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Food allergy prevention -

The greatest increase has been observed in infants and children with food allergies or atopic eczema [ 4, 5 ]. Overall, prevalence figures for food allergy and anaphylaxis appear to be steadily rising [ 7 ]. Effective allergy prevention has therefore become a global public health priority [ 8 ].

Nutritional interventions play a central role in the prevention and treatment of food allergies Table 1. In recent years, clinical approaches have undergone significant changes [ 3 ]. In the food allergy prevention space, greater focus has been placed on the early introduction of the complementary diet in infancy [ 9 ] Fig.

This is in contrast to the previous approach of prolonged food allergen avoidance which, in hindsight, may have paradoxically increased the rate of food allergies [ ]. In the area of food allergy treatment, there have also been major advances, including a shift from mere food allergen avoidance to proactive food allergen immunotherapy [ 13 ].

In addition, there is renewed interest in the role of gut microbiome-modifying therapies in an attempt to promote immunological tolerance development via the gut-associated immune system [ ].

This review summarizes the previous and current approaches to dietary food allergy prevention and treatment and highlights areas of uncertainty or controversy, as well as priorities for future research. Breastfeeding is one of the main pillars in both food allergy prevention and treatment [ ].

Breast milk provides the most appropriate source of nutrition for the young infant as it contains a specific nutrient mixture, growth factors, and protective maternal antibodies.

The World Health Organization WHO guidelines on complementary feeding of recommend exclusive breastfeeding for at least 6 months. However, this recommendation has been challenged in countries with a high prevalence of food allergies, as the early dietary introduction of allergens appears to protect from food allergies [ 22, 23 ].

Recent guidelines on the prevention of food allergies from Europe, the USA, and Australia have recommended the introduction of solids from 4—6 months of age [ ]. Breastfeeding is associated with the establishment of fecal microbiota high in Bifidobacteria [ 29 ]. Human milk oligosaccharides HMO promote the colonization of the gut with Bifidobacteria which is thought to promote mucosal tolerance via interaction with regulatory T-lymphocytes and Toll-like receptors [ 30 ].

Breastfeeding itself does not appear to confer a strong protective effect against food allergies [ 21 ]. However, the duration of exclusive breastfeeding appears to influence the risk of allergic disease [ 31, 32 ]. The protective effect of breastfeeding on eczema in the first 2 years of life appears to be modified by maternal allergy status [ 33 ].

Exclusively breastfed infants can express clinical manifestations of food allergy, including food protein-induced proctocolitis and multiple food intolerance of infancy [ ].

In some infants who failed a trial of maternal dietary elimination, treatment with a hypoallergenic formula may be required [ ]. Maternal elimination diets during pregnancy and lactation for the purpose of allergy prevention are not recommended [ 18, 43 ]. By contrast, secondary prevention aims to prevent the clinical expression of allergic disease in individuals who are either allergen sensitized or who already manifest other allergic disorders, such as atopic dermatitis or asthma.

The prevention of food allergies and atopic dermatitis by nutritional interventions has been explored for the past 2 decades with a broad range of approaches. In addition to the promotion of breastfeeding, these have included the use of partially hydrolyzed formula PHF and a range of maternal elimination diets [ 43, 45 ].

Supplementation with probiotics, prebiotics, and specific nutrients has also been explored [ 46, 47 ]. Some of these interventions have been trialed in high-risk populations, either in families with a history of allergies, or in infants who are showing evidence of food sensitization or eczema.

Other studies have assessed the preventive effect of interventions at the population level without selecting for allergic history. This distinction is important when the findings of prevention trials are translated into population-based health policies [ 22, 48 ].

Prevention strategies have been developed around 3 main hypotheses on the etiology of food allergies: the hygiene hypothesis, the dual allergen exposure hypothesis, and the vitamin D hypothesis [ 11, 49, 50 ]. The following sections will summarize current preventive strategies in the context of these hypotheses.

Gut microbiota and environmental microbial burden play a central role in early immune development and are likely to influence immunological events that lead to allergy [ 49, 51, 52 ]. The hygiene hypothesis assumes that there is an immune deviation to T-helper 2 reactions due to reduced early microbial exposure and a lack of fecal microbial diversity [ 53, 54 ].

For example, growing up in a rural farm environment has been shown to significantly reduce the risk of asthma and allergic disease in children [ 49, 55 ]. There are significant differences in the gut microbiota profiles between allergic and nonallergic infants and children [ 56, 57 ].

Infants with IgE-associated eczema have significantly reduced fecal microbial diversity in the first month of life, compared to nonatopic infants [ 54, 58 ]. Modification of early gut colonization and fecal microbial diversity in infancy may thus provide an avenue for preventive or therapeutic strategies [ 59 ].

Probiotic or prebiotic supplementation has been shown to modify the risk of allergies, particularly for atopic dermatitis in infancy [ ]. The World Allergy Organization Guidelines recommend the use of probiotics and prebiotics for the prevention of eczema and allergies, but caution that the available evidence is of very low certainty [ 63, 64 ].

Infants with allergies have been shown to have significantly lower numbers of fecal Bifidobacteria, compared to healthy infants [ 65 ]. Allergy prevention via supplementation with probiotic bacteria therefore appears to be a promising approach.

The effects of probiotics are mainly mediated via the innate immune system Toll-like receptors , resulting in the promotion of T-helper 1 differentiation, production of regulatory cytokines IL and TGF-beta and enhanced intestinal IgA responses [ 66 ].

Several studies have demonstrated that perinatal administration of probiotics to mothers in the last weeks of pregnancy and to infants in the first few months of life was associated with a significant reduction in atopic eczema [ ].

Nevertheless, results have been varied, depending on the probiotic strain, dose, timing and food matrix used. A study using Lactobacillus acidophilus LAVRI A1 even showed a paradoxical increase in allergic sensitization [ 70 ].

These studies highlight that clinical outcomes depend on the specific probiotic strains used. The role of probiotics in allergy prevention requires further study [ 46 ]. HMO are complex, nondigestible oligosaccharides with prebiotic properties in breast milk which provide a specialized substrate for Bifidobacteria.

In the past, infant formulas were devoid of prebiotic oligosaccharides [ 71 ]. Over the past decade, several manufactured prebiotics have been added to infant formula, including plant-based long-chain fructo-oligosaccharides FOS and short-chain galacto-oligosaccharides GOS.

GOS and FOS have been shown to increase counts of fecal Bifidobacteria in formula-fed infants [ 72, 73 ]. A more recent European multi-center randomized controlled trial assessed the effect of prebiotics in healthy, low-risk infants from 8 weeks to 12 months [ 75 ]. Again, disease severity was not affected.

Further studies are needed to assess the role of GOS and FOS in allergy prevention [ 62 ]. HMO in breast milk provide the substrate for specific microbes and significantly influence early microbial gut colonization [ 76, 77 ]. The role of HMO in the prevention and treatment of food allergies is at this stage not clearly defined but represents a promising area for future research [ 80, 81 ].

The dual allergen exposure hypothesis via skin and gut is based on the observation that infants with eczema have a high risk of developing IgE-mediated food allergies [ 11 ]. While allergen contact via eczematous skin may cause allergic sensitization, the exposure via the gastrointestinal tract is more likely to induce immunological tolerance [ 11, 82, 83 ].

Prolonged avoidance of a food allergen in infants with eczema may paradoxically increase the risk of food allergies [ 12, 84 ]. This reflects feeding practices in many European countries, but is not supported by the WHO guidelines on complementary feeding.

The Australian HealthNuts Study showed that the risk of developing egg allergy increased significantly if egg was introduced after 12 months of age [ 85 ]. This finding prompted to question the recommendation of delaying the introduction of egg beyond 12 months of age.

The LEAP Learning Early about Peanut study was the pivotal study demonstrating that the early introduction of peanut into the infants diet from 4 months conferred a protective effect against peanut allergy in high-risk infants [ 86 ]. This study was based on the observation that infants in Israel who were exposed to peanut in a teething snack had a low risk of peanut allergy, while Jewish infants in the United Kingdom who introduced peanut generally after 12 months of age had a high risk.

The subsequent clinical study enrolled infants with pre-existing egg allergy or eczema and randomized them to introduce peanut from 4 months, or to continue strict peanut avoidance. A supplementary analysis found that the skin prick test wheal diameter at the time of peanut introduction predicted the tolerance development in those who avoided peanut, with the greatest benefit seen between 6 and 11 months [ 87 ].

This analysis provided additional insights on the best timing of the dietary introduction of food allergens in high-risk infants. A second study, the Enquiring about Tolerance EAT study, prospectively examined if the early introduction of 6 food allergens from 4 months of age while breastfeeding could reduce the risk of food allergy in a nonallergic population [ 88 ].

On per-protocol analysis, there was a significant protective effect against food allergy. However, the study overall failed on intention-to-treat analysis due to a large proportion of participants who were unable to adhere to the study regimen.

This raised questions around the logistics of introducing foods early in infancy, including finding suitable food formats that would allow the delivery of food proteins in adequate doses to breastfed infants [ 22, 27 ].

The role of hydrolyzed formula in allergy prevention has been studied for more than 2 decades. The German Infant Nutritional Intervention GINI study is to date the largest, quasi-randomized trial examining the role of hydrolyzed formula in the prevention of allergies [ 89 ].

That study found a sustained protective effect against atop ic eczema for whey-based PHF and casein-based EHF [ 89 ]. Two other meta-analyses also confirmed a preventive effect, mainly for atopic dermatitis [ 92, 93 ]. Others have questioned the role of PHF and cautioned against overstating its preventive effects [ 94, 95 ].

Boyle et al. However, pooling of data on hydrolyzed formulas in meta-analyses may be problematic due to significant heterogeneity of PHF products. That study found a preventive effect for all allergies and eczema, but acknowledged limitations in the certainty of available data.

The current Allergy Prevention Guidelines by the European Academy of Allergy and Clinical Immunology EAACI recommend the use of PHF with a documented preventive effect in infants at high-risk of allergy if breastfeeding is insufficient or not possible [ 98 ]. Several studies have demonstrated an association between low vitamin D levels and food allergy [ 99, ].

This finding concurred with the observation that the prevalence of food allergy and eczema follows a north-south gradient, being more common in regions with less sun exposure and lower skin-derived vitamin D levels [ ]. Adequate vitamin D levels in the first year of life may therefore provide protection against the development of food allergies.

By contrast, vitamin D may also have undesirable immune-modulating effects and, in high doses, increase the risk of allergic sensitization. Vitamin D has been shown to inhibit the maturation of dendritic cells and impede the development of T-helper 1 responses.

In theory, vitamin D therefore could increase the risk of allergic disorders in infancy [ ]. This is supported by a recent German birth cohort study LINA study which found that high vitamin D levels during pregnancy and at birth were associated with an increased risk of food allergy [ ].

The varying effects of vitamin D on allergy risk have been explained by a U-shaped dose response curve, i. The aforementioned studies suggest that both vitamin D insufficiency and oversupplementation are risk factors for allergies [ 99 ]. The VITALITY trial, a prospective randomized trial, is currently underway to assess the role of postnatal vitamin D supplementation as a preventive strategy against IgE-mediated food allergy, eczema, and lower respiratory tract infections [ ].

Maternal diets high in omega-3 long-chain polyunsaturated fatty acids LCPUFA are thought to have a protective effect against the development of allergies in the newborn [ ]. Supplementation with docosahexaenoic acid and eicosapentaenoic acid during pregnancy has been shown to increase LCPUFA concentrations in breast milk [ ].

A large randomized clinical trial of maternal fish oil supplementation during pregnancy demonstrated a significant decrease in cord blood concentrations of Th-2 cytokines IL-4 and IL as well as increased levels of oral tolerance-inducing TGF-beta [ ].

Palmer et al. Primary outcomes were infantile eczema and food sensitization at 12 months of age. Infants in the fish oil-supplemented group had significantly lower rates of atopic eczema and egg sensitization. In another study by the same group [ ], high-risk infants were randomized to mg docosahexaenoic acid plus mg eicosapentaenoic acid daily or olive oil control from birth to 6 months of age.

In that study, between-group comparisons revealed no differences in allergic sensitization, eczema, asthma, or food allergy. In summary, fish oil supplementation during pregnancy reduced the risk of atopic eczema and food sensitization, whereas dietary supplementation after birth appeared to be ineffective.

The treatment of food allergies relies on the strict elimination of the offending allergens. In exclusively breastfed infants who react to allergens via breast milk, maternal elimination diets have been shown to be effective [ 34, 38 ].

The complementary diet also needs to be free of the food allergen. The main types of these treatment formulas are EHF and amino acid-based formula AAF [ 40, , ].

Hypoallergenic elimination diets need to be carefully supervised for nutritional adequacy [ 38 ]. Despite attempts to strictly eliminate offending food allergens from the diet, accidental reactions are relatively common. The risk of inadvertent allergic reactions and anaphylaxis significantly impacts the quality of life of patients and families [ , ].

Precautionary allergen labelling is in many instances still confusing or incomplete [ , ]. Reassuringly, several countries have introduced legislation towards more consistent allergen labelling [ ]. Food allergens that are secreted into breast milk may elicit allergic symptoms in the infant [ ]. While maternal elimination diets have no role in primary food allergy prevention, they have become a widely used intervention in breastfed infants with food allergies [ 38 ].

Poorly supervised or broad-based maternal elimination diets are not without nutritional risks for both mother and infant [ ].

The nutritional adequacy of the maternal diet should be assessed and monitored by a pediatric dietitian [ ]. Whey- or casein-based EHF are considered the first-line treatment of formula-fed infants with CMA [ ]. There are significant differences in the molecular weights and profiles of peptides in EHF.

This may explain differences in the risk of allergic reactions to various EHF [ , ]. A task force of the European Academy of Allergy and Clinical Immunology EAACI has therefore called for stricter standards for the definition of EHF marketed in Europe, including preclinical testing, quality assurance, and labelling requirements [ ].

Some recently developed EHF contain highly purified lactose. Contrary to common perception, lactose is tolerated well by most infants with CMA [ ]. These infants may develop increased diarrhea after lactose ingestion.

However, a lactose-containing EHF can generally be reintroduced once the diarrhea has settled and the small intestinal mucosal integrity has been restored. As young infants do not absorb all ingested lactose, it is considered a prebiotic compound with positive effects on the gut microbiome of infants [ ].

Compared to lactose-free formula, lactose-containing formula is associated with increased counts of Bifidobacteria and increased concentrations of short-chain fatty acids. This may confer a protective effect on colonic mucosal integrity and have a beneficial effect on early immune development [ 53 ].

There is to date no data showing a direct effect on tolerance development or allergic risk. EHF contains trace amount of allergenic peptides and therefore has a small residual allergenicity with the risk of allergic reactions [ ].

Conversely, the antigenic content in EHF may have the potential to actively promote tolerance development [ ]. This ability may be further enhanced by the addition of probiotic bacteria or other ingredients. Berni Canani et al. This effect appeared to be, at least in part, modulated by an expansion of buty-rate-producing gut microbiota [ ].

At the 3-year follow-up of another cohort, there appeared to be a greater rate of resolution of IgE-mediated CMA as well as a lower incidence of other allergic manifestations in response to LGG-supplemented EHF [ 15 ]. These studies highlight the potential for probiotic supplementation of EHF to hasten tolerance development as well as the importance of butyrate as a likely key mediator in tolerance acquisition.

However, further clinical trials are required to confirm the tolerogenic effects of LGG and assess the potential benefits of other probiotic strains with regard to early immune development. As tolerance development is thought to be an antigen-driven process [ ], AAF is unlikely to promote tolerance development [ ].

The addition of prebiotics or probiotics to AAF may have beneficial effects on gut microbiome, but clinical outcome data are not currently available [ ]. Should EHF or AAF not be available, other formula options may be considered.

Soy formula is frequently used for economic reasons in countries with limited access to hypoallergenic formulas [ ]. However, the role of soy formula in the treatment of infants with CMA remains controversial.

Generally, soy formula is not recommended as a first-line treatment in infants with CMA under 6 months of age [ ]. Hydrolyzed rice-based formula has become available in recent years as a hypoallergenic formula in infants with CMA [ , ].

The hydrolysis is required due to the poor solubility and hydrophobic properties of rice protein. These formulas are tolerated well and may have a taste advantage over casein- or whey-based EHF.

The exact role of hydrolyzed rice-based formulas needs to be clarified. The concept of food allergen immunotherapy is not new. The concept was first described by Schofield in in a year-old boy with egg allergy who was successfully desensitized by introducing egg in incremental doses [ ].

Since then, 3 main clinical immunotherapy concepts to food allergens have emerged: oral, sublingual, and epicutaneous immunotherapy. Oral immunotherapy OIT involves the stepwise introduction of a food allergen via the oral route, starting with milligram doses [ ] Fig.

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Robert Hamilton, M. Board-certified Pediatrician. Yes, early allergen introduction is safe. Feeding allergens to kids under 1 year of age is the safest time to start.

Less than one percent of children under the age of 1 have any reaction at all, and when they do, it is mild. Learn more about the safety of early allergen introduction here. Early allergen introduction is the process of gradually introducing common allergenic foods to your baby as early as four months of age.

Recent groundbreaking clinical trials have showed that early allergen introduction can help prevent food allergies, which have been followed by guidelines from leading health organizations all recommending early allergen introduction.

NIAID Role in Research. Food allergy prevention a Funding Preevntion. Apply for a Grant. After You Submit an Application. Manage Your Award. Funding News. Illustration of an antibody, a three-pronged protein made by the immune system. Ralf Grapefruit electrolyte drink. Heine; Detox herbal tea Allergy Prevention and Treatment by Targeted Prevemtion. Ann Pevention Metab 18 April ; 72 Hydration tips for outdoor enthusiasts. In view of the dramatic rise in the prevalence of food allergy globally, effective prevention strategies have become a public health priority. Several models have emerged around the etiology of food allergy, including the hygiene hypothesis, dual allergen exposure hypothesis, and vitamin D hypothesis. These form the basis for current and potential prevention strategies. Breastfeeding remains a key pillar of primary allergy prevention.