidence suggests that the prevalence of IgE‐mediated FA may be rising in the developing regions, although the pattern is highly heterogeneous across Asia. In contrast, non‐IgE–mediated FA is rising in Westernized countries. Although the West generally supports the early introduction of allergenic solids, including peanuts [29, 30, 31], this approach may not be as relevant in the East [32], where the background prevalence of peanut allergies is much lower. Culturally, peanuts are not commonly used as first complementary foods in many Asian countries [33]. Moreover, evidence from Asian cities like Singapore indicates that despite the delayed introduction of peanuts, the prevalence of peanut allergies remains low [18]. This suggests that different dietary practices and cultural contexts may play a significant role in the development of food allergies in these regions.
3. The Relationship Between Diet and FA
3.1. Relationship Between Dietary Fiber and FA Protection
Urbanization and Westernized diets are believed to be major factors driving the disparity between the East and the West. Previous articles have summarized in detail the differences in the pattern of FA and anaphylaxis between the East and the West [34]. We propose that leveraging the modifiable nature of dietary habits is key to addressing the growing FA crisis and improving outcomes through region‐specific, evidence‐based approaches.
Early observational studies found that an anthroposophic lifestyle, characterized by a vegetable‐rich diet and reduced use of antibiotics, may lower the incidence of allergic sensitization in children from these families. The PARSIFAL study compared farm children and those from anthroposophic families, finding a reduced prevalence of allergic symptoms and sensitization in both groups, although the difference was less consistent in the anthroposophic group. The ALADDIN birth cohort study further demonstrated that children from anthroposophic households had a significantly lower risk of atopic sensitization during the first 2 years of life compared to those from non‐anthroposophic families [35]. The anthroposophic diet, similar to a Mediterranean diet, was identified as a potential contributing factor, although other aspects of the lifestyle, such as restricted vaccinations and antibiotics, may have also played a role. Moreover, these studies only demonstrated differences in atopic sensitization and not in the prevalence of FA specifically. In a longitudinal prospective cohort study conducted in the United Kingdom, the Prevalence of Infant Food Allergy (PIFA) study found that a high‐vegetable, fruit, and home‐cooked infant diet is related to a reduced risk of FA by 2 years of age [36]. A recent pre‐birth cohort study, Healthy Start in the United States, involving 1410 mothers, found that a maternal diet high in vegetables and yogurt was protective against the development of airway and skin allergies in the offspring by age four [37]. However, the study did not find a significant association between the maternal diet and the later development of FA, likely due to the relatively lower incidence of FA compared to that of the other allergic conditions examined. Being another significant component of a Mediterranean diet, the effect of fish consumption was also examined in a prospective birth cohort of 4089 infants. In this study, regular fish consumption during the first year was associated with a reduced risk of allergic disease (OR 0.76) and sensitization (OR 0.76) by age four [38]. Despite these promising findings, an earlier systematic review and meta‐analyses involving 62 articles, including cohorts, case–control, and cross‐sectional studies, found weak evidence that vitamins A, D, and E; zinc; fruits and vegetables; and a Mediterranean diet are associated with protection against asthma, but not other allergic diseases including FA [39].
Interventional studies showed that supplementation with n‐3 long‐chain polyunsaturated fatty acid (n‐3 LC‐PUFA) was able to alter the plasma levels of fatty acid but did not translate into a reduced prevalence of FA and other atopic conditions in these studies on infants and children [40, 41]. Recently, a systematic review of 46 interventional studies during pregnancy, lactation, and infancy found no specific dietary components that significantly prevented FA. This includes vitamins, fish oil, and pre/pro/synbiotic supplements [42, 43]. Instead, the ways that cow's milk and eggs were introduced, and the timing of the introduction of eggs and peanuts were important factors in reducing the risk of specific FA.
It is interesting to note the disparity between the observed clinical findings in prospective cohort studies and the outcomes of interventional trials assessing the clinical impact of various dietary components. The reasons for the differing results are not fully understood, but it is likely that the overall dietary pattern plays a crucial role rather than isolated dietary components. This perspective aligns with the concept of “food synergy,” which suggests that the health benefits of foods stem from the interactions among their various components rather than just individual nutrients [44]. Findings from the KOALA Birth Cohort Study in the Netherlands support this idea, showing that healthier dietary patterns associated with organic food consumption, characterized by a high ratio of vegetables to fast food, instead of the organic products themselves, were linked to a more favorable pre‐pregnancy BMI and a lower prevalence of gestational diabetes [45]. Additionally, diet should be considered alongside changes in gut microbial composition and metabolic profiles. This highlights the connection between nutrition, immune function, and allergic disease, which is increasingly referred to as an “immune‐supportive diet,” referring to a diverse diet rich in fresh, whole, and minimally processed plant‐based foods, fermented foods, and moderate amounts of omega‐3‐rich and animal‐based products that can synergistically improve immune function and gut health [46]. Figure 2 summarizes the influence of dietary patterns on the risk of developing FA.
FIGURE 2.

The potential risk factors and protective elements related to various dietary practices, and how different foods and dietary patterns may influence the likelihood of developing food allergies.
Dietary patterns consisting of a diverse array of dietary fatty acids and fiber types and sources have been proven more effective for managing allergy risk and symptoms than simply focusing on individual supplements [40, 44, 46, 47]. Dietary fibers are plant‐based, nondigestible carbohydrates that provide nourishment for the gut microbiome, leading to the production of short‐chain fatty acids (SCFAs) as a result of microbial fermentation. By forming SCFAs, dietary fiber‐fermenting bacteria modulate the gut barrier's function and help build a tolerogenic environment through different cellular pathways in the epithelial, dendritic, and T cells [48, 49]. In a study that recruited healthy lactating women, butyrate in human breast milk reduced allergic responses in both in vivo and in vitro models [50]. A high‐fiber diet has been shown to increase the production of SCFAs and provide protection against FA in a murine model [51]. Depriving mice of dietary fiber led to a gut microbiome signature characterized by increases in the mucin‐degrading bacterium Akkermansia muciniphila [52]. This gut microbial profile was associated with impaired intestinal barrier function, elevated expression of type 1 and type 2 cytokines, and the presence of IgE‐coated commensal bacteria in the colon. These changes exacerbated allergic reactions to food allergens such as ovalbumin (OVA) and peanuts. Furthermore, in a synthetic human gut microbiome in gnotobiotic mice, the presence of A. muciniphila , combined with fiber deprivation, resulted in stronger anti‐commensal IgE coating and increased innate type 2 immune responses, further worsening FA symptoms. SCFAs diffuse passively and systemically, primarily acting as signaling molecules via binding to different GPCRs to exhibit anti‐inflammatory actions [53, 54]. Through SCFA‐GPCR activation and histone deacetylase (HDAC) inhibition, SCFA stimulated the growth and expansion of Treg [55, 56, 57]. Other experimental models have consistently demonstrated that SCFAs play a significant role in the growth of immunological oral tolerance and have potent anti‐inflammatory actions in allergic disorders [55, 56, 58].
In human studies, Cait et al., using metagenomics sequencing, uncovered that infants who later developed allergic sensitization in childhood had gut microbiomes lacking the necessary genes for carbohydrate breakdown and butyrate production [59]. These findings suggest that a butyrate‐producing gut microbiome in early infancy may protect against the development of childhood allergies. Children who had high amounts of butyrate and propionate in their feces at 1 year old had a lower risk of developing FA and asthma later in life [60, 61]. Researchers have also consistently observed that children with both IgE‐mediated and non‐IgE–mediated cow's milk allergies exhibited a state of gut microbial imbalance, or dysbiosis, characterized by reduced levels of the SCFA butyrate in their stool samples when compared to healthy control children without milk allergies [62, 63]. The resolution of non‐IgE–mediated cow's milk allergies occurred more quickly in individuals with an abundance of butyrate‐producing bacteria [64]. Despite the promising results from experimental models, mixed results were reported in a systematic review and meta‐analyses of observational and intervention studies that evaluated the relationship between the SCFA level and allergic outcomes, likely due to differences in methodologies used [65]. Figure 3 presents an outline of how diet may offer protection and pose risks for FA.
FIGURE 3.

The mechanisms by which diet can both protect against and contribute to the risk of food allergies. It illustrates how certain dietary components may enhance immune tolerance, whereas others could trigger allergic responses, highlighting the complex interplay between nutrition and allergy development.
Overall, evidence has shown promise that a diet rich in fiber and diverse plant‐based foods can foster a healthy gut microbiome, promoting immune tolerance and reducing the risk of FA. This needs to be considered alongside the timing and manner of introducing allergenic foods during early life, which can also influence the gut microbiome and the risk of developing FA [66]. This is supported by findings from the CORAL cohort, which demonstrate that the introduction of foods, such as beans, nuts, seeds, oils, and cow's milk, significantly impacts microbiota composition during early life [67]. Although the effects of oil, beans, and nuts were similar to those of breastfeeding and vaginal birth—promoting the growth of beneficial bacteria such as Bifidobacterium and Lactobacillus—animal‐derived products, particularly cow's milk, shifted the microbiota away from a composition dominated by Bifidobacterium and Bacteroides. Further studies that evaluate how dietary patterns and the introduction of specific foods during early life may influence gut health and immunity are needed to inform strategies for preventing and managing food allergies. Clinical trials examining the targeted use of SCFAs as an intervention for treating FA are much needed [49, 66, 68].
3.2. Evidence on UPFs and FA Risk
Although there is a strong interest in the role of dietary fiber and SCFA in protecting infants from developing an FA, there is concurrently an increased focus on the harmful influences of certain dietary components of allergic disease outcomes. Among 1628 infants born between 2007 and 2015 from the COhort for Childhood Origin of Asthma and allergic diseases (COCOA) cohort in South Korea, a maternal confectionery diet during pregnancy, characterized by a higher intake of baked and sugary products, was associated with a higher prevalence of FA (aOR = 1.517, p = 0.02) [69]. Furthermore, the research group found that the confectionery diet was more significant in infants with specific genetic polymorphisms in CD14 and GST genes. Researchers from the EDEN birth cohort analyzed the associations between the immune and growth factor concentrations in early breast milk and childhood FA outcomes [70]. A core cluster of the breast milk components was found to be negatively associated with a “Western” dietary pattern during late pregnancy, which was characterized by a diet rich in processed foods such as French fries and soda; sugar‐loaded foods such as snacks, cakes, and chocolates; and processed meat. This implies that the immune factors passed to the newborn through breast milk were associated with the mother's dietary habits and lifestyle. This suggests that a Western lifestyle influences health from an early age. In a murine model, treatment with the artificial sweetener saccharin led to a dose‐dependent increase in OVA‐specific IgE and IgG1 antibodies in mice. Mice treated with 100 mg of saccharin and then challenged with 30 mg of the allergen OVA developed anaphylactic reactions [71]. Further analysis of the mesenteric lymph nodes of mice given 100 mg of saccharin showed that saccharin upregulated the Th2 cytokine IL‐4 while downregulating the Th1 cytokine IFN‐γ and the regulatory cytokine TGF‐β. This suggests that saccharin disrupted the induction of regulatory T cells, which are important for oral tolerance. However, the amount of additive was much higher than the typical consumptive dose. In a study that included 2211 adult and pediatric participants, with a mean age of 39.5 years, from the United States, urine dichlorophenol levels (derived from pesticides) at or above the 75th percentile were associated with the presence of sensitization to food allergens (OR, 1.8; 95% CI, 1.2–2.5; p = 0.003) [72]. However, this was a cross‐sectional study and the study did not include children younger than 6 years.
The increased risk conferred by a “Western diet” is considered a key contributor to the growth in FA prevalence. The Western diet typically features a higher intake of UPFs, refined carbohydrates, added sugars, unhealthy fats, and animal‐based proteins, while comprising fewer whole, minimally processed plant‐based foods such as fruits, vegetables, and whole grains. Western food cultures adopt frying, baking, and processed ingredients, unlike non‐Western cuisines that favor traditional cooking methods and spices. UPFs have become central to modern diets, offering convenience and enhanced flavors, but are calorie dense and high in refined grains, added salt, sugar, and saturated fats [73, 74]. All nations are shifting toward UPF‐dominated diets, especially in the West [75], where they now account for nearly half of total caloric intake in the United States [76, 77, 78], the United Kingdom [79], Canada [80], and Australia [81], with rising consumption also noted in Asia [82, 83].
UPFs, which frequently have added sugars, are considered to contribute to the production of advanced glycation end products (AGEs) [84]. In vitro studies have shown that roasting enhances the glycation and allergenicity of peanuts; as a result, peanut butter made from roasted peanuts with added sugar will result in AGEs [85, 86]. AGE‐rich meals are also those that have experienced the Maillard reaction (also known as “glycation”), which explains a series of chemical interactions involving carbonyl chemicals, such as reducing sugar and amino compounds. They generally come from high‐temperature–heated animal proteins and lipids, such as French fries, microwaved meals, and grilled meat. The innate immune system may then respond to AGEs as a “false alarm” in response to dietary antigens [84]. A receptor specific to the AGEs (RAGE) appears to be an important driver in priming the innate signaling, which results in allergic phenotypes [87]. It is believed that the increasing reliance on processed foods depleted from natural compounds can promote hormesis effects—a dose–response phenomenon characterized by low‐dose stimulation and high‐dose inhibition [88]. More research is needed to determine how consuming processed and high‐AGE foods affects the development of atopy and FA mechanistically.
3.3. UPFs, Emulsifiers, and the Epithelial Barrier
Research indicates that the first 3 years of life are critical for establishing the gut microbiome, primarily shaped by environmental factors rather than genetics [89]. Microbial maturation is essential for immune system development, with weaning marking a significant increase in gut microbiome diversity [90, 91]. Early onset dysbiosis and delayed microbiota maturation have been linked to later FAs [92, 93]. Thus, early life food choices greatly influence microbiota composition and long‐term allergic outcomes [66].
Recent studies show that over 30% of infant food items in the EU and the United Kingdom are UPFs—products with additives including flavorings, and emulsifiers [94, 95], with 39% containing sugar [96]. Common first foods, such as baby biscuits and cereals, have high sugar content (14–16 g per 100 g of food), exceeding recommended limits for infants (7.6–9.4 g) [97]. In Brazil, 79% of infant meals were UPFs, including follow‐up formulas [98]. Emulsifiers, such as lecithin and modified starches, are prevalent in infant formulas and raise concerns globally. Although the trend of consuming ultra‐processed infant foods is evident worldwide, it is particularly pronounced in Europe and is rising in Asia (Figure 4a) [100].
FIGURE 4.

The global food supply quantity (kg/capita/year) of (A) infant food and (B) sweeteners between 2010 and 2020 [99]. Although the total supply of commercial infant formula and sweeteners in Asia remained low, there has been a notable increase in sales of infant formula in Asia.
The two most frequently researched emulsifiers are carboxymethylcellulose and polysorbate 80, both of which have been demonstrated to encourage bacterial translocation across mucosal surfaces, alter the composition of the microbiota, increase their pro‐inflammatory potential, and trigger low‐grade inflammation that leads to chronic gut inflammatory disease [101, 102, 103, 104, 105]. Polysorbate 80 has been demonstrated to disrupt the function of the tight junction at low cytotoxic levels, facilitating the ability for allergens to pass through the gut's epithelial barrier [106]. Besides, household cleaning products are popular consumer commodities utilized by a substantial portion of the global population. Soaps and detergents, in particular, have gone from a luxury to a necessity due to the rising influence of the modern lifestyle. Recent research has demonstrated that alcohol ethoxylates, a key component of professional dishwashing detergents called rinse aids, are harmful and damaging to gut epithelial cells, compromising their integrity and activating the pro‐inflammatory response [107]. The detergent residue was present in substantial amounts on both washed and prepped dishware.
The “epithelial barrier hypothesis” provides further insights into how modern food processing impacts FA; emulsifiers in processed foods and detergent residue from dishwasher‐prepped dishware can impair the epithelial barrier in the gut mucosa, which becomes leaky, leading to microbial dysbiosis, bacterial translocation to interepithelial and subepithelial regions, and tissue microinflammation [108]. Recent experimental studies have shown that exposure to 5000 ng/mL sodium dodecyl sulfate (SDS) in a human esophageal epithelium air–liquid interface caused barrier dysfunction, an eosinophilic esophagitis‐like pathology, increased innate and adaptive immune responses, and potential sensitization to food components [109].
In discussing the Western diet, the focus has primarily been on the lack of dietary fiber, UPFs, AGEs, and emulsifiers. However, it is important to recognize that many other chemically modified food substances may also have detrimental effects on allergic diseases, particularly food allergies. For instance, additives such as artificial colors [110], preservatives [111], and flavor enhancers [112] have been implicated in allergic reactions and sensitivities. A comprehensive examination of the components of the Western diet, along with further mechanistic studies, is essential to clarify how exposure to environmental substances brought about by contemporary food processing might harm the epithelial barriers and enhance susceptibility to FA [108].
4. Epidemiological Link Between Diet and FA in West Versus East
4.1. Introducing the Global Pattern of Nutritional Transition
The global phenomenon of “nutritional transition” has resulted in a shift from traditional, home‐based, fiber‐rich diets, which were believed to be beneficial for preventing allergic diseases, to modern dietary patterns that could have negative influences on the immune system. These modern diets are characterized by a high consumption of processed foods, refined grains, and animal products and a low consumption of fruits, vegetables, and nuts. At the same time, physical activity and energy expenditure decrease [113, 114, 115]. Income growth often leads to a shift towards a more diverse diet that includes a larger share of animal protein and fats and oils. However, this transition has concurrently resulted in a decrease in the diversity of grain consumption, with a predominant reliance on wheat. This phenomenon is also referred to as Bennett's law [116]. This transition occurs at different paces and is primarily driven by wealth but varies according to culture, tradition, geography, and religion.
The Industrial Revolution (1760–1840) transformed food processing in Western countries, leading to a diet dominated by dairy, cereals, refined sugars, vegetable oils, and alcohol, which now account for 72% of the daily energy intake for Americans—items that contributed minimally to pre‐agricultural diets [117]. From the 1970s to the 1990s, the consumption of processed foods (refined sugar and vegetable oils [trans‐fans]) surged [118]. Between 1999 and 2018, energy intake from UPFs consistently increased among US youths, now representing the majority of their total intake [78]. This shift from minimally processed foods to UPFs negatively impacts dietary variables such as glycemic load, fiber content, fatty acid composition, and acid–base balance. Although the mechanism by which diet impacts the gut microbiome is beyond the scope of this review, there is evidence that consuming an animal‐based diet [119, 120] and omega‐6 polyunsaturated fatty acids [121] can negatively impact gut health. This dietary transition in the late 19th and early 20th centuries coincided with rising cases of food allergies and anaphylaxis beginning in 1990 [12, 122, 123], marking a “second wave” of the allergy epidemic occurring 10–15 years after a respiratory epidemic [124].
China's agricultural output only started to rise after the famines of 1959 and 1961 through a “rural scientific‐experiment movement” during the Mao period [125]. Between 1960 and 2020, wheat yields tripled, whereas rice and maize yields doubled [126]. The growth and production of peanuts increased by 10 times during this period [127]. Similar agricultural development has occurred in Malaysia, Thailand, and Indonesia since the 1960s, whereas that in Vietnam and Bangladesh only started in the 1990s. Since 1980, there has been rapid economic growth, but it was not uniform across Asia. The economic growth and protein transition were first notable in Thailand and Malaysia. This was quickly followed by rapid growth in China, succeeded by a slower pace in countries such as Vietnam, Indonesia, India, and Bangladesh [128]. A decline was observed in the consumption of cereals as a source of calories, whereas there was an increase in calories from animal products, sugars, sweeteners, and fats, mirroring that of the Western diet [129]. However, global trade only opened up during the structural reforms in the 2000s, leading to a “supermarket revolution” in different periods in Asia, which provided a conduit for processed food products to reach Asian populations [130]. From 2010 to 2020, the growth of packaged food revenue ranged from 5% to 34% across Asia, most notably in transitional countries such as India and Vietnam.
Although the “Westernized” lifestyle and diet took shape in the United Kingdom and the United States between 1970 and 1990, there was a significant increase in FA and anaphylaxis observed in these Westernized countries since the 1990s and peaked in the 2000s [124, 131]. On the other hand, many parts of Asia were still grappling with poverty and famine in the 1970s, and globalization only began to emerge and thrive in most parts of Asia in 2000–2020. Inferring from this observation, one can anticipate that FA prevalence in Asia will follow a similar pattern of increase in Western countries over the coming decade (2020–2030), parallel to the West. However, the rate of increase is expected to vary in different parts of Asia.
4.2. Individualized Modernity in the East
A common understanding of “modernity” is that it refers to a state of perpetual societal progress, beginning with agriculture and continuing through urbanization, industrialization, and westernization, along with the advancement of technology and social structure [132].
Although there is a significant leap in modernization across Asia, the countries in the region are experiencing varying levels of economic growth. Meat consumption increased primarily in East Asia, such as China, Japan, and Korea, and was slower in South Asia, such as Thailand, Vietnam, and Indonesia [133]. In contrast, vegetable consumption in Asia continues to rise from 57 to 116 kg per capita per year, with rice and leafy vegetables being the most common food groups (Figure 5). Traditional Chinese diets (TCDs) are typically fiber rich and inversely associated with obesity risk and weight gain [134]. Sweetener consumption in Asia is low relative to the global average (Figure 4b) [99], but disproportionately increased in developing countries like India and Vietnam [126]. Meanwhile, although the total sales of commercial milk formula in South Asia remained low at 1.5 kg/c, there has been a significant increase in sales in East Asia and the Pacific (Figure 4a), approaching the levels of sales in Western countries [135].
FIGURE 5.

The global ratio of vegetable‐to‐meat supply (kg/capita/year) [99], showing that this ratio has consistently remained higher in Asia over time compared to other regions over time.
Despite heavy global and Western influences, traditional customs and ideology continue to shape modernity in most Asian countries. In China, the rural poverty rate dropped from 97.5% to 0.6% between 1978 and 2019 [136], although income inequality persists due to rural–urban gap [137]. In rural China, homemade peanut oil remains the primary cooking oil, valued for its affordability and flavor [138, 139]. A recent study (2021–2022) carried out in Guangxi, southwestern China, found that 82% of 1611 pregnant women consumed homemade peanut oil, which was associated with a higher risk of low birth weight and preterm births [140]. Additionally, peanuts are commonly consumed peanuts for their rich folate content [141] and are significant in traditional Han weddings symbolizing fertility [142].
Despite significant global and Western influences, traditional customs and cultural norms continue to play a profound role in shaping modernity across most Asian countries. Although some parts of Asia have modernized quickly, they have not fully embraced Western culture. Importantly, there is still a proportion of populations in Asia who live in a rural environment and have retained their traditional dietary habits that may be protective against allergies. Further studies are needed to assess the impact of these dietary patterns on allergic outcomes.
5. Conclusion
Unlike the pattern of FA observed in the Western world since 1990, with peanuts/nuts‐induced anaphylaxis as a hallmark, the epidemiology of FA in Asia in the past decade has shown differences in prevalence and patterns. Even within the same country, the prevalence and pattern of FA and anaphylaxis differ between urban and rural areas in China. Although FA prevalence is gradually stabilizing in the West, there is preliminary evidence that FA is rising in the East, specifically concerning countries with rapidly developing economies like China. FPIES, which was once thought to be rare, is now increasing in incidence in Westernized countries. Anticipating the increase in the prevalence of FA in Asia in the next decade, it is crucial to identify the important environmental factors that may contribute to the development of FA.
The process of modernization, especially the industrialization of the food system, has resulted in the well‐known “Western diet.” Epidemiological evidence suggests that the shift towards a more Westernized, processed, and UPF‐rich diet, as part of the broader process of modernization, has been accompanied by a rise in the prevalence of FAs, autoimmune diseases, and other immune‐mediated disorders in many parts of the world. The incorporation of emulsifiers, sweeteners, and other additives into processed foods and UPFs is particularly concerning. Emulsifiers are used to improve the texture, stability, and shelf life of these foods, but have been shown to harm epithelial barriers and increase susceptibility to FAs. On the other hand, a diet rich in fiber nourishes the gut microbiome and produces SCFAs through microbial fermentation, which in turn, modulates the gut barrier's function and builds a tolerogenic environment.
The delayed and accumulative effects of industrialization and the modern food system are akin to the gradual unfolding of climate change. Just as we are now witnessing the profound impacts of climate change that have built up over decades, the adverse effects of nutritional transition and the predominance of processed foods on human health may only become fully apparent in the coming decade. However, the implications could be equally devastating, leading to a rise in FAs and other immune‐related disorders. This persistent interplay between tradition and modernity is a critical factor in understanding the regional variations in FA patterns between Asia and the West. We need to take proactive steps to address these issues and mitigate the adverse outcomes on the immune system related to the modernization of the food system.
Author Contributions
A.S.‐Y.L. conceptualization and interpretation of relevant literature, and writing of first draft. Y.X., G.W.‐K.W., and M.F.‐R. conceptualization and critical revision of final draft. All authors have read and agreed to the published version of the manuscript.
Consent
The authors have nothing to report.
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
We would like to express our gratitude to Ms. Vanessa Tang and Ms. Ann Au for their invaluable assistance in developing the figures for this article. The figures were created with BioRender.com.
Funding: The authors received no specific funding for this work.
Data Availability Statement
The authors have nothing to report.
References
- 1. Leung A. S. Y., Wong G. W. K., and Tang M. L. K., “Food Allergy in the Developing World,” Journal of Allergy and Clinical Immunology 141, no. 1 (2018): 76–78.e1. [DOI] [PubMed] [Google Scholar]
- 2. Celebi Sozener Z., Ozdel Ozturk B., Cerci P., et al., “Epithelial Barrier Hypothesis: Effect of the External Exposome on the Microbiome and Epithelial Barriers in Allergic Disease,” Allergy 77, no. 5 (2022): 1418–1449. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Lewis S. L. and Maslin M. A., “Defining the Anthropocene,” Nature (London) 519, no. 7542 (2015): 171–180. [DOI] [PubMed] [Google Scholar]
- 4. Platts‐Mills T. A. E., “The Allergy Epidemics: 1870–2010,” Journal of Allergy and Clinical Immunology 136, no. 1 (2015): 3–13. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5. Venter C., Hasan Arshad S., Grundy J., et al., “Time Trends in the Prevalence of Peanut Allergy: Three Cohorts of Children From the Same Geographical Location in the UK,” Allergy 65, no. 1 (2010): 103–108. [DOI] [PubMed] [Google Scholar]
- 6. Venter C., Maslin K., Patil V., et al., “The Prevalence, Natural History and Time Trends of Peanut Allergy Over the First 10 Years of Life in Two Cohorts Born in the Same Geographical Location 12 Years Apart,” Pediatric Allergy and Immunology 27, no. 8 (2016): 804–811. [DOI] [PubMed] [Google Scholar]
- 7. Osborne N. J., Koplin J. J., Martin P. E., et al., “Prevalence of Challenge‐Proven IgE‐Mediated Food Allergy Using Population‐Based Sampling and Predetermined Challenge Criteria in Infants,” Journal of Allergy and Clinical Immunology 127, no. 3 (2011): 668–676.e2. [DOI] [PubMed] [Google Scholar]
- 8. Soriano V. X., Peters R. L., Moreno‐Betancur M., et al., “Association Between Earlier Introduction of Peanut and Prevalence of Peanut Allergy in Infants in Australia,” Journal of the American Medical Association 328, no. 1 (2022): 48–56. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9. Ma Z., Chen L., Xian R., Fang H., Wang J., and Hu Y., “Time Trends of Childhood Food Allergy in China: Three Cross‐Sectional Surveys in 1999, 2009, and 2019,” Pediatric Allergy and Immunology 32, no. 5 (2021): 1073–1079. [DOI] [PubMed] [Google Scholar]
- 10. Rangkakulnuwat P. and Lao‐Araya M., “The Prevalence and Temporal Trends of Food Allergy Among Preschool Children in Northern Thailand Between 2010 and 2019,” World Allergy Organization Journal 14, no. 10 (2021): 100593. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11. Yoshisue H., Homma Y., Ito C., and Ebisawa M., “Prevalence of Food Allergy Increased 1.7 Times in the Past 10 Years Among Japanese Patients Below 6 Years of Age,” Pediatric Allergy and Immunology 35, no. 7 (2024): e14192. [DOI] [PubMed] [Google Scholar]
- 12. Sicherer S. H., Muñoz‐Furlong A., Godbold J. H., and Sampson H. A., “US Prevalence of Self‐Reported Peanut, Tree Nut, and Sesame Allergy: 11‐Year Follow‐Up,” Journal of Allergy and Clinical Immunology 125, no. 6 (2010): 1322–1326. [DOI] [PubMed] [Google Scholar]
- 13. Gupta R. S., Springston E. E., Warrier M. R., et al., “The Prevalence, Severity, and Distribution of Childhood Food Allergy in the United States,” Pediatrics 128, no. 1 (2011): e9–e17. [DOI] [PubMed] [Google Scholar]
- 14. Gupta R. S., Warren C. M., Smith B. M., et al., “The Public Health Impact of Parent‐Reported Childhood Food Allergies in the United States,” Pediatrics 142, no. 6 (2018): e20181235. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Wang Y., Allen K. J., Suaini N. H. A., McWilliam V., Peters R. L., and Koplin J. J., “The Global Incidence and Prevalence of Anaphylaxis in Children in the General Population: A Systematic Review,” Allergy 74, no. 6 (2019): 1063–1080. [DOI] [PubMed] [Google Scholar]
- 16. Leung A. S. Y., Tham E. H., Pacharn P., et al., “Disparities in Pediatric Anaphylaxis Triggers and Management Across Asia,” Allergy 79, no. 5 (2024): 1317–1328. [DOI] [PubMed] [Google Scholar]
- 17. Li J., Ogorodova L. M., Mahesh P. A., et al., “Comparative Study of Food Allergies in Children From China, India, and Russia: The EuroPrevall‐INCO Surveys,” Journal of Allergy and Clinical Immunology: In Practice 8, no. 4 (2020): 1349–1358.e16. [DOI] [PubMed] [Google Scholar]
- 18. Tham E. H., Lee B. W., Chan Y. H., et al., “Low Food Allergy Prevalence Despite Delayed Introduction of Allergenic Foods‐Data From the GUSTO Cohort,” Journal of Allergy and Clinical Immunology: In Practice 6, no. 2 (2018): 466–475.e1. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19. Lieberman J. A., Gupta R. S., Knibb R. C., et al., “The Global Burden of Illness of Peanut Allergy: A Comprehensive Literature Review,” Allergy 76, no. 5 (2021): 1367–1384. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20. Sugizaki C., Takahashi K., Sato S., Yanagida N., and Ebisawa M., “National Survey of Immediate Type Food Allergies in Japan in 2020: A Report Supported by A Grant From the Consumer Affairs Agency, Government of Japan,” Arerugī 72, no. 8 (2023): 1032–1037. [DOI] [PubMed] [Google Scholar]
- 21. Kitamura K., Ito T., and Ito K., “Comprehensive Hospital‐Based Regional Survey of Anaphylaxis in Japanese Children: Time Trends of Triggers and Adrenaline Use,” Allergology International 70, no. 4 (2021): 452–457. [DOI] [PubMed] [Google Scholar]
- 22. Nowak‐Węgrzyn A., Chehade M., Groetch M. E., et al., “International Consensus Guidelines for the Diagnosis and Management of Food Protein‐Induced Enterocolitis Syndrome: Executive Summary‐Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology,” Journal of Allergy and Clinical Immunology 139, no. 4 (2017): 1111–1126.e4. [DOI] [PubMed] [Google Scholar]
- 23. Mehr S., Frith K., and Campbell D. E., “Epidemiology of Food Protein‐Induced Enterocolitis Syndrome,” Current Opinion in Allergy and Clinical Immunology 14, no. 3 (2014): 208–216. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24. Akashi M., Kaburagi S., Kajita N., and Morita H., “Heterogeneity of Food Protein‐Induced Enterocolitis Syndrome (FPIES),” Allergology International 73, no. 2 (2024): 196–205. [DOI] [PubMed] [Google Scholar]
- 25. Ruffner M. A., Wang K. Y., Dudley J. W., et al., “Elevated Atopic Comorbidity in Patients With Food Protein–Induced Enterocolitis,” Journal of Allergy and Clinical Immunology: In Practice 8, no. 3 (2020): 1039–1046. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26. Lopes J. P., Cox A. L., Baker M. G., et al., “Peanut‐Induced Food Protein‐Induced Enterocolitis Syndrome (FPIES) in Infants With Early Peanut Introduction,” Journal of Allergy and Clinical Immunology: In Practice 9, no. 5 (2021): 2117–2119. [DOI] [PubMed] [Google Scholar]
- 27. Robbins K. A., Ackerman O. R., Carter C. A., Uygungil B., Sprunger A., and Sharma H. P., “Food Protein‐Induced Enterocolitis Syndrome to Peanut With Early Introduction: A Clinical Dilemma,” Journal of Allergy and Clinical Immunology: In Practice 6, no. 2 (2018): 664–666. [DOI] [PubMed] [Google Scholar]
- 28. Akashi M., Hayashi D., Kajita N., et al., “Recent Dramatic Increase in Patients With Food Protein‐Induced Enterocolitis Syndrome (FPIES) Provoked by Hen's Egg in Japan,” Journal of Allergy and Clinical Immunology: In Practice 10, no. 4 (2022): 1110–1112.e2. [DOI] [PubMed] [Google Scholar]
- 29. Joshi P. A., Smith J., Vale S., and Campbell D. E., “The Australasian Society of Clinical Immunology and Allergy Infant Feeding for Allergy Prevention Guidelines,” Medical Journal of Australia 210, no. 2 (2019): 89–93. [DOI] [PubMed] [Google Scholar]
- 30. Fleischer D. M., Chan E. S., Venter C., et al., “A Consensus Approach to the Primary Prevention of Food Allergy Through Nutrition: Guidance From the American Academy of Allergy, Asthma, and Immunology; American College of Allergy, Asthma, and Immunology; and the Canadian Society for Allergy and Clinical Immunology,” Journal of Allergy and Clinical Immunology: In Practice 9, no. 1 (2021): 22–43.e4. [DOI] [PubMed] [Google Scholar]
- 31. Abrams E. M., Watson W., Vander Leek T. K., et al., “Dietary Exposures and Allergy Prevention in High‐Risk Infants,” Allergy, Asthma and Clinical Immunology 18, no. 1 (2022): 36. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32. Tham E. H., Shek L. P., Van Bever H. P., et al., “Early Introduction of Allergenic Foods for the Prevention of Food Allergy From an Asian Perspective–An Asia Pacific Association of Pediatric Allergy, Respirology & Immunology (APAPARI) Consensus Statement,” Pediatric Allergy and Immunology 29, no. 1 (2018): 18–27. [DOI] [PubMed] [Google Scholar]
- 33. Leung A. S.‐Y., Pacharn P., Tangvalelerd S., et al., “Food Allergy in a Changing Dietary Landscape: A Focus on the Asia Pacific Region,” Pediatric Allergy and Immunology 35, no. 8 (2024): e14211. [DOI] [PubMed] [Google Scholar]
- 34. Tham E. H., Leung A. S. Y., Pacharn P., et al., “Anaphylaxis – Lessons Learnt When East Meets West,” Pediatric Allergy and Immunology 30, no. 7 (2019): 681–688. [DOI] [PubMed] [Google Scholar]
- 35. Stenius F., Swartz J., Lilja G., et al., “Lifestyle Factors and Sensitization in Children – The ALADDIN Birth Cohort,” Allergy 66, no. 10 (2011): 1330–1338. [DOI] [PubMed] [Google Scholar]
- 36. Grimshaw K. E. C., Maskell J., Oliver E. M., et al., “Diet and Food Allergy Development During Infancy: Birth Cohort Study Findings Using Prospective Food Diary Data,” Journal of Allergy and Clinical Immunology 133, no. 2 (2014): 511–519. [DOI] [PubMed] [Google Scholar]
- 37. Venter C., Palumbo M. P., Glueck D. H., et al., “The Maternal Diet Index in Pregnancy Is Associated With Offspring Allergic Diseases: The Healthy Start Study,” Allergy 77, no. 1 (2022): 162–172. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38. Kull I., Bergström A., Lilja G., Pershagen G., and Wickman M., “Fish Consumption During the First Year of Life and Development of Allergic Diseases During Childhood,” Allergy 61, no. 8 (2006): 1009–1015. [DOI] [PubMed] [Google Scholar]
- 39. Nurmatov U., Devereux G., and Sheikh A., “Nutrients and Foods for the Primary Prevention of Asthma and Allergy: Systematic Review and Meta‐Analysis,” Journal of Allergy and Clinical Immunology 127, no. 3 (2011): 724–733.e1‐30. [DOI] [PubMed] [Google Scholar]
- 40. Venter C., Meyer R. W., Nwaru B. I., et al., “EAACI Position Paper: Influence of Dietary Fatty Acids on Asthma, Food Allergy, and Atopic Dermatitis,” Allergy 74, no. 8 (2019): 1429–1444. [DOI] [PubMed] [Google Scholar]
- 41. Hoppenbrouwers T., Cvejić Hogervorst J. H., Garssen J., Wichers H. J., and Willemsen L. E. M., “Long Chain Polyunsaturated Fatty Acids (LCPUFAs) in the Prevention of Food Allergy,” Frontiers in Immunology 10 (2019): 1118. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 42. de Silva D., Halken S., Singh C., et al., “Preventing Food Allergy in Infancy and Childhood: Systematic Review of Randomised Controlled Trials,” Pediatric Allergy and Immunology 31, no. 7 (2020): 813–826. [DOI] [PubMed] [Google Scholar]
- 43. Halken S., Muraro A., de Silva D., et al., “EAACI Guideline: Preventing the Development of Food Allergy in Infants and Young Children (2020 Update),” Pediatric Allergy and Immunology 32, no. 5 (2021): 843–858. [DOI] [PubMed] [Google Scholar]
- 44. Jacobs D. R., Gross M. D., and Tapsell L. C., “Food Synergy: An Operational Concept for Understanding nutrition,” American Journal of Clinical Nutrition 89, no. 5 (2009): 1543S–1548S. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45. Simões‐Wüst A. P., Moltó‐Puigmartí C., Jansen E. H., van Dongen M. C., Dagnelie P. C., and Thijs C., “Organic Food Consumption During Pregnancy and Its Association With Health‐Related Characteristics: The KOALA Birth Cohort Study,” Public Health Nutrition 20, no. 12 (2017): 2145–2156. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46. Vlieg‐Boerstra B., Groetch M., Vassilopoulou E., et al., “The Immune‐Supportive Diet in Allergy Management: A Narrative Review and Proposal,” Allergy 78, no. 6 (2023): 1441–1458. [DOI] [PubMed] [Google Scholar]
- 47. Venter C., Meyer R. W., Greenhawt M., et al., “Role of Dietary Fiber in Promoting Immune Health—An EAACI Position Paper,” Allergy 77, no. 11 (2022): 3185–3198. [DOI] [PubMed] [Google Scholar]
- 48. Koh A., De Vadder F., Kovatcheva‐Datchary P., and Bäckhed F., “From Dietary Fiber to Host Physiology: Short‐Chain Fatty Acids as Key Bacterial Metabolites,” Cell 165, no. 6 (2016): 1332–1345. [DOI] [PubMed] [Google Scholar]
- 49. Luu M., Monning H., and Visekruna A., “Exploring the Molecular Mechanisms Underlying the Protective Effects of Microbial SCFAs on Intestinal Tolerance and Food Allergy,” Frontiers in Immunology 11 (2020): 1225. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 50. Paparo L., Nocerino R., Ciaglia E., et al., “Butyrate as a Bioactive Human Milk Protective Component Against Food Allergy,” Allergy 76, no. 5 (2021): 1398–1415. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 51. Tan J., McKenzie C., Vuillermin P. J., et al., “Dietary Fiber and Bacterial SCFA Enhance Oral Tolerance and Protect Against Food Allergy Through Diverse Cellular Pathways,” Cell Reports 15, no. 12 (2016): 2809–2824. [DOI] [PubMed] [Google Scholar]
- 52. Parrish A., Boudaud M., Grant E. T., et al., “ Akkermansia muciniphila Exacerbates Food Allergy in Fibre‐Deprived Mice,” Nature Microbiology 8, no. 10 (2023): 1863–1879. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 53. Oh D. Y., Talukdar S., Bae E. J., et al., “GPR120 Is an Omega‐3 Fatty Acid Receptor Mediating Potent Anti‐Inflammatory and Insulin‐Sensitizing Effects,” Cell 142, no. 5 (2010): 687–698. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 54. Thorburn Alison N., Macia L., and Mackay C. R., “Diet, Metabolites, and “Western‐Lifestyle” Inflammatory Diseases,” Immunity 40, no. 6 (2014): 833–842. [DOI] [PubMed] [Google Scholar]
- 55. Arpaia N., Campbell C., Fan X., et al., “Metabolites Produced by Commensal Bacteria Promote Peripheral Regulatory T‐Cell Generation,” Nature 504, no. 7480 (2013): 451–455. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 56. Furusawa Y., Obata Y., Fukuda S., et al., “Commensal Microbe‐Derived Butyrate Induces the Differentiation of Colonic Regulatory T Cells,” Nature 504, no. 7480 (2013): 446–450. [DOI] [PubMed] [Google Scholar]
- 57. Park J., Kim M., Kang S. G., et al., “Short‐Chain Fatty Acids Induce Both Effector and Regulatory T Cells by Suppression of Histone Deacetylases and Regulation of the mTOR–S6K Pathway,” Mucosal Immunology 8, no. 1 (2015): 80–93. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 58. Smith P. M., Howitt M. R., Panikov N., et al., “The Microbial Metabolites, Short‐Chain Fatty Acids, Regulate Colonic Treg Cell Homeostasis,” Science 341, no. 6145 (2013): 569–573. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 59. Cait A., Cardenas E., Dimitriu P. A., et al., “Reduced Genetic Potential for Butyrate Fermentation in the Gut Microbiome of Infants Who Develop Allergic Sensitization,” Journal of Allergy and Clinical Immunology 144, no. 6 (2019): 1638–1647.e3. [DOI] [PubMed] [Google Scholar]
- 60. Roduit C., Frei R., Ferstl R., et al., “High Levels of Butyrate and Propionate in Early Life Are Associated With Protection Against Atopy,” Allergy 74, no. 4 (2019): 799–809. [DOI] [PubMed] [Google Scholar]
- 61. Sandin A., Bråbäck L., Norin E., and Björkstén B., “Faecal Short Chain Fatty Acid Pattern and Allergy in Early Childhood,” Acta Paediatrica 98, no. 5 (2009): 823–827. [DOI] [PubMed] [Google Scholar]
- 62. Berni Canani R., Sangwan N., Stefka A. T., et al., “ Lactobacillus rhamnosus GG‐Supplemented Formula Expands Butyrate‐Producing Bacterial Strains in Food Allergic Infants,” ISME Journal 10, no. 3 (2016): 742–750. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 63. Berni Canani R., De Filippis F., Nocerino R., et al., “Gut Microbiota Composition and Butyrate Production in Children Affected by Non‐IgE‐Mediated Cow's Milk Allergy,” Scientific Reports 8, no. 1 (2018): 1–10. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 64. Bunyavanich S., Shen N., Grishin A., et al., “Early‐Life Gut Microbiome Composition and Milk Allergy Resolution,” Journal of Allergy and Clinical Immunology 138, no. 4 (2016): 1122–1130. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 65. Sasaki M., Suaini N. H. A., Afghani J., et al., “Systematic Review of the Association Between Short Chain Fatty Acids and Allergic Diseases,” Allergy 79, no. 7 (2024): 1789–1811. [DOI] [PubMed] [Google Scholar]
- 66. Stephen‐Victor E., Crestani E., and Chatila T. A., “Dietary and Microbial Determinants in Food Allergy,” Immunity 53, no. 2 (2020): 277–289. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 67. Korpela K., Hurley S., Ford S. A., et al., “Association Between Gut Microbiota Development and Allergy in Infants Born During Pandemic‐Related Social Distancing Restrictions,” Allergy 79, no. 7 (2024): 1938–1951. [DOI] [PubMed] [Google Scholar]
- 68. Di Costanzo M., Carucci L., Berni Canani R., and Biasucci G., “Gut Microbiome Modulation for Preventing and Treating Pediatric Food Allergies,” International Journal of Molecular Sciences 21, no. 15 (2020): 5275. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 69. Kim Y. H., Kim K. W., Lee S. Y., et al., “Maternal Perinatal Dietary Patterns Affect Food Allergy Development in Susceptible Infants,” Journal of Allergy and Clinical Immunology: In Practice 7, no. 7 (2019): 2337–2347.e7. [DOI] [PubMed] [Google Scholar]
- 70. Berdi M., de Lauzon‐Guillain B., Forhan A., et al., “Immune Components of Early Breastmilk: Association With Maternal Factors and With Reported Food Allergy in Childhood,” Pediatric Allergy and Immunology 30, no. 1 (2019): 107–116. [DOI] [PubMed] [Google Scholar]
- 71. Yamashita H., Matsuhara H., Miotani S., et al., “Artificial Sweeteners and Mixture of Food Additives Cause to Break Oral Tolerance and Induce Food Allergy in Murine Oral Tolerance Model for Food Allergy,” Clinical and Experimental Allergy 47, no. 9 (2017): 1204–1213. [DOI] [PubMed] [Google Scholar]
- 72. Jerschow E., McGinn A. P., de Vos G., et al., “Dichlorophenol‐Containing Pesticides and Allergies: Results From the US National Health and Nutrition Examination Survey 2005–2006,” Annals of Allergy, Asthma & Immunology 109, no. 6 (2012): 420–425. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 73. Popkin B. M. and Hawkes C., “Sweetening of the Global Diet, Particularly Beverages: Patterns, Trends, and Policy Responses,” Lancet Diabetes and Endocrinology 4, no. 2 (2016): 174–186. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 74. Baker P., Machado P., Santos T., et al., “Ultra‐Processed Foods and the Nutrition Transition: Global, Regional and National Trends, Food Systems Transformations and Political Economy Drivers,” Obesity Reviews 21, no. 12 (2020): e13126. [DOI] [PubMed] [Google Scholar]
- 75. Azzam A., “Is the World Converging to a 'Western diet'?,” Public Health Nutrition 24, no. 2 (2021): 309–317. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 76. Baraldi L. G., Martinez Steele E., Canella D. S., and Monteiro C. A., “Consumption of Ultra‐Processed Foods and Associated Sociodemographic Factors in the USA Between 2007 and 2012: Evidence From a Nationally Representative Cross‐Sectional Study,” BMJ Open 8, no. 3 (2018): e020574. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 77. Juul F., Parekh N., Martinez‐Steele E., Monteiro C. A., and Chang V. W., “Ultra‐Processed Food Consumption Among US Adults From 2001 to 2018,” American Journal of Clinical Nutrition 115, no. 1 (2022): 211–221. [DOI] [PubMed] [Google Scholar]
- 78. Wang L., Steele E. M., Du M., et al., “Trends in Consumption of Ultraprocessed Foods Among US Youths Aged 2–19 Years, 1999–2018,” Journal of the American Medical Association 326, no. 6 (2021): 519–530. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 79. Rauber F., Louzada M., Martinez Steele E., et al., “Ultra‐Processed Foods and Excessive Free Sugar Intake in the UK: A Nationally Representative Cross‐Sectional Study,” BMJ Open 9, no. 10 (2019): e027546. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 80. Polsky J. Y., Moubarac J.‐C., and Garriguet D., “Consumption of Ultra‐Processed Foods in Canada,” Health Reports 31, no. 11 (2020): 3–15. [DOI] [PubMed] [Google Scholar]
- 81. Marchese L., Livingstone K. M., Woods J. L., Wingrove K., and Machado P., “Ultra‐Processed Food Consumption, Socio‐Demographics and Diet Quality in Australian Adults,” Public Health Nutrition 25, no. 1 (2022): 94–104. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 82. Sung H., Park J. M., Oh S. U., Ha K., and Joung H., “Consumption of Ultra‐Processed Foods Increases the Likelihood of Having Obesity in Korean Women,” Nutrients 13, no. 2 (2021): 698. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 83. Koiwai K., Takemi Y., Hayashi F., et al., “Consumption of Ultra‐Processed Foods Decreases the Quality of the Overall Diet of Middle‐Aged Japanese Adults,” Public Health Nutrition 22, no. 16 (2019): 2999–3008. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 84. Smith P. K., Masilamani M., Li X. M., and Sampson H. A., “The False Alarm Hypothesis: Food Allergy Is Associated With High Dietary Advanced Glycation End‐Products and Proglycating Dietary Sugars That Mimic Alarmins,” Journal of Allergy and Clinical Immunology 139, no. 2 (2017): 429–437. [DOI] [PubMed] [Google Scholar]
- 85. Maleki S. J., Chung S.‐Y., Champagne E. T., and Raufman J.‐P., “The Effects of Roasting on the Allergenic Properties of Peanut Proteins,” Journal of Allergy and Clinical Immunology 106, no. 4 (2000): 763–768. [DOI] [PubMed] [Google Scholar]
- 86. Chung S.‐Y. and Champagne E. T., “Association of End‐Product Adducts With Increased IgE Binding of Roasted Peanuts,” Journal of Agricultural and Food Chemistry 49, no. 8 (2001): 3911–3916. [DOI] [PubMed] [Google Scholar]
- 87. Sick E., Brehin S., André P., et al., “Advanced Glycation End Products (AGEs) Activate Mast Cells,” British Journal of Pharmacology 161, no. 2 (2010): 442–455. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 88. Florsheim E. B., Sullivan Z. A., Khoury‐Hanold W., and Medzhitov R., “Food Allergy as a Biological Food Quality Control System,” Cell 184, no. 6 (2021): 1440–1454. [DOI] [PubMed] [Google Scholar]
- 89. Rothschild D., Weissbrod O., Barkan E., et al., “Environment Dominates Over Host Genetics in Shaping Human Gut Microbiota,” Nature 555, no. 7695 (2018): 210–215. [DOI] [PubMed] [Google Scholar]
- 90. Fallani M., Amarri S., Uusijarvi A., et al., “Determinants of the Human Infant Intestinal Microbiota After the Introduction of First Complementary Foods in Infant Samples From Five European Centres,” Microbiology (Reading) 157, no. Pt 5 (2011): 1385–1392. [DOI] [PubMed] [Google Scholar]
- 91. Bäckhed F., Roswall J., Peng Y., et al., “Dynamics and Stabilization of the Human Gut Microbiome During the First Year of Life,” Cell Host & Microbe 17, no. 5 (2015): 690–703. [DOI] [PubMed] [Google Scholar]
- 92. Gensollen T., Iyer S. S., Kasper D. L., and Blumberg R. S., “How Colonization by Microbiota in Early Life Shapes the Immune System,” Science 352, no. 6285 (2016): 539–544. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 93. Hoskinson C., Dai D. L. Y., Del Bel K. L., et al., “Delayed Gut Microbiota Maturation in the First Year of Life Is a Hallmark of Pediatric Allergic Disease,” Nature Communications 14, no. 1 (2023): 4785. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 94. Khandpur N., Neri D. A., Monteiro C., et al., “Ultra‐Processed Food Consumption Among the Paediatric Population: An Overview and Call to Action From the European Childhood Obesity Group,” Annals of Nutrition & Metabolism 76, no. 2 (2020): 109–113. [DOI] [PubMed] [Google Scholar]
- 95. Monteiro C. A., Cannon G., Levy R. B., et al., “Ultra‐Processed Foods: What They Are and How to Identify Them,” Public Health Nutrition 22, no. 5 (2019): 936–941. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 96. Grammatikaki E., Wollgast J., and Caldeira S., “High Levels of Nutrients of Concern in Baby Foods Available in Europe That Contain Sugar‐Contributing Ingredients or Are Ultra‐Processed,” Nutrients 13, no. 9 (2021): 3105. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 97. World Health Organization , Guideline: Sugars Intake for Adults and Children (Geneva: World Health Organization, 2015). [PubMed] [Google Scholar]
- 98. Chen M. and Sun Q., “Current Knowledge in the Stabilization/Destabilization of Infant Formula Emulsions During Processing as Affected by Formulations,” Trends in Food Science & Technology 109 (2021): 435–447. [Google Scholar]
- 99. FAOSTAT , accessed July 24, 2024, https://www.fao.org/faostat/en/#data.
- 100. McSweeney S. L., “Emulsifiers in Infant Nutritional Products,” in Food Emulsifiers and Their Applications, 2nd ed., eds. Hasenhuettl G. L. and Hartel R. W. (New York, NY: Springer New York, 2008), 233–261. [Google Scholar]
- 101. Chassaing B., Koren O., Goodrich J. K., et al., “Dietary Emulsifiers Impact the Mouse Gut Microbiota Promoting Colitis and Metabolic Syndrome,” Nature 519, no. 7541 (2015): 92–96. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 102. Chassaing B., Van de Wiele T., De Bodt J., Marzorati M., and Gewirtz A. T., “Dietary Emulsifiers Directly Alter Human Microbiota Composition and Gene Expression Ex Vivo Potentiating Intestinal Inflammation,” Gut 66, no. 8 (2017): 1414–1427. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 103. Roberts C. L., Keita A. V., Duncan S. H., et al., “Translocation of Crohn's Disease Escherichia coli Across M‐Cells: Contrasting Effects of Soluble Plant Fibres and Emulsifiers,” Gut 59, no. 10 (2010): 1331–1339. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 104. Roberts C. L., Rushworth S. L., Richman E., and Rhodes J. M., “Hypothesis: Increased Consumption of Emulsifiers as an Explanation for the Rising Incidence of Crohn's Disease,” Journal of Crohn's and Colitis 7, no. 4 (2013): 338–341. [DOI] [PubMed] [Google Scholar]
- 105. Cani P. D. and Everard A., “Keeping Gut Lining at Bay: Impact of Emulsifiers,” Trends in Endocrinology and Metabolism 26, no. 6 (2015): 273–274. [DOI] [PubMed] [Google Scholar]
- 106. Khuda S. E., Nguyen A. V., Sharma G. M., Alam M. S., Balan K. V., and Williams K. M., “Effects of Emulsifiers on an in Vitro Model of Intestinal Epithelial Tight Junctions and the Transport of Food Allergens,” Molecular Nutrition & Food Research 66, no. 4 (2022): 2100576. [DOI] [PubMed] [Google Scholar]
- 107. Ogulur I., Pat Y., Aydin T., et al., “Gut Epithelial Barrier Damage Caused by Dishwasher Detergents and Rinse Aids,” Journal of Allergy and Clinical Immunology 151 (2022): 469–484. [DOI] [PubMed] [Google Scholar]
- 108. Akdis C. A., “Does the Epithelial Barrier Hypothesis Explain the Increase in Allergy, Autoimmunity and Other Chronic Conditions?,” Nature Reviews. Immunology 21, no. 11 (2021): 739–751. [DOI] [PubMed] [Google Scholar]
- 109. Doyle A. D., Masuda M. Y., Pyon G. C., et al., “Detergent Exposure Induces Epithelial Barrier Dysfunction and Eosinophilic Inflammation in the Esophagus,” Allergy 78, no. 1 (2023): 192–201. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 110. Feketea G. and Tsabouri S., “Common Food Colorants and Allergic Reactions in Children: Myth or Reality?,” Food Chemistry 230 (2017): 578–588. [DOI] [PubMed] [Google Scholar]
- 111. Zaknun D., Schroecksnadel S., Kurz K., and Fuchs D., “Potential Role of Antioxidant Food Supplements, Preservatives and Colorants in the Pathogenesis of Allergy and Asthma,” International Archives of Allergy and Immunology 157, no. 2 (2011): 113–124. [DOI] [PubMed] [Google Scholar]
- 112. Andreozzi L., Giannetti A., Cipriani F., Caffarelli C., Mastrorilli C., and Ricci G., “Hypersensitivity Reactions to Food and Drug Additives: Problem or Myth?,” Acta Bio‐Medica 90, no. 3‐S (2019): 80–90. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 113. da Costa G. G., da Conceição N. G., da Silva P. A., and Simões B. F. T., “Worldwide Dietary Patterns and Their Association With Socioeconomic Data: An Ecological Exploratory Study,” Globalization and Health 18, no. 1 (2022): 31. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 114. Popkin B. M., “Nutritional Patterns and Transitions,” Population and Development Review 19, no. 1 (1993): 138–157. [Google Scholar]
- 115. Popkin B. M., “The Nutrition Transition: An Overview of World Patterns of Change,” Nutrition Reviews 62, no. 7 Pt 2 (2004): S140–S143. [DOI] [PubMed] [Google Scholar]
- 116. Bennett M. K., “International Contrasts in Food Consumption,” Geographical Review 31, no. 3 (1941): 365–376. [Google Scholar]
- 117. Cordain L., Miller J. B., Eaton S. B., Mann N., Holt S. H., and Speth J. D., “Plant‐Animal Subsistence Ratios and Macronutrient Energy Estimations in Worldwide Hunter‐Gatherer Diets,” American Journal of Clinical Nutrition 71, no. 3 (2000): 682–692. [DOI] [PubMed] [Google Scholar]
- 118. Cordain L., Eaton S. B., Sebastian A., et al., “Origins and Evolution of the Western Diet: Health Implications for the 21st Century,” American Journal of Clinical Nutrition 81, no. 2 (2005): 341–354. [DOI] [PubMed] [Google Scholar]
- 119. Khan M. T., Nieuwdorp M., and Bäckhed F., “Microbial Modulation of Insulin Sensitivity,” Cell Metabolism 20, no. 5 (2014): 753–760. [DOI] [PubMed] [Google Scholar]
- 120. David L. A., Maurice C. F., Carmody R. N., et al., “Diet Rapidly and Reproducibly Alters the Human Gut Microbiome,” Nature 505, no. 7484 (2014): 559–563. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 121. Miyamoto J., Igarashi M., Watanabe K., et al., “Gut Microbiota Confers Host Resistance to Obesity by Metabolizing Dietary Polyunsaturated Fatty Acids,” Nature Communications 10, no. 1 (2019): 4007. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 122. Gupta R., Sheikh A., Strachan D. P., and Anderson H. R., “Time Trends in Allergic Disorders in the UK,” Thorax 62, no. 1 (2007): 91–96. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 123. Mullins R. J., “Paediatric Food Allergy Trends in a Community‐Based Specialist Allergy Practice, 1995–2006,” Medical Journal of Australia 186, no. 12 (2007): 618–621. [DOI] [PubMed] [Google Scholar]
- 124. Prescott S. and Allen K. J., “Food Allergy: Riding the Second Wave of the Allergy Epidemic,” Pediatric Allergy and Immunology 22, no. 2 (2011): 155–160. [DOI] [PubMed] [Google Scholar]
- 125. Saha M. and Schmalzer S., “Green‐Revolution Epistemologies in China and India: Technocracy and Revolution in the Production of Scientific Knowledge and Peasant Identity,” BJHS Themes 1 (2016): 145–167. [Google Scholar]
- 126. Pingali P. and Abraham M., “Food Systems Transformation in Asia – A Brief Economic History,” Agricultural Economics 53, no. 6 (2022): 895–910. [Google Scholar]
- 127. “Peanut Production and Utilization in The People's Republic of China, ” (2004), http://peanutgr.fafu.edu.cn/supply_documents/china_peanut_production.pdf.
- 128. Wan G., Wang C., and Zhang X., “The Poverty‐Growth‐Inequality Triangle: Asia 1960s to 2010s,” Social Indicators Research 153 (2021): 795–822. [Google Scholar]
- 129. Pingali P., “Agricultural Policy and Nutrition Outcomes–Getting Beyond the Preoccupation With Staple Grains,” Food Security 7 (2015): 583–591. [Google Scholar]
- 130. Reardon T., Timmer C. P., and Minten B., “Supermarket Revolution in Asia and Emerging Development Strategies to Include Small Farmers,” Proceedings of the National Academy of Sciences of the United States of America 109, no. 31 (2012): 12332–12337. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 131. Ben‐Shoshan M., Turnbull E., and Clarke A., “Food Allergy: Temporal Trends and Determinants,” Current Allergy and Asthma Reports 12, no. 4 (2012): 346–372. [DOI] [PubMed] [Google Scholar]
- 132. Hidaka B. H., “Depression as a Disease of Modernity: Explanations for Increasing Prevalence,” Journal of Affective Disorders 140, no. 3 (2012): 205–214. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 133. “3. Global and Regional Food Consumption Patterns and Trends,” Food and Agriculture Organization (FAO), accessed July 24, 2024, https://www.fao.org/4/ac911e/ac911e05.htm.
- 134. Niu J., Li B., Zhang Q., Chen G., and Papadaki A., “Exploring the Traditional Chinese Diet and Its Association With Health Status—A Systematic Review,” Nutrition Reviews (2024), 10.1093/nutrit/nuae013. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 135. Baker P., Santos T., Neves P. A., et al., “First‐Food Systems Transformations and the Ultra‐Processing of Infant and Young Child Diets: The Determinants, Dynamics and Consequences of the Global Rise in Commercial Milk Formula Consumption,” Maternal & Child Nutrition 17, no. 2 (2021): e13097. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 136. “Four Decades of Poverty Reduction in China,” (2022), The World Bank, Development Research Center of the State Council, the People's Republic of China, https://thedocs.worldbank.org/en/doc/bdadc16a4f5c1c88a839c0f905cde802‐0070012022/original/Poverty‐Synthesis‐Report‐final.pdf.
- 137. Xie Y. and Zhou X., “Income Inequality in Today's China,” National Academy of Sciences of the United States of America 111, no. 19 (2014): 6928–6933. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 138. Lei L., Liu S., Ye Y., et al., “Associations Between Serum Aflatoxin‐B1 and Anemia in Pregnant Women: Evidence From Guangxi Zhuang Birth Cohort in China,” Toxins (Basel) 13, no. 11 (2021): 806. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 139. Qi N., Yu H., Yang C., Gong X., Liu Y., and Zhu Y., “Aflatoxin B1 in Peanut Oil From Western Guangdong, China, During 2016–2017,” Food Additives & Contaminants: Part B 12, no. 1 (2019): 45–51. [DOI] [PubMed] [Google Scholar]
- 140. Zhong Y., Lu H., Jiang Y., Rong M., Zhang X., and Liabsuetrakul T., “Effect of Homemade Peanut Oil Consumption During Pregnancy on Low Birth Weight and Preterm Birth Outcomes: A Cohort Study in Southwestern China,” Global Health Action 17, no. 1 (2024): 2336312. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 141. Arya S. S., Salve A. R., and Chauhan S., “Peanuts as Functional Food: A Review,” Journal of Food Science and Technology 53, no. 1 (2016): 31–41. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 142. Han M., “The Logic Between Nature and Culture: Food in the Wedding Traditions Across East Asia,” International Journal of Anthropology and Ethnology 7, no. 1 (2023): 9. [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The authors have nothing to report.
