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Introducing highly allergenic foods to infants

Introducing highly allergenic foods to infants
Author:
David M Fleischer, MD
Section Editor:
Scott H Sicherer, MD, FAAAAI
Deputy Editor:
Elizabeth TePas, MD, MS
Literature review current through: Apr 2025. | This topic last updated: Sep 18, 2024.

INTRODUCTION — 

Introduction of highly allergenic foods to infants is discussed here. The general approach to introduction of solid foods during infancy is reviewed in greater detail separately, as is use of formula in infants at higher risk for allergic disease. (See "Introducing solid foods and vitamin and mineral supplementation during infancy" and "Introducing formula to infants at risk for allergic disease".)

Other aspects of the primary prevention of allergic disease are also discussed in greater detail separately. (See "Primary prevention of allergic disease: Maternal diet in pregnancy and lactation" and "The impact of breastfeeding on the development of allergic disease".)

COMPLEMENTARY FOOD INTRODUCTION — 

Complementary foods are solid foods and liquids other than human milk or infant formula. The timing of complementary food introduction is based on neurodevelopmental maturation and physiologic and nutritional needs of the infant. Both American and European allergy expert committee guidelines recommend that solid foods be introduced between four to six months of age in all infants [1-4]. Other organizations have also concluded that complementary foods may be safely introduced between four and six months of age [5-8], although many still recommend or prefer exclusive breastfeeding for the first six months of life [6,9-12]. We support introducing complementary foods, including those with high allergenic potential, between four and six months of age if the infant has the necessary developmental skills (eg, sits with support, has good head and neck control). Introducing complementary foods to infants is discussed in greater detail separately. (See "Introducing solid foods and vitamin and mineral supplementation during infancy", section on 'When to initiate complementary foods'.)

HIGHLY ALLERGENIC FOODS — 

While any food has the potential to cause allergy, certain foods are more common triggers of significant acute allergic reactions due to various factors. The most common food allergens in children in the United States and many other countries include cow's milk (CM), hen's egg, soy, wheat, peanut, tree nuts, sesame, and seafood (shellfish and fish). (See "Pathogenesis of food allergy", section on 'Factors influencing sensitization or tolerance' and "History and physical examination in the patient with possible food allergy", section on 'Common culprit foods' and "Food allergy in children: Prevalence, natural history, and monitoring for resolution", section on 'Prevalence of childhood food allergy' and "Food allergens: Clinical aspects of cross-reactivity".)

IDENTIFYING HIGH-RISK INFANTS — 

The primary risk factors for the development of food allergy in infants and young children are a family history of atopy and a personal history of atopy, particularly severe eczema.

An ascending pyramidal gradient of risk assessment for the possible development of food allergy was developed [13]. At the bottom (lowest risk) is infants in the general population who do not have identifiable risk factors. These infants still have some inherent risk of developing food allergy. In ascending order of increasing risk after this base group are infants with a parental history of allergic disease, infants with mild-to-moderate eczema, infants with a known food allergy, and finally the highest-risk group, infants with severe eczema.

While this ranking of risk is helpful for families to understand the relative risk of developing food allergy based on these factors, there is no existing evidence that shows the pathophysiologic mechanisms of allergy sensitization differ amongst these infants. This has led to the notion that recommendations for at-risk infants are applicable to general-population infants [14].

TIMING OF INTRODUCTION

Immunologic window and primary prevention — Recommendations regarding when to introduce highly allergenic foods, particularly in high-risk infants, have shifted over time. While the origins and causes of food allergy are complex, studies support the existence of a critical time during which an infant is at higher risk for developing allergic sensitization to common food allergens if they are not incorporated into the regular diet when other complementary foods are introduced [15,16].

For many years, it was thought that sensitization to food occurred via the gut by breastfeeding or early consumption, hence the previous recommendations in 2000 to delay the introduction of common food allergens until later in toddlerhood rather than earlier in infancy. However, recommendations shifted to promote earlier oral introduction of common allergens around the time other complementary foods are introduced due to the growing evidence that early-life sensitization to foods may occur through the skin, especially through eczematous skin, and may lead to eventual food allergy [15]. The goal of this approach is to possibly induce tolerance to foods through the gastrointestinal tract and prevent food allergy (dual-allergen exposure hypothesis).

Dietary interventions in the first years of life subsequent to the change in recommended approach have been analyzed for their effects on the prevalence of allergic disease, including food allergy [17-19]. Data from Australian studies suggest the prevalence of food allergy is not rising as rapidly or has leveled off for certain food allergies with earlier introduction of common allergens [18,19].

Limitations — There are few studies examining the safest time to introduce highly allergenic foods in infants. One challenge is that reactions can occur in response to the first known ingestion [20]. Another limitation is that results from studies that focused on a specific, study-defined, high-risk group or specific form of a food may not be broadly generalizable to other foods or the same food in a different form, to infants at higher risk for allergy for other reasons, or to infants at lower risk for allergy.

Standard-risk infants — A number of studies, most of which were performed in population-based, prospective birth cohorts not selected for food allergy risk status, have not supported delaying the introduction of solid foods beyond four to six months for the prevention of allergic disease [21-32] and, for cow's milk (CM) protein, suggest that an even earlier introduction may be beneficial [33-36]. Delayed introduction of solid foods [22] and restricting the diversity of complementary foods introduced in the first year of life [37] may increase the risk of allergy, whereas earlier introduction may decrease the risk [38], as is also seen in high-risk populations. It is still possible that some children in this lower-risk stratum will have allergic reactions with introduction since some infants are already allergic to foods such as hen's egg by four to six months of age [39]. Introduction of solids during infancy in the general population is reviewed in detail separately. (See "Introducing solid foods and vitamin and mineral supplementation during infancy".)

Cow's milk – One small, randomized trial and several observational studies in populations not selected by risk status suggest that introduction of cow's milk (CM) protein in early infancy can decrease the risk of developing CM allergy. The Strategy for Prevention of Milk Allergy by Daily Ingestion of Infant Formula in Early Infancy (SPADE) trial recruited newborns within five days of birth from four hospitals in Okinawa, Japan [34]. Infants were randomly assigned to ingestion at least 10 mL of a cow's milk formula (CMF) daily or avoidance of CMF between one and two months of age; the avoidance group was supplemented with soy formula as needed. Ongoing breastfeeding for both groups were recommended until six months of age, and food challenges were performed at six months of age to assess CM allergy. In the intention-to-treat (ITT) analysis population, 2 of 242 (0.8 percent) infants in the ingestion group had oral food challenge (OFC) confirmed CM allergy at six months of age compared with 17 of 249 (6.8 percent) infants in the avoidance group (relative risk [RR] 0.12, 95% CI 0.01-0.50; risk difference 6 percent, 95% CI 2.7-9.3).

One prospective study that examined feeding history and probable adverse reactions to CM in 13,019 infants found that earlier exposure to CMF (within the first 14 days of life) or other CM protein (mean 62 days of age) was associated with a lower rate of CM allergy compared with later introduction [33]. Another prospective cohort study that examined timing of exposure to CMF or other CM products in 1298 infants and development of adverse reactions to CM during childhood found that children who both received CMF supplementation in the hospital after delivery and who had CM protein introduced into their diet at less than two weeks of age were at the lowest risk of developing an adverse reaction to CM (reference group) compared with a four- to fivefold increased risk in the other exposure groups [36].

Hen's egg – Data regarding introduction of hen's egg are mixed, possibly in part due to the form of egg used (from most to least allergenic: raw, lightly cooked, or in baked goods). The Hen's Egg Allergy Prevention (HEAP) trial randomly assigned 383 infants four to six months of age who were recruited from the general population and had egg-specific immunoglobulin E (IgE) <0.35 kUA/L to increasing doses of raw, pasteurized egg white three times per week (0.83 g/dose during week 1, 1.67 g/dose during week 2, and 2.5 g/dose during week three until 12 months of age) or placebo [39]. There was no difference between the two groups with regard to egg sensitization or egg allergy confirmed by OFC. The adjusted prevalence of egg allergy in the 406 infants screened for the study was 5.3 percent. The authors noted a high rate of anaphylaxis at entry egg introduction, which may be partially attributed to the raw pasteurized form and the relatively larger amounts of egg protein consumed compared with other early egg introduction randomized, controlled trials.

A population-based, cross-sectional study examined the prevalence of egg allergy at 12 months of age (based upon positive egg-specific IgE testing followed by confirmation of allergy with an OFC to egg or a prior history of a reaction) in 2589 infants [27]. Later introduction of egg was associated with an increased risk of egg allergy (5.6, 7.8, 10.1, and 27.6 percent of infants at 12 months of age had egg allergy with introduction at 4 to 6, 7 to 9, 10 to 12, and >12 months of age, respectively), with significant differences seen with introduction at 10 to 12 and >12 months compared with 4 to 6 months (adjusted odds ratio [OR] 1.6, 95% CI 1.0-2.6 and OR 3.4, 95% CI 1.8-6.5, respectively). A lower risk of egg allergy was seen in infants who were given lightly cooked egg first rather than egg in baked goods first (OR 0.2, 95% CI 0.06-0.71).

Multiple highly allergenic foods – One trial, Enquiring about Tolerance (EAT), highlighted the challenge of introducing six of the most allergenic foods into an infant's diet [32]. The regimen used in this trial did not reduce the risk of food allergies, but it also did not support the prior recommendation to delay introduction of allergenic foods. In addition, earlier introduction did not appear to effect rates of concomitant breastfeeding.

In this trial, 1303 exclusively breast milk-fed infants were randomly assigned to introduction of six highly allergenic foods (egg, CM, sesame, whitefish, peanut, and wheat) between three to six months of age or continued exclusive breastfeeding until six months of age. Infants were recruited from the general population, but the group was self-enriched for atopy. Milk in the form of yogurt was always the first food introduced and wheat the last, with the other foods introduced in random order. There was no difference in the prevalence of food allergy at one and three years of age between the two groups in the ITT analysis. However, adherence to the food regimen was problematic, with 43 percent of the participants in the early-introduction group adhering to the protocol (ie, able to consume all six allergenic foods in the required amount and by the required time).

High-risk infants — The American Academy of Pediatrics (AAP) had previously suggested in 2000 that the introduction of certain highly allergenic foods be delayed further in high-risk infants and children: CM until age one year; hen's egg until age two years; and peanuts, tree nuts, and fish until age three years [40]. This recommendation was based upon early studies that suggested that delayed introduction of solid foods might help prevent some allergic diseases, particularly atopic dermatitis (AD) [41-43]. (See "Introducing formula to infants at risk for allergic disease", section on 'Infants at high risk for developing allergy'.)

However, this advice was modified in 2008 with consensus that there was insufficient evidence to recommend any specific practices concerning the introduction of these foods after four to six months for the prevention of allergic disease in high-risk infants [4,5,44-46]. To the contrary, data demonstrated that delayed introduction of solid foods may increase the risk of allergy [47,48], and early introduction of certain foods (eg, egg, peanut) between four to six months of age may decrease the risk of allergy to that specific food [38,49]. These findings suggest that the increased risk of peanut allergy seen in younger siblings of a child with peanut allergy, for example, is partly due to delayed introduction, in addition to an underlying genetic susceptibility [50]. Other risk factors, such as moderate-to-severe eczema, may also play a role in increasing this risk.

Hen's egg – Trials of earlier introduction of egg (at four to six months of age) demonstrated unclear benefit and a high rate of egg allergy at enrollment without known history of direct egg ingestion [51-54]. Variations in the studies included the factors used to determine high-risk status (severe to no eczema, environmental allergen sensitization, first-degree relative with atopic disease), the form of egg used for consumption and for challenges (raw whole egg powder, heated egg powder, whole cooked egg), and whether a pretreatment OFC was performed to determine presence of egg allergy. In addition, two trials were terminated early, one for benefit and one for safety reasons, and loss to follow-up was also an issue.

In the first trial, 86 high-risk infants with moderate-to-severe eczema were randomly assigned to daily consumption of 1 teaspoon of pasteurized raw whole-egg powder or rice powder from four to eight months of age [51]. A medically supervised feeding of 2 teaspoons of whole cooked egg was performed at eight months of age, with egg introduced into the diet after that if the feeding was successful. An OFC with one-half of a whole pasteurized raw egg was performed at 12 months of age. Although the infants in this study had no known prior direct ingestion of egg, egg-specific IgE was >0.35 kUA/L in 36 percent (24 of 67) of infants with this measurement at the start of the study. In addition, 31 percent (15 of 49) in the egg group reacted to the egg powder, most on initial exposure, and did not continue ingestion. At 12 months, 33 percent (14 of 42) in the egg group were diagnosed with egg allergy (elevated egg-specific IgE and a positive raw egg challenge or history of an allergic reaction to egg) compared with 51 percent (18 of 35) in the control group, a nonsignificant difference. However, the trial was terminated early for safety reasons due to the large percentage of infants allergic at four months and significant allergic reactions at the entry OFC.

In the Prevention of Egg Allergy with Tiny Amount Intake (PETIT) trial, 147 infants with eczema and no prior direct ingestion of egg or history of an allergic reaction to egg were randomly assigned to daily consumption of heated egg powder (50 mg daily from 6 to 9 months of age and 250 mg daily thereafter until 12 months of age) or placebo, along with aggressive treatment of eczema in both groups [52]. Participants underwent an OFC to 7 grams of heated whole-egg powder equivalent to 32 grams of boiled, whole egg at 12 months of age. After a planned interim analysis, the trial was stopped early due to benefit. The 121 infants who performed the egg OFC at 12 months were included in the ITT analysis. Of the infants in the treatment group, 8 percent (5 of 60) had egg allergy confirmed by OFC compared with 38 percent (23 of 61) in the placebo group (risk ratio [RR] 0.22, 95% CI 0.09-0.54). Limitations of this study include stopping early for benefit, which tends to overestimate treatment effect, especially if the event rate is low, as in this case. In addition, baseline eczema was more severe in the placebo group compared with the treatment group based upon the mean Scoring Atopic Dermatitis (SCORAD) score (42 versus 27.5, respectively), and the mean egg-specific IgE was higher in the placebo group as well (4.46 versus 0.73, respectively).

Two other trials of egg introduction beginning at four to six months of age were performed in infants at risk for food allergies based upon family history of atopic disease. The first of these, the Starting Time of Egg Protein (STEP) trial, enrolled 820 infants of atopic mothers with allergic disease and a positive environmental skin prick test (SPT) who were aged four to six months and did not have a history of eczema or known prior direct ingestion of egg [53]. Testing for egg sensitization was not performed prior to starting the treatment phase of the study. Infants were randomly assigned at four to six months of age to daily ingestion of 900 mg of pasteurized, raw whole-egg protein or placebo daily until 10 months of age. Cooked egg was introduced into the diet in both groups at 10 months of age, and a raw egg OFC was performed at 12 months of age. There was no difference in the percent of infants who reacted to the egg OFC at 12 months of age (7 percent in the treatment group compared with 10.3 percent in the placebo group). However, a higher percentage of infants stopped taking the study powder due to confirmed allergic reactions compared with the placebo group (6.1 versus 1.5 percent, respectively), suggesting that some of these infants were already allergic to egg.

The second trial, the Beating Egg Allergy Trial (BEAT), enrolled 319 infants who were SPT negative to egg but had a first-degree relative with atopic disease [54]. These infants were randomly assigned at four months of age to 350 mg pasteurized, raw whole-egg protein or placebo daily and were treated until eight months of age, at which time egg was introduced into the diet. At 12 months of age, egg sensitization was significantly lower in the treatment group (13 of 122, 10.7 percent) compared with placebo (25 of 122, 20.5 percent). However, there was a significant loss to follow-up, with only 254 infants having at least partial assessment at 12 months of age. In addition, 14 of the infants in the treatment group were lost to follow-up because they reacted to the egg powder at introduction. Presumably, there would have been no difference in the rates of sensitization had those children been evaluated at 12 months. Furthermore, there was no difference in the number of infants with probable egg allergy, a more clinically relevant outcome than sensitization, at 12 months of age.

Peanut – The data on earlier introduction of peanut are primarily derived from a single randomized trial with long-term follow-up. The Learning Early about Peanut Allergy (LEAP) trial was the first randomized trial to show benefit of earlier introduction of a major food allergen, with a decreased risk of developing peanut allergy in high-risk infants seen with earlier introduction of peanut at 4 to 11 months of age compared with continued avoidance through 60 months of age [47]. Peanut allergy continued to be significantly more common in the avoidance group despite both groups avoiding peanut consumption between 60 to 72 months of age (LEAP-On study) [48] and longer periods with lack of ingestion of peanut through 12 years of age [55].

In the LEAP study, 640 children aged 4 to <11 months with severe eczema and/or egg allergy and an SPT wheal of ≤4 mm to peanut were stratified based upon peanut sensitization (sensitized: SPT wheal 1 to 4 mm; n = 98, or not sensitized: no wheal on SPT; n = 542) and then randomly assigned to either consumption or avoidance of peanut until 60 months of age [47]. Absence of peanut allergy was confirmed by OFC for infants assigned to the consumption group. Those with a positive OFC (one in nonsensitized group, six in sensitized group) were told to avoid peanut. Those with a negative OFC were fed at least 6 grams of peanut protein per week (consumed in three or more meals per week). Among the 530 children in the nonsensitized group who underwent peanut OFC at 60 months of age, 13.7 percent of the avoidance group and 1.9 percent of the consumption group were allergic to peanut (absolute risk difference 11.8, 95% CI 3.4-20.3; 86 percent relative risk reduction). All 98 children in the sensitized group were evaluated at 60 months; 35.3 percent of the avoidance group and 10.6 percent of the consumption group were allergic to peanuts (absolute risk difference 24.7, 95% CI 4.9-43.3; 70 percent relative risk reduction). The retention rate of the study was 98.4 percent, and adherence to the assigned treatment was also high.

In the follow-up (LEAP-On) study that included 550 of the participants from the primary trial, both groups were asked to avoid peanut for 12 months until 72 months (6 years) of age [48]. Compliance with avoidance was 90.4 percent in the original avoidance group and 69.3 percent in the original consumption group. Peanut allergy continued to be significantly more common in the peanut avoidance group (18.6 percent, 52 of 280 children) than the early peanut consumption group (4.8 percent, 13 of 270 children). Three children in the consumption group who were previously tolerant developed peanut allergy during the 12-month avoidance period. In the group that continued avoidance, three children developed peanut allergy, and four had resolution of the allergy during the follow-up period. Development of peanut allergy in previously tolerant children who cease consumption is consistent with data on peanut allergy recurrence in patients who had outgrown their peanut allergy but did not go on to eat it regularly after a successful OFC. (See "Food allergy in children: Prevalence, natural history, and monitoring for resolution", section on 'Recurrence'.)

In a further continuation of the LEAP study (LEAP-Trio) that included 508 of the original participants, peanut tolerance at 12 years of age was determined by OFC in 80.5 percent, history of no reaction to consumption of 2 g of peanut on at least one occasion in the past year in 12.3 percent, and via use of a prediction model in 7 percent (primary endpoint not determined in 0.2 percent) [55]. Peanut allergy continued to remain more prevalent in the original peanut avoidance group than in the original peanut consumption group (15.4 versus 4.4 percent, respectively) despite periods of prolonged avoidance of peanut in both groups.

TESTING — 

Screening with skin prick tests (SPTs) or serum IgE testing and/or in-office supervised introduction is not required prior to introducing potentially allergenic complementary foods, regardless of risk level [13]. However, parent/caregiver preference for testing should be considered, especially if they will not introduce the food(s) without performing a test. An alternative is to perform supervised oral food challenge (OFC) without prior testing. An OFC is also advised if testing is done and is positive in the setting of no prior ingestion of the food and no history of an allergic reaction to the food given the high false-positive rate of allergy testing in this setting. (See "Diagnostic evaluation of IgE-mediated food allergy" and "Oral food challenges for diagnosis and management of food allergies".)

GENERAL APPROACH — 

We suggest introduction of highly allergenic, complementary foods (eg, cow's milk [CM] products, peanut, cooked hen's egg, soy, wheat, tree nuts, sesame, fish, and shellfish) beginning at approximately four to six months of age for all infants, regardless of allergic risk. This recommendation is based upon accumulating evidence that earlier introduction results in lower rates of food allergy in both high-risk and standard-risk infants. (See 'High-risk infants' above and 'Standard-risk infants' above.)

It is not known what dose and frequency of ingestion for each allergen are necessary to maintain tolerance after they are introduced into the diet. Thus, the general approach is to try to incorporate these foods into the infant's regular diet by focusing less on the amounts and more on the forms that the child likes and is willing to eat, with a general target of at least weekly consumption [13].

We counsel parents/caregivers to introduce highly allergenic foods in the following manner:

First, the child should be at least four months of age and have shown developmental readiness to consume complementary foods. Some allergens can be choking hazards for infants. Specific infant-safe forms, such as nut butter smoothed out by mixing with a fruit or vegetable puree, should be used. (See "Introducing solid foods and vitamin and mineral supplementation during infancy", section on 'Developmental skills'.)

In addition, the child should have tolerated a few of the more typical, initial complementary foods (such as cereals, meats, fruits, or vegetables).

If these two criteria are met, then the child can be given an initial taste of one of these foods at home (rather than at daycare or at a restaurant).

If there is no apparent reaction, the food can be introduced in gradually increasing amounts.

For further practical advice on how to introduce major allergens, please refer to Appendix A of the 2021 American Academy of Allergy, Asthma and Immunology (AAAAI), American College of Allergy, Asthma and Immunology (ACAAI), and Canadian Society for Allergy and Clinical Immunology (CSACI) Consensus Approach to the Primary Prevention of Food Allergy Through Nutrition.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Food allergy".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Beyond the Basics topic (see "Patient education: Starting solid foods with babies (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Optimal initial source of nutrition for term infants – Human milk is the optimal source of nutrition for all term infants during the first four to six months of life, regardless of their risk for allergic disease. (See "Infant benefits of breastfeeding".)

Most common highly allergenic foods – The most common highly allergenic foods include cow's milk (CM), hen's egg, soy, wheat, peanut, tree nuts, sesame, shellfish, and fish. (See 'Highly allergenic foods' above.)

Determining risk Infants at highest risk for developing food allergy are, in descending order, those with severe eczema, mild-to-moderate eczema, and parental history of allergic disease. However, infants in the general population who do not have identifiable risk factors can still develop food allergy. (See 'Identifying high-risk infants' above.)

Approach to introduction of potentially allergenic complementary foods – Previous guidelines recommended delayed introduction of highly allergenic complementary foods for the purpose of preventing allergic disease in high-risk infants. However, subsequent evidence has suggested that this practice may increase rather than decrease the incidence of food allergies in both high-risk and standard-risk infants. (See 'High-risk infants' above and 'Standard-risk infants' above.)

For all infants, regardless of allergic risk, we suggest not delaying introduction of highly allergenic complementary foods (eg, CM products, peanut, cooked hen's egg, soy, wheat, tree nuts, sesame, fish, and shellfish) once introduction of complementary food is started (Grade 2C). The most robust data available for earlier introduction is for peanut and egg, and the greatest potential for benefit with this approach is for high-risk infants.

Infants should be at least four months of age, be developmentally ready, and have tolerated a few less allergenic complementary foods. Infant-safe forms of the foods should be used. Testing is not required prior to introduction. Incorporating the food into the regular diet is encouraged once the food is introduced, with a target of at least weekly consumption since more frequent exposure may help maintain tolerance to the food. (See 'General approach' above and 'Testing' above.)

The general approach to introduction of complementary foods during infancy is discussed separately. (See "Introducing solid foods and vitamin and mineral supplementation during infancy", section on 'When to initiate complementary foods' and 'General approach' above.)

  1. Greer FR, Sicherer SH, Burks AW, et al. The Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Hydrolyzed Formulas, and Timing of Introduction of Allergenic Complementary Foods. Pediatrics 2019; 143.
  2. Muraro A, Dreborg S, Halken S, et al. Dietary prevention of allergic diseases in infants and small children. Part III: Critical review of published peer-reviewed observational and interventional studies and final recommendations. Pediatr Allergy Immunol 2004; 15:291.
  3. Grimshaw KE, Allen K, Edwards CA, et al. Infant feeding and allergy prevention: a review of current knowledge and recommendations. A EuroPrevall state of the art paper. Allergy 2009; 64:1407.
  4. Fleischer DM, Spergel JM, Assa'ad AH, Pongracic JA. Primary prevention of allergic disease through nutritional interventions. J Allergy Clin Immunol Pract 2013; 1:29.
  5. Agostoni C, Decsi T, Fewtrell M, et al. Complementary feeding: a commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr 2008; 46:99.
  6. Section on Breastfeeding. Breastfeeding and the use of human milk. Pediatrics 2012; 129:e827.
  7. European Food, Safety Authority. Scientific opinion on the appropriate age for introduction of complementary feeding of infants. EFSA Journal 2009; 7:1423.
  8. Netting MJ, Campbell DE, Koplin JJ, et al. An Australian Consensus on Infant Feeding Guidelines to Prevent Food Allergy: Outcomes From the Australian Infant Feeding Summit. J Allergy Clin Immunol Pract 2017; 5:1617.
  9. World Health Organization. Global Strategy for Infant and Young Child Feeding (2003). Available at: www.who.int/nutrition/publications/infantfeeding/en/index.html (Accessed on April 10, 2009).
  10. Committee on Health Care for Underserved Women, American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 361: Breastfeeding: maternal and infant aspects. Obstet Gynecol 2007; 109:479.
  11. Boland M. Exclusive breastfeeding should continue to six months. Paediatr Child Health 2005; 10:148.
  12. US Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, et al. Primary Care Interventions to Support Breastfeeding: US Preventive Services Task Force Recommendation Statement. JAMA 2016; 316:1688.
  13. Fleischer DM, Chan ES, 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. J Allergy Clin Immunol Pract 2021; 9:22.
  14. Togias A, Cooper SF, Acebal ML, et al. Addendum Guidelines for the Prevention of Peanut Allergy in the United States: Report of the National Institute of Allergy and Infectious Diseases-Sponsored Expert Panel. Pediatr Dermatol 2017; 34:e1.
  15. Brough HA, Nadeau KC, Sindher SB, et al. Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented? Allergy 2020; 75:2185.
  16. Zeiger RS. Food allergen avoidance in the prevention of food allergy in infants and children. Pediatrics 2003; 111:1662.
  17. Pali-Schöll I, Renz H, Jensen-Jarolim E. Update on allergies in pregnancy, lactation, and early childhood. J Allergy Clin Immunol 2009; 123:1012.
  18. Soriano VX, Allen KJ, Dharmage SC, et al. Prevalence and Determinants of Food Allergy in the Era of Early Allergen Introduction: The EarlyNuts Population-Based Study. J Allergy Clin Immunol Pract 2024; 12:3068.
  19. Soriano VX, Peters RL, Moreno-Betancur M, et al. Association Between Earlier Introduction of Peanut and Prevalence of Peanut Allergy in Infants in Australia. JAMA 2022; 328:48.
  20. Sicherer SH, Burks AW, Sampson HA. Clinical features of acute allergic reactions to peanut and tree nuts in children. Pediatrics 1998; 102:e6.
  21. Du Toit G, Katz Y, Sasieni P, et al. Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy. J Allergy Clin Immunol 2008; 122:984.
  22. Zutavern A, von Mutius E, Harris J, et al. The introduction of solids in relation to asthma and eczema. Arch Dis Child 2004; 89:303.
  23. Zutavern A, Brockow I, Schaaf B, et al. Timing of solid food introduction in relation to eczema, asthma, allergic rhinitis, and food and inhalant sensitization at the age of 6 years: results from the prospective birth cohort study LISA. Pediatrics 2008; 121:e44.
  24. Snijders BE, Thijs C, van Ree R, van den Brandt PA. Age at first introduction of cow milk products and other food products in relation to infant atopic manifestations in the first 2 years of life: the KOALA Birth Cohort Study. Pediatrics 2008; 122:e115.
  25. Poole JA, Barriga K, Leung DY, et al. Timing of initial exposure to cereal grains and the risk of wheat allergy. Pediatrics 2006; 117:2175.
  26. Nwaru BI, Erkkola M, Ahonen S, et al. Age at the introduction of solid foods during the first year and allergic sensitization at age 5 years. Pediatrics 2010; 125:50.
  27. Koplin JJ, Osborne NJ, Wake M, et al. Can early introduction of egg prevent egg allergy in infants? A population-based study. J Allergy Clin Immunol 2010; 126:807.
  28. Tromp II, Kiefte-de Jong JC, Lebon A, et al. The introduction of allergenic foods and the development of reported wheezing and eczema in childhood: the Generation R study. Arch Pediatr Adolesc Med 2011; 165:933.
  29. Joseph CL, Ownby DR, Havstad SL, et al. Early complementary feeding and risk of food sensitization in a birth cohort. J Allergy Clin Immunol 2011; 127:1203.
  30. Grimshaw KE, Maskell J, Oliver EM, et al. Introduction of complementary foods and the relationship to food allergy. Pediatrics 2013; 132:e1529.
  31. Luccioli S, Zhang Y, Verrill L, et al. Infant feeding practices and reported food allergies at 6 years of age. Pediatrics 2014; 134 Suppl 1:S21.
  32. Perkin MR, Logan K, Tseng A, et al. Randomized Trial of Introduction of Allergenic Foods in Breast-Fed Infants. N Engl J Med 2016; 374:1733.
  33. Katz Y, Rajuan N, Goldberg MR, et al. Early exposure to cow's milk protein is protective against IgE-mediated cow's milk protein allergy. J Allergy Clin Immunol 2010; 126:77.
  34. Sakihara T, Otsuji K, Arakaki Y, et al. Randomized trial of early infant formula introduction to prevent cow's milk allergy. J Allergy Clin Immunol 2021; 147:224.
  35. Sakihara T, Otsuji K, Arakaki Y, et al. Early Discontinuation of Cow's Milk Protein Ingestion Is Associated with the Development of Cow's Milk Allergy. J Allergy Clin Immunol Pract 2022; 10:172.
  36. Switkowski KM, Oken E, Rifas-Shiman SL, et al. Timing of Cow's Milk Protein Introduction and Childhood Adverse Reactions to Cow's Milk. J Allergy Clin Immunol Pract 2022; 10:2713.
  37. Roduit C, Frei R, Depner M, et al. Increased food diversity in the first year of life is inversely associated with allergic diseases. J Allergy Clin Immunol 2014; 133:1056.
  38. Ierodiakonou D, Garcia-Larsen V, Logan A, et al. Timing of Allergenic Food Introduction to the Infant Diet and Risk of Allergic or Autoimmune Disease: A Systematic Review and Meta-analysis. JAMA 2016; 316:1181.
  39. Bellach J, Schwarz V, Ahrens B, et al. Randomized placebo-controlled trial of hen's egg consumption for primary prevention in infants. J Allergy Clin Immunol 2017; 139:1591.
  40. American Academy of Pediatrics. Committee on Nutrition. Hypoallergenic infant formulas. Pediatrics 2000; 106:346.
  41. Fergusson DM, Horwood LJ, Beautrais AL, et al. Eczema and infant diet. Clin Allergy 1981; 11:325.
  42. Fergusson DM, Horwood LJ, Shannon FT. Early solid feeding and recurrent childhood eczema: a 10-year longitudinal study. Pediatrics 1990; 86:541.
  43. Fergusson DM, Horwood LJ, Shannon FT. Asthma and infant diet. Arch Dis Child 1983; 58:48.
  44. Sicherer SH, Burks AW. Maternal and infant diets for prevention of allergic diseases: understanding menu changes in 2008. J Allergy Clin Immunol 2008; 122:29.
  45. Greer FR, Sicherer SH, Burks AW, et al. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics 2008; 121:183.
  46. Høst A, Halken S, Muraro A, et al. Dietary prevention of allergic diseases in infants and small children. Pediatr Allergy Immunol 2008; 19:1.
  47. Du Toit G, Roberts G, Sayre PH, et al. Randomized trial of peanut consumption in infants at risk for peanut allergy. N Engl J Med 2015; 372:803.
  48. Du Toit G, Sayre PH, Roberts G, et al. Effect of Avoidance on Peanut Allergy after Early Peanut Consumption. N Engl J Med 2016; 374:1435.
  49. Sicherer SH, Allen K, Lack G, et al. Critical Issues in Food Allergy: A National Academies Consensus Report. Pediatrics 2017; 140.
  50. Abrams EM, Chan ES, Sicherer SH. Should Younger Siblings of Peanut Allergic Children Be Screened for Peanut Allergy? J Allergy Clin Immunol Pract 2018; 6:414.
  51. Palmer DJ, Metcalfe J, Makrides M, et al. Early regular egg exposure in infants with eczema: A randomized controlled trial. J Allergy Clin Immunol 2013; 132:387.
  52. Natsume O, Kabashima S, Nakazato J, et al. Two-step egg introduction for prevention of egg allergy in high-risk infants with eczema (PETIT): a randomised, double-blind, placebo-controlled trial. Lancet 2017; 389:276.
  53. Palmer DJ, Sullivan TR, Gold MS, et al. Randomized controlled trial of early regular egg intake to prevent egg allergy. J Allergy Clin Immunol 2017; 139:1600.
  54. Wei-Liang Tan J, Valerio C, Barnes EH, et al. A randomized trial of egg introduction from 4 months of age in infants at risk for egg allergy. J Allergy Clin Immunol 2017; 139:1621.
  55. Du Toit G, Huffaker MF, Radulovic S, et al. Follow-up to Adolescence after Early Peanut Introduction for Allergy Prevention. NEJM Evid 2024; 3:EVIDoa2300311.
Topic 107525 Version 24.0

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