INTRODUCTION — Peanut, tree nut, and seed allergies are some of most common food allergies in both children and adults. These allergies tend to cause severe reactions and usually persist over time.
The epidemiology, pathogenesis, and clinical features of peanut, tree nut, and seed allergies are presented in this topic review. Diagnosis and management of these allergies are discussed separately, as is treatment for food-induced anaphylaxis. General discussions of food allergy are presented separately in appropriate topic reviews. (See "Peanut, tree nut, and seed allergy: Diagnosis" and "Peanut, tree nut, and seed allergy: Management" and "Food-induced anaphylaxis".)
EPIDEMIOLOGY — The prevalence of peanut allergy is variable worldwide. The highest rates are seen in westernized countries such as the United States, the United Kingdom, Canada, and Australia, where the prevalence is approximately 1 to 2 percent [1-10]. However, rates are lower in other westernized countries such as France (0.3 to 0.7 percent) [11], Denmark (0.2 to 0.6 percent) [12,13], and Israel (0.04 to 0.17 percent) [6,14]. Peanut allergy is rare in Asia, where peanut is often not found on the list of most common allergenic foods [15-17]. Regional dietary habits and pollen exposure may influence the epidemiology of allergy to legumes, such as peanut [6,18-20]. (See "Food allergens: Clinical aspects of cross-reactivity" and 'Pathogenesis' below and "Food allergy in children: Prevalence, natural history, and monitoring for resolution".)
Data suggest that the rate of peanut allergy is increasing in some countries, such as the US and UK [1,2,21], although it may be leveling off [22]. The rate appears stable in other countries including Canada [5]. Hypotheses regarding the apparent increase in prevalence of food allergies are discussed in detail separately [23]. (See "Pathogenesis of food allergy", section on 'Prevalence'.)
Tree nuts and seeds are also common food allergens [1,24-28]. Sesame and mustard are the most common seed allergies reported, but allergy to other seeds can occur [26]. The reported prevalence of sesame seed allergy in France, based upon data from the national databank, was 2 percent in children and 5 percent in adults [29]. However, patient-reported food allergy typically exceeds challenge-proven symptomatic allergy. Studies in the US using symptom-report criteria convincing for immunoglobulin E (IgE) mediated allergy reported a sesame allergy prevalence of 0.2 percent, and an Australian study of food challenge-confirmed allergy found a sesame allergy prevalence of 0.8 percent [30,31]. The prevalence of tree nut allergy was similar to that of peanut allergy in a general population survey in the United States [1]. Walnut was the most commonly reported tree nut allergy, followed by cashew and almond.
Coexisting food allergy is discussed below. (See 'Allergies to other foods' below.)
PATHOGENESIS — Nine major and minor allergenic proteins in peanut (Arachis hypogaea), designated Ara h 1 to 9, have been identified that are responsible for IgE-mediated reactions [18,19,32,33]. The dominant allergens in most populations are Ara h 1 to 3, which are vicilin, conglutin, and glycinin seed storage proteins, respectively. Ara h 4, 6, and 7 are also seed storage proteins. Ara h 4 is a nearly identical isoform of Ara h 3. Ara h 6 is highly homologous to Ara h 2, and Ara h 7 is also a conglutin.
Ara h 5, 8, and 9 are proteins that are associated with pollen-food allergy syndrome (oral allergy syndrome). Ara h 5 is a profilin, Ara h 8 is a Bet v 1 (a birch allergen) homolog [18], and Ara h 9 is a nonspecific lipid transfer protein similar to Pru p 3 (a peach allergen) [18,19]. (See "Pathogenesis of oral allergy syndrome (pollen-food allergy syndrome)", section on 'Allergens in PFS'.)
In the United States and Europe, 44 to 77 percent of patients with peanut allergy have specific IgE to Ara h 1 and 2, and 25 to 77 percent have specific IgE to Ara h 3 [34,35]. In contrast, specific IgE to Ara h 8 or 9 is more common in individuals with concomitant birch pollen or peach sensitization, especially in Northern and Southern Europe, respectively [18,19]. The presence of IgE antibodies to Ara h 2 is most closely associated with systemic reactions to peanut [36]. (See "Component testing for pollen-related, plant-derived food allergies", section on 'Peanut'.)
Tree nut and seed allergens are less well characterized than peanut allergens, although a number of tree nut and seed allergens have been identified [37,38]. These allergens include pollen allergen homologs, such as Bet v 1-like proteins and profilins, and more stable allergens, such as seed storage proteins and some lipid transfer proteins. Issues of crossreactivity between allergens are discussed in greater detail separately. (See "Food allergens: Clinical aspects of cross-reactivity" and 'Allergies to other foods' below.)
Allergy to peanut, tree nuts, and seeds can develop through primary sensitization to the food itself or through secondary sensitization via sensitization to cross-reactive allergens (eg, birch pollen). (See "Pathogenesis of food allergy", section on 'Routes of allergen sensitization' and "Pathogenesis of oral allergy syndrome (pollen-food allergy syndrome)".)
Results from one study suggest that the development of atopic sensitization to peanut occurs after birth rather than in utero. T cell cytokine responses and antibody assays of peanut-specific IgE and immunoglobulin G4 (IgG4) were investigated in a cohort of 200 high-risk infants at birth (cord blood) and at 6, 12, and 24 months of age [39]. Skin prick testing was also performed, although food challenges were not done, and data on parental peanut ingestion were not collected. No association was found between cord blood T cell reactivity and the subsequent postnatal IgE or skin test responses to peanut (presence or absence of peanut sensitization), whereas an increasingly strong association developed between these parameters beyond six months of age.
Several reasons have been proposed to explain why peanut (and possibly tree nuts and seeds) are more allergenic than other foods:
●Seed storage proteins contain disulfide bonds that give these proteins high thermostability and resistance to extreme pH values. In addition, these proteins are often glycosylated, which further increases thermal and proteolytic stability. Ara h 1 in the glycosylated form can act as a T helper type 2 (Th2) adjuvant, activating dendritic cells to induce maturation and proliferation of Th2 cells, which promote IgE production [40]. (See "Molecular features of food allergens".)
●Certain factors involved in harvesting and processing may also make these foods more allergenic. A greater amount of Ara h 1 is found in larger, more mature peanut kernels and in peanuts dried or cured at higher temperatures [41]. High-heat roasting leads to glycation reactions that increase protein stability and allergenicity. (See "Pathogenesis of food allergy", section on 'Antigen form'.)
●Metabolized vegetable oils, such as peanut oil, can serve as adjuvants, increasing the immune response to antigens [42]. Whipping or emulsifying peanut butter to prevent the oil from separating from the peanut solids brings more of the water-soluble protein into direct contact with the oil, potentially increasing the immunogenicity of peanut proteins. (See "Molecular features of food allergens".)
The pathogenesis of non-IgE-mediated peanut, tree nut, and seed allergy is less clear.
RISK FACTORS FOR DEVELOPMENT OF PEANUT ALLERGY — Risk factors for the development of peanut allergy include severe atopic dermatitis and/or hen's egg allergy in young infants [43]. Peanut allergy is also associated with the use of skin care products containing crude peanut oil in young children with a history of atopic dermatitis [44] and the degree of household peanut consumption [45]. Specific factors associated with increased risk of tree nut or seed allergy have not been elucidated.
Familial factors — Initial data from observational studies suggested that younger siblings of children with peanut allergy were at increased risk of developing peanut allergy [46,47]. However, data from subsequent studies indicate that this finding is due in part to delayed introduction in this population [48-50]. (See "Peanut, tree nut, and seed allergy: Management", section on 'Management of younger siblings'.)
Genetic factors — In a case-control study, loss-of-function mutations in filaggrin were associated with oral food challenge-positive peanut allergy (odds ratio [OR] 5.3) [51]. These findings were replicated in a different population (OR 1.9) in the same study.
Skin care products — A British study found that the development of peanut allergy was associated with the use of skin care products that contain peanut protein in the form of crude oil in children with atopic dermatitis, particularly those with active eczematous rashes [44]. Only highly refined oils are used in skin preparations in the United States. These oils contain almost no detectable allergen. It is not known if there is an association with the use of refined peanut, tree nut, or seed oils in skin care products and the development of peanut allergy. Nor is it known whether there is a similar risk if these oils are applied to noninflamed skin.
Timing of first exposure — The timing of introduction of a food probably influences the development of allergy versus tolerance. Peanut allergy has more than doubled in young children in countries where delayed introduction of peanut until at least three years of age was recommended [1,4]. In addition, the rate of peanut allergy is lower in countries where peanuts are introduced at a younger age [6,14,52]. However, dietary advice was generally poorly followed in countries that recommended delayed introduction, so the impact of these recommendations is unclear [4]. One study noted that the age at first exposure in children who developed peanut allergy and age at initial reaction (19 and 21 months) were lower during the period in which delayed introduction was recommended compared with the age of exposure and allergy onset (22 and 24 months) in the period prior to those recommendations [53].
The Learning Early about Peanut Allergy (LEAP) trial was the first randomized trial to show benefit of early introduction of a major food allergen, with earlier introduction of peanut at 4 to 11 months of age associated with a decreased risk of developing peanut allergy [43]. Introduction of highly allergenic foods is reviewed in greater detail separately. (See "Introducing highly allergenic foods to infants and children", section on 'Suggested approach'.)
Other factors that may determine whether an individual becomes sensitized or tolerant to a food allergen are discussed in detail separately. (See "Pathogenesis of food allergy", section on 'Factors influencing sensitization or tolerance' and "Pathogenesis of oral allergy syndrome (pollen-food allergy syndrome)" and "Introducing highly allergenic foods to infants and children", section on 'Introduction in higher-risk populations'.)
Other risk factors — Factors that have been associated with increased risk of food allergy in general in observational studies include older maternal age, maternal dietary factors, higher parental levels of education and income, delivery via cesarean section, vitamin supplementation, and use of antiulcer drugs. However, observational studies are prone to bias, and many of these factors may be confounders. These issues are reviewed in greater detail separately. (See "Pathogenesis of food allergy".)
Factors found to not increase risk
Soy consumption — Consumption of soy formula or milk was associated with peanut allergy in one study [44]. However, a subsequent study confirmed the suspicion that this association was not causal, but was due to preferential use of soy formula/milk in children who had a known or suspected allergy to cow's milk based upon personal and family history [54]. In addition, an increased risk of peanut allergy was not seen in infants fed soy formula in a randomized trial of soy versus extensively hydrolyzed formula in infants with cow's milk allergy [55].
Maternal ingestion of food allergens — Evidence suggests that maternal avoidance of allergenic foods during pregnancy and lactation does not reduce the risk of atopic disease in infants. As such, the American Academy of Pediatrics (AAP) and European Academy of Allergy and Clinical Immunology (EAACI) do not recommend maternal avoidance diets during pregnancy [56,57]. (See "Primary prevention of allergic disease: Maternal diet in pregnancy and lactation".)
TYPES OF REACTIONS — Most allergic reactions to peanut, tree nuts, and seeds are IgE mediated. These reactions can range from mild symptoms isolated to the oropharynx to severe anaphylaxis (table 1). Peanut is also implicated as a trigger in non-IgE-mediated or mixed IgE and non-IgE-mediated disorders, such as atopic dermatitis and occasionally eosinophilic esophagitis.
Systemic IgE-mediated reactions — The majority of allergic reactions to peanut, tree nuts, or seeds are systemic. Symptoms can be isolated to a single organ system, most commonly the skin (eg, urticaria, angioedema), or involve multiple organ systems (anaphylaxis) [58,59]. In one study of children, 89 percent of initial reactions to peanut or tree nuts involved the skin, one-half involved the respiratory tract, and one-third affected the gastrointestinal tract [59]. One-half of all reactions involved two or more organ systems in this study. Similar findings are reported for sesame allergy [14,28,60]. The clinical features of IgE-mediated reactions are discussed in more detail elsewhere. (See "Clinical manifestations of food allergy: An overview".)
Peanut, tree nut, and seed allergies are among the most common causes of food-induced anaphylaxis. Concomitant asthma and peanut allergy developing at a later age were associated with an increased risk of anaphylaxis in one study [8]. In another study, coexisting atopic diseases of greater severity and lower serum angiotensin-converting enzyme concentrations were associated with increased risk of life-threatening anaphylaxis [61]. Peanut and tree nut allergies are risk factors for, and are rarely responsible for, fatal anaphylaxis. A prospective study of nut and sesame allergy assessed by food challenges found that almond, hazelnut, and pine nut reactions were associated with the lowest severity scores [62]. Food-induced anaphylaxis and fatal anaphylaxis are discussed in greater detail separately. (See "Food-induced anaphylaxis" and "Anaphylaxis in infants" and "Fatal anaphylaxis".)
Reactions due to skin contact — Reactions due to skin contact with a food allergen (eg, peanut butter) are typically limited to the site of contact and are unlikely to trigger systemic symptoms [63-67]. Inadvertent contact in the eye, typically due to rubbing the eye with residual food on the finger, can lead to marked periorbital edema, erythema, and pruritus. (See "Management of food allergy: Avoidance", section on 'Skin contact and inhalation'.)
Reactions due to inhalation exposure — Inhalation of peanut, tree nut, or seed proteins can trigger allergic reactions in particularly sensitive patients or in patients exposed to large amounts of allergen, such as with an occupational exposure [67-70]. Inhalation exposure can occur when particles become airborne (eg, peanut dust from bags of peanuts or peanut flour) or aerosolized (eg, peanut protein in cooking vapors). The smell of peanut butter, which contains volatile organic compounds, but not peanut protein, did not trigger any reactions in one study of patients with peanut allergy [63]. (See "Management of food allergy: Avoidance", section on 'Airline travel'.)
Reactions due to allergen exposure through saliva — Exposure to allergens such as peanut through another person's saliva (kissing, sharing utensils or straws) can rarely trigger local and systemic allergic reactions in sensitized individuals [71,72]. (See "Management of food allergy: Avoidance", section on 'Interpersonal contact'.)
Oral allergy syndrome — Reactions localized and limited to the oropharynx can occur upon ingestion of peanut and certain tree nuts in individuals who are sensitized to homologous plant allergens (figure 1 and figure 2). As examples, Bet v 1 (birch pollen allergen) cross-reacts with homologous proteins in peanut, hazelnut, almond, and several seeds, and mugwort pollen cross-reacts with mustard and other seeds [18,37,73]. In addition, almond and peanut contain proteins homologous to peach allergens [19]. These reactions tend to occur in older children and adults. Oral allergy syndrome is discussed in greater detail separately. (See "Pathogenesis of oral allergy syndrome (pollen-food allergy syndrome)" and 'Pathogenesis' above.)
Non-IgE-mediated reactions — Peanut allergy is associated with atopic dermatitis that is earlier in onset, more severe, and more persistent than in most patients without peanut allergy. Ingestion of peanut can exacerbate atopic dermatitis in individuals with peanut allergy. (See "Role of allergy in atopic dermatitis (eczema)".)
Food allergy is associated with allergic gastrointestinal disorders. Peanut and tree nuts are uncommon reported triggers for food protein-induced enterocolitis syndrome [74]. Eosinophilic esophagitis can also be triggered by peanut and tree nut allergy [75]. Removal of suspected food allergens from the diet can lead to clinical and histologic improvement. (See "Treatment of eosinophilic esophagitis (EoE)" and "Food protein-induced enterocolitis syndrome (FPIES)".)
Skin contact with lignin-like molecules in sesame oil can cause delayed-type hypersensitivity reactions, primarily contact dermatitis with angioedema [76]. (See "Allergic contact dermatitis in children".)
CLINICAL FEATURES
Threshold dose — The typical threshold dose for triggering objective symptoms is equivalent to one to three peanut kernels [77]. Peanut kernels vary in size, with peanut protein content ranging from 161 to 325 mg per peanut kernel (average 223 mg). Peanut flour is partially defatted and most commonly is 50 percent protein (12 percent fat). Patients with severe reactions typically have lower threshold doses of peanut protein than patients with mild symptoms [78]. The dose predicted to elicit a reaction in 5 percent of patients (ED05) with peanut allergy is 1.5 mg of peanut protein. However, in a study of 378 children with peanut allergy of any severity, only eight patients (2.1 percent) challenged with 1.5 mg of peanut protein had an objective reaction that met the predetermined reaction criteria [79]. No association was seen between reacting at this threshold dose and peanut skin prick test responses or Ara h 2-specific IgE levels. The lowest reported level of peanut triggering an IgE-mediated reaction in both children and adults is 0.05 mg of peanut protein [78,80].
There are limited data on threshold doses for tree nuts and seeds. The lowest observed adverse effect level (LOAEL) for triggering anaphylaxis was 30 mg for sesame seed and 1 to 5 mL for sesame oil in one study [81].
Allergies to other foods — In a longitudinal population-based study that included 5276 children recruited at one year of age and followed up at six years of age, 45 percent of children with peanut allergy had allergies to one or more tree nuts [82]. Among children with tree nut allergy, 47.8 percent had allergy to more than one tree nut. Some of this co-allergy is due to cross-reactive homologous IgE-binding epitopes [83-88]. Peanut-specific IgE cross-reacts with pecan, almond, Brazil nut, and hazelnut allergens, and certain tree nut pairs commonly cross-react (walnut and pecan, cashew and pistachio, and almond and hazelnut) [62,89]. The rate of sensitization and allergy to multiple nuts increases with age in children with peanut and/or tree nut allergy [90]. (See 'Pathogenesis' above and "Food allergens: Clinical aspects of cross-reactivity", section on 'Tree nuts'.)
There are limited data on the rate of co-allergy to sesame in patients with peanut allergy [62]. In a prospective study evaluating challenge-defined allergies, 8.3 percent of persons with peanut allergy (n = 60) were also reactive to sesame, whereas 41.7 percent of those with sesame allergy (n = 12) had peanut co-allergy [62]. In one retrospective survey, children who had a positive skin test to peanut or tree nuts were more likely to also test positive to sesame [91]. However, there was no systematic evaluation of the clinical outcomes (eg, whether there was a significant risk of clinical allergy to sesame). In contrast, children with peanut and tree nut sensitization or allergy were not more likely to be sensitized or allergic to coconut. One known IgE-binding epitope of the peanut allergen Ara h 1 has 80 percent homology with the corresponding area of the sesame allergen Ses i 3 [92]. However, the clinical relevance of this homology is not known.
Concurrent sensitization and allergy to other foods is common in patients with peanut allergy. In one study, sensitization or co-allergy to another food was seen in two-thirds of patients with peanut allergy [53]. Hen's egg was the most common (53 percent), followed by cow's milk (26 percent), fish (11 percent), shellfish (9 percent), soy (7 percent), wheat (6 percent), and sesame seed (6 percent). Thirty-seven percent of children with peanut and hen's egg allergy at one year of age have tree nut allergy by six years of age [82]. Similarly, 70 percent of patients with sesame allergy were allergic to other foods [76]. An estimated 17 percent of children with at least one food allergy were also found to have a sesame allergy in one study [93].
Less than 5 to 10 percent of patients with peanut allergy have clinical reactions to other legumes [77]. Cross-sensitization to multiple legumes (eg, soy, peas, green beans) is common in patients with peanut allergy, although there is little clinical crossreactivity between peanut and most other legumes except lupine beans. (See "Food allergens: Clinical aspects of cross-reactivity", section on 'Legumes: Peanut, soy, and others'.)
Many seed allergens are seed storage proteins that share IgE epitopes with peanut, tree nuts, kiwi, and other seeds [26]. Some of these allergens are cross-reactive. The full clinical implications of these findings are not established. (See "Food allergens: Clinical aspects of cross-reactivity", section on 'Seeds'.)
Associated atopic diseases — Most patients with peanut, tree nut, and/or seed allergy have concomitant atopic disease. Over three-quarters of patients with sesame allergy had other atopic conditions in one study [76]. Patients with peanut allergy often have asthma (60 to 75 percent), atopic dermatitis (60 to 75 percent), and/or allergic rhinitis (55 to 60 percent) [94]. Coexisting asthma is a risk factor for anaphylactic reactions to peanut [8]. However, a prospective multicenter study defining challenge-proven peanut, tree nut, and sesame allergy found that age, sex, asthma, allergic rhinitis, current atopic dermatitis, and increased number of peanut, tree nut, or sesame seed allergies were not associated with reaction severity at oral food challenge [62]. (See 'Systemic IgE-mediated reactions' above.)
Natural history and prognosis — The age at first exposure and age at first reaction are commonly between one to two years of age, although allergy to peanut, tree nuts, and seeds can develop later in life [8,53,60,73,95]. In a large survey of over 40,000 American adults, 17 percent of those with peanut allergy reported that the allergy developed in adulthood [96]. Symptoms occur with first known direct ingestion in up to three-quarters of children [59,97]. Subsequent reactions when the child is older are often more severe than the initial episode [8,58,98].
Accidental exposures are relatively common. In one study, the median time from diagnosis of allergy to first accidental ingestion was four months [58]. In several series, accidental ingestions occurred in 55 to 75 percent of children with peanut allergy and 30 percent of children with tree nut allergy over a period of approximately five years [59,98,99]. The annual incidence rate of accidental exposures to peanut was 14 percent in another study [100].
Development of tolerance does occur in children with peanut, tree nut, and seed allergies, although it is uncommon (approximately 10 to 20 percent in young children). (See "Food allergy in children: Prevalence, natural history, and monitoring for resolution", section on 'Natural history of specific allergies' and "Clinical manifestations and diagnosis of oral allergy syndrome (pollen-food allergy syndrome)", section on 'Birch' and "Management and prognosis of oral allergy syndrome (pollen-food allergy syndrome)".)
The size of the skin test reaction or level of specific IgE for peanut and tree nuts and specific IgE levels to component proteins for peanut are the most reliable predictors of resolution versus persistence of the allergy, although up to 25 percent of children may have mean wheal diameters to peanut >10 mm, peanut-specific IgE >15 kU/L, or IgE to the peanut protein Ara h 2 and be nonreactive to oral challenge [101-103]. In contrast, clinical features do not reliably predict persistence. (See "Peanut, tree nut, and seed allergy: Diagnosis", section on 'Diagnosis of IgE-mediated reactions' and "Food allergy in children: Prevalence, natural history, and monitoring for resolution", section on 'Prognostic factors' and "Diagnostic evaluation of IgE-mediated food allergy" and "Component testing for pollen-related, plant-derived food allergies", section on 'Peanut'.)
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 email 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.)
●Basics topic (see "Patient education: Peanut, tree nut, and seed allergy (The Basics)")
●Beyond the Basics topics (see "Patient education: Food allergy symptoms and diagnosis (Beyond the Basics)" and "Patient education: Food allergen avoidance (Beyond the Basics)")
SUMMARY
●Prevalence – Peanut, tree nut, and seed allergies are among the most common food allergies. The prevalence of these allergies appears to be increasing in some countries, particularly in those with the highest rates of food allergy. (See 'Epidemiology' above.)
●Types of reactions – Most allergic reactions to peanut, tree nuts, and seeds are immunoglobulin E (IgE) mediated and range in severity from mild symptoms isolated to the oropharynx to severe anaphylaxis (table 1). Peanut is also implicated as a trigger in non-IgE-mediated or mixed disorders, such as atopic dermatitis and eosinophilic esophagitis. (See 'Types of reactions' above.)
●Pathogenesis – IgE-mediated allergy to peanut, tree nuts, and seeds can develop through primary sensitization to the food itself or through secondary sensitization via sensitization to cross-reactive allergens (eg, birch pollen). The pathogenesis of non-IgE-mediated peanut, tree nut, and seed allergy is less clear. (See 'Pathogenesis' above and "Pathogenesis of food allergy", section on 'Routes of allergen sensitization' and "Pathogenesis of oral allergy syndrome (pollen-food allergy syndrome)".)
●Risk factors – Infants with severe atopic dermatitis and/or hen's egg allergy are at increased risk of developing peanut allergy. (See 'Risk factors for development of peanut allergy' above.)
●Maternal avoidance and timing of introduction – There is insufficient evidence to suggest that maternal avoidance of food allergens during pregnancy and lactation prevents the development of allergy to those foods. Data suggest that early introduction of peanut in high-risk infants is more likely to lead to the development of tolerance peanut. (See 'Risk factors for development of peanut allergy' above and "Introducing formula to infants at risk for allergic disease" and "Introducing highly allergenic foods to infants and children".)
●Natural history – Peanut, tree nut, and seed allergies are typically lifelong, although a small percentage of patients may outgrow these allergies. (See 'Clinical features' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Hugh A Sampson, MD, who contributed to earlier versions of this topic review.
39 : Prenatal versus postnatal sensitization to environmental allergens in a high-risk birth cohort.
47 : Familial aggregation of food allergy and sensitization to food allergens: a family-based study.
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