Food Allergies

Etiology

The development of food allergies in infants and children is driven by a complex interplay of genetic, environmental, and immunological factors. A strong genetic predisposition is evident, particularly in individuals with a family history of atopic conditions such as asthma, eczema, and allergic rhinitis. Research indicates that genetic variations affecting immune regulation and epithelial barrier function significantly contribute to the risk of developing food allergies. A notable example is the loss-of-function mutations in the filaggrin (FLG) gene, which encodes a protein essential for maintaining the integrity of the skin barrier. When this barrier is compromised, environmental allergens, including food proteins, can penetrate the skin and interact with immune cells, triggering sensitization. This mechanism is especially relevant in children with atopic dermatitis, who are at increased risk of food allergy development.[1] 

In addition to FLG mutations, other genetic variants involved in immune system regulation also affect food allergy susceptibility. For example, variations in the interleukin-4 (IL-4) gene can lead to an exaggerated T-helper type 2 (Th2) immune response, promoting the development of IgE-mediated allergies. Furthermore, specific human leukocyte antigen (HLA) variants have been linked to an increased risk of peanut allergy, further highlighting the influence of genetic factors in food allergy pathogenesis.[2][3]

Environmental factors play a critical role in modulating immune function and influencing the risk of food allergy development. Factors such as mode of delivery (cesarean section versus vaginal delivery), early antibiotic exposure, and alterations in the gut microbiome can influence immune tolerance and the integrity of the intestinal barrier.[4] Children delivered via cesarean section face a higher risk of developing food allergies, possibly related to the lack of exposure to beneficial microbes encountered during vaginal delivery.[4] Early antibiotic use in childhood may increase the risk of developing food allergies, likely due to disruption of the gut microbiome and impaired immune regulation.[5] Additionally, the timing of introducing potentially allergenic solid foods to infants plays a significant role in the risk of food allergies, a topic further explored in the Deterrence and Patient Education section below.

Finally, alterations in immune function are central to the pathogenesis of food allergies. A loss of immune tolerance to otherwise harmless food proteins can trigger inappropriate immune activation. Depending on the specific immunological pathways involved, this response may manifest as either IgE-mediated or non-IgE–mediated hypersensitivity reactions.

Epidemiology

Healthcare experts increasingly recognize food allergies as a growing global public health concern, with rising prevalence in both high-income and resource-limited countries. An estimated 250 million people worldwide are affected by one or more food allergies.[6] In the United States, approximately 8% of children and up to 10% of adults are affected by this condition.[7] Notably, around 40% of affected children have multiple food allergies.[8] The most common allergenic foods include cow milk, eggs, peanuts, tree nuts, soy, wheat, fish, shellfish, and sesame.

Although cow’s milk and egg allergies are among the most commonly reported food allergies worldwide, geographic variations exist, likely determined by cultural feeding patterns.[9] Many children eventually outgrow allergies to milk, eggs, or soy; however, allergies to peanuts, tree nuts, and shellfish are more likely to persist into adulthood.[10][6] Additionally, individuals with a history of allergies to bee venom, medications, or latex have an elevated risk of developing food allergies later in life.[8]

Prevalence of food allergies varies widely and is influenced by factors such as geography, dietary habits, environmental exposures, access to healthcare, and the diagnostic criteria applied.[11] Higher rates are observed in Westernized countries, particularly in urban areas, where food allergies affect up to 10% of infants.[7] In contrast, prevalence tends to be lower in rural and resource-limited regions. These regional differences may be attributed to variations in early-life microbial exposure, air pollution, ingestion of microplastics, and contact with natural environments, including exposure to tree pollen, insects, and animals.[5][12][13][14][15]

Racial and ethnic differences in food allergies are also observed within countries. For instance, Black children in the United States have higher rates of peanut and shellfish allergies compared to White children.[7] The impact of food allergies extends beyond the individual, contributing to increased emergency department visits, hospital admissions, healthcare costs, and significant psychosocial stress for affected individuals and families.[16] The incidence of food-induced anaphylaxis has also risen, particularly among children and adolescents.[17] Understanding these epidemiological patterns is crucial for clinicians to guide screening, patient education, and preventive strategies tailored to the needs of diverse populations.

Pathophysiology

Food allergy results from an abnormal immune response to dietary antigens, leading to either IgE-mediated or non-IgE–mediated hypersensitivity reactions. In sensitized individuals, exposure to specific food proteins triggers immune activation instead of tolerance, causing the release of inflammatory mediators and the development of allergic symptoms. In IgE-mediated food allergies, initial sensitization begins with antigen presentation by dendritic cells, which activates Th2 lymphocytes. This leads to the production of allergen-specific IgE antibodies by B cells. These antibodies then bind to IgE receptors on mast cells and basophils.

Re-exposure to the offending food allergen triggers the release of histamine and other pro-inflammatory mediators, leading to smooth muscle contraction, vasodilation, and increased mucus secretion. Symptoms of immediate hypersensitivity can range from urticaria to anaphylaxis, the latter being a severe, potentially life-threatening systemic allergic reaction. Anaphylaxis develops rapidly and typically involves at least 2 organ systems or presents with hypotension, airway compromise, or significant respiratory distress.[18][13]

Oral allergy syndrome, also known as pollen food allergy syndrome, is an IgE-mediated allergic reaction caused by cross-reactivity between structurally similar proteins in pollen and certain raw fruits, vegetables, and nuts. In sensitized individuals—typically those with pollen allergies—the immune system misidentifies specific food proteins as allergens due to their resemblance to pollen antigens. Upon ingestion of these raw foods, IgE antibodies bound to mast cells and basophils in the oral mucosa recognize the allergens and initiate the release of histamine, prostaglandins, and leukotrienes. This immune response leads to localized symptoms such as itching, tingling, and swelling of the lips, tongue, mouth, and throat. These symptoms usually resolve within minutes to hours and rarely progress to systemic reactions or anaphylaxis.[19][20] 

Cooking denatures the proteins responsible for cross-reactivity with pollen allergens, rendering them unrecognizable to the immune system. As a result, most individuals with oral allergy syndrome can tolerate cooked forms of these foods. Apples, peaches, cherries, and bananas are among the most common foods associated with oral allergy syndrome.

In contrast, non-IgE–mediated food allergies, including food protein–induced enterocolitis syndrome (FPIES), food protein–induced enteropathy, and allergic proctocolitis, are driven by cell-mediated immune mechanisms. These conditions involve delayed hypersensitivity (type IV) reactions, characterized by T-cell–mediated inflammation, epithelial barrier dysfunction, and immune pathways unrelated to IgE-mediated responses.[20] Affected individuals typically present with delayed-onset gastrointestinal symptoms, such as vomiting and diarrhea.[21]

In summary, the pathophysiology of food allergies occurs when the immune system loses tolerance to typically harmless dietary proteins. Genetic predisposition, impaired epithelial barrier function, and environmental factors collectively contribute to the breakdown of immune regulation, triggering a dysregulated immune response. As a result, exposure to specific food allergens can provoke either IgE-mediated or non-IgE–mediated allergic reactions.

History and Physical

The approach to evaluating a patient with possible food allergies depends on whether the clinician investigates a known reaction following food ingestion or considers food allergy as one of several potential diagnoses. When a food allergy is suspected based on a reaction, the clinical history should detail the exposure and characterize the timing and nature of the symptoms. Key questions include:

• What did the patient consume? In what quantity?
• Was the food cooked or raw?
• Did it contain a known allergen such as peanuts, tree nuts, milk, egg, fish, shellfish, wheat, soy, or sesame?
• How much time elapsed before symptom onset?

In IgE-mediated food allergies, symptoms typically develop within minutes to 2 hours of exposure to the allergen. Although individuals may initially present with mild symptoms, subsequent exposures can result in more severe and potentially life-threatening reactions.

Clinicians should gather a detailed account of the reaction, including the severity, progression, and duration of symptoms. Presentations may involve multiple organ systems, such as skin (urticaria, swelling), gastrointestinal (nausea, vomiting), respiratory (wheezing, respiratory distress), or cardiovascular (tachycardia, syncope). Notably, it is important to determine whether the patient has reacted to this food or a related one in the past, and whether the severity of their response has changed over time. Clinicians should also assess for contributing factors, such as physical exertion, medications, alcohol intake, or underlying medical conditions, that may have influenced the reaction. Finally, details about any treatments used, including antihistamines, epinephrine, or emergency care, should be documented.

When food allergy is one of several potential explanations for a patient's symptoms, the goal of the history is to assess whether it is the most likely cause. The clinician should investigate the patient's typical diet, particularly focusing on common allergenic foods, and identify any consistent patterns between food intake and the onset of symptoms. A food diary can be especially helpful in pinpointing food-related triggers, especially in patients with chronic or recurrent symptoms. Timing and reproducibility are key factors; the clinician should ask whether symptoms occur regularly after eating specific foods. Recurrent hives, vomiting, diarrhea, abdominal pain, or respiratory issues following meals should raise suspicion for food allergies.

Additionally, clinicians should inquire about any personal or family history of atopic conditions such as asthma, eczema, or allergic rhinitis, as these increase the likelihood of food allergies. A feeding history is important for young children, including information on breastfeeding and the introduction of solid or allergenic foods. Considering other potential causes, including environmental or medication exposures, nonallergic food intolerances, or gastrointestinal conditions that may mimic food allergies, is important. 

Non-IgE–mediated food allergies, including irritability, vomiting or frequent spitting up, diarrhea, and poor weight gain, commonly present with gastrointestinal symptoms in infants and young children. In FPIES, affected infants typically experience vomiting 1 to 3 hours after ingestion of the triggering food. With continued exposure, symptoms may progress to include abdominal distention, bloody diarrhea, lethargy, anemia, and failure to thrive. The most frequently implicated foods in FPIES include cow's milk, soy, oats, and rice.

Food protein–induced allergic proctocolitis (FPIAP) typically presents as blood-streaked stools in otherwise healthy infants during the first few months of life. Approximately 60% of cases occur in exclusively breastfed infants. Cow's milk protein is the most common trigger, although other allergens such as soy, egg, and wheat may also be involved. FPIAP is generally a benign, self-limiting condition, with most cases resolving spontaneously within the first year of life.[22][23] 

Patients with food protein–induced enteropathy often present with chronic steatorrhea, protein-losing enteropathy, malabsorption, and poor weight gain during the first few months of life. The malabsorption can lead to anemia, hypoalbuminemia, protein-losing enteropathy, and vitamin deficiencies. While grossly bloody stools are typically absent, occult blood may be present. Cow's milk is the most common trigger for FPE, followed by soy, wheat, and rice. Symptoms generally resolve in individuals by the age of 2 to 3.[24]

In IgE-mediated allergic reactions, cutaneous symptoms such as acute urticaria, flushing, pruritic eyes, and angioedema typically appear within minutes to 2 hours after allergen exposure. Common triggers include milk, egg, peanuts, tree nuts, sesame, and certain fruits like kiwi. Notably, about 30% of children with moderate-to-severe atopic dermatitis also have coexisting food allergies, highlighting a potential link between skin barrier dysfunction and allergic sensitization. 

Breathing-related symptoms, including nasal congestion, sneezing, coughing, and wheezing, can also manifest, particularly in IgE-mediated reactions. However, isolated respiratory symptoms are rare. Wheezing occurs in approximately 25% of patients with IgE-mediated food allergy reactions, although only 10% of individuals with asthma experience food-induced respiratory symptoms.

Respiratory compromise may indicate progression toward anaphylaxis and warrants immediate recognition and intervention. In the United States, food allergy reactions are the leading cause of anaphylaxis presenting to hospital emergency departments. Patients often report generalized malaise, a sense of impending doom, and lethargy, along with symptoms affecting multiple organ systems, including the skin, respiratory tract, gastrointestinal system, and cardiovascular system. Cardiovascular involvement typically manifests as hypotension, tachycardia, pallor, dizziness, syncope, or collapse.[8]

Evaluation

Specific IgE-mediated food allergies can be confirmed or ruled out using 3 principal tests, including skin prick testing (SPT), serum-specific IgE testing (sIgE), and an oral food challenge (OFC). Evaluation should be reserved for patients with a high pre-test probability of food allergy, based on a history of allergic symptoms following the consumption of a particular food. Both SPT and sIgE testing have a high negative predictive value, helping to rule out food allergies and prevent unnecessary dietary restrictions when results are negative. However, since SPT and sIgE testing only identify sensitization rather than clinical allergy, positive results without a corresponding clinical history have limited diagnostic value. When the history and initial test results—either SPT or sIgE—fail to provide clarity, an oral food challenge remains the diagnostic "gold standard."

Several factors determine the choice of the initial test. Patients at high risk for anaphylaxis, those with asthma symptoms, or individuals who cannot tolerate SPT due to dermatological conditions may be better suited for sIgE testing. The RadioAllergoSorbent Test (RAST), developed in the 1970s, was the original method for detecting allergen-specific IgE antibodies in serum using radioactive labeling. However, newer methods that directly measure allergen-specific IgE antibodies offer higher sensitivity and reproducibility, and have largely replaced RAST. Despite this, "RAST" is still commonly used colloquially to refer to any sIgE assay.

An advantage of sIgE testing over SPT is that primary care clinicians can order the assay and interpret the results without consulting an allergy specialist. Although high concentrations of sIgE are typically associated with an increased likelihood of a clinical reaction, the levels do not always correlate with the severity of symptoms. A negative result can help rule out a food allergy, but it may also reflect a lack of prior exposure to the allergen, underscoring the importance of testing only when there is a clear history of symptoms following ingestion of a likely allergen.

Allergists typically perform SPT as part of a comprehensive food allergy evaluation. Although SPT is more sensitive than sIgE testing, it must be conducted in a setting that recognizes and manages anaphylaxis. During the procedure, a small drop of allergen extract is placed onto the skin's surface, usually on the forearm or back, and a tiny prick or scratch introduces the allergen into the epidermis. In patients sensitized to the allergen, a localized wheal, resembling a mosquito bite, typically forms within 15 minutes. The size of the wheal generally correlates with the severity of the allergy. However, children aged 2 or younger and adults aged 70 or older may experience smaller dermal reactions. Certain systemic medications, such as antihistamines and tricyclic antidepressants, can interfere with test results and should be discontinued approximately 1 week before testing.[8] 

Intradermal testing involves injecting a small amount of allergen extract into the dermis. Although this technique is more sensitive than SPT, it is less specific, resulting in a higher rate of false positives and an increased risk of systemic reactions. For these reasons, allergists typically perform intradermal testing to evaluate environmental or drug allergies, and it is not recommended for diagnosing food allergies.

When the clinical history and initial testing are inconclusive, an OFC may be necessary to confirm a diagnosis of food allergy. This procedure involves the supervised ingestion of the suspected allergenic food in gradually increasing amounts, with close monitoring for allergic reactions. Similar to the SPT testing, the OFC must be conducted in a setting equipped to treat anaphylaxis. Patients should avoid the suspected food for at least 2 weeks before the challenge and discontinue medications that could interfere with the test, such as antihistamines and beta-adrenergic bronchodilators.[25]

The OFC can be conducted as a double-blind placebo-controlled challenge to minimize bias, or as an open or single-blind test if the clinician believes the risk of bias is low. If the blinded challenge result is negative, it can be repeated with an open, supervised feeding of a typical serving of the food to rule out a false-negative result. In addition to confirming a food allergy diagnosis, allergists use the OFC to determine the threshold dose that triggers a reaction and to assess whether a patient has outgrown a previously diagnosed food allergy. Although the OFC is effective, it is costly, resource-intensive, and carries a low but significant risk of anaphylaxis and potentially fatal outcomes.[26]

When individuals present with a clear history of an immediate allergic reaction to a specific food and have a positive SPT or elevated sIgE, an OFC is often unnecessary to confirm the diagnosis. If symptoms resolve following the elimination of the suspected food, clinicians and families can reasonably conclude a food allergy without proceeding to an OFC. However, patients with uncontrolled asthma, recent anaphylaxis, acute illness, or those in settings lacking immediate access to emergency care should not undergo an OFC, as it carries a higher risk of severe allergic reactions compared to skin and serum testing.

Currently, no reliable testing exists to diagnose non-IgE–mediated food allergies, such as FPIES, food protein–induced enteropathy, and FPIAP. These conditions are diagnosed clinically, based on a detailed history and physical examination findings. A supportive history includes the timing and pattern of symptoms following food exposure, symptom improvement after eliminating the suspected allergen, and symptom recurrence upon reintroduction of the food.

Treatment / Management

Managing food allergies requires strict avoidance of allergenic foods, patient-specific education, and regular follow-up to reassess tolerance and adjust dietary plans as necessary.[27] An exception to strict avoidance is seen in patients with oral allergy syndrome, where heat-induced protein denaturation enables them to tolerate certain allergenic foods when cooked or baked, despite experiencing symptoms when consuming the same foods raw. The American College of Allergy, Asthma & Immunology and the National Institute of Allergy and Infectious Diseases provide comprehensive guidelines, including counseling families on proper food preparation, reading ingredient labels, and understanding the risks of cross-contamination and hidden allergens. Over time, many children and some adults with food allergies may develop tolerance, making regular reassessment critical to determine if the allergy persists.[20] If symptoms persist despite adherence to an elimination diet, food allergies are unlikely to be the cause.

Prompt administration of epinephrine is the first-line treatment for anaphylaxis. Patients or caregivers should administer an epinephrine autoinjector (EAI) at the first sign of anaphylactic symptoms, followed by immediate transfer to an emergency facility for further evaluation and treatment.[10] Due to epinephrine’s short half-life, a second injection is often required 5 to 15 minutes after the initial injection. The recommended dose of epinephrine is 0.1 mg/kg, with a maximum dose of 0.3 mg for children and 0.5 mg for adults. In the United States, epinephrine autoinjectors are available in 3 strengths—0.1 mg, 0.15 mg, and 0.3 mg. A 0.5 mg dose is also available in Canada and some European countries.

Although the US Food and Drug Administration (FDA) recommends 0.3 mg epinephrine dose for patients with a body weight of 30 kg or more, several medical organizations, including the American Academy of Allergy, Asthma & Immunology, American Academy of Pediatrics (AAP), Canadian Society of Allergy and Clinical Immunology, and European Academy Allergy and Clinical Immunology), advocate for its use in children with a body weight of 25 to 30 kg to avoid underdosing. The AAP also recommends the 0.1 mg dose for children with a body weight of 7.5 to 13 kg and the 0.15 mg dose for those between 13 and 25 kg. If the 0.1 mg EAI is unavailable, the AAP recommends using the 0.15 mg dose of EAIs for children with a body weight of less than 15 kg.[28]

The FDA approved inhaled epinephrine (brand name Neffy) in 2025 for the emergency treatment of type I allergic reactions, including anaphylaxis, in patients aged 4 and older with a body weight of at least 15 kg. This needle-free alternative is beneficial for patients who fear injections or struggle to use an EAI correctly.[29][30] Inhaled epinephrine also offers a longer shelf life than EAI, providing additional convenience for patients.

Clinicians may administer adjunctive medications, such as antihistamines, corticosteroids, and inhaled beta-agonists, to reduce symptoms of anaphylaxis. However, these medications should never replace epinephrine as the initial treatment of choice.[31] In community settings, patients frequently attempt to manage systemic allergic reactions with antihistamines before administering an EAI, delaying appropriate intervention and increasing the risk of anaphylaxis.

Allergen immunotherapy, including oral, sublingual, and epicutaneous approaches, aims to desensitize individuals with food allergies to specific antigens, thereby reducing the severity of reactions and improving their quality of life.[32] This approach induces tolerance by gradually increasing exposure to allergenic extracts over weeks to months.[8][33] Newer biological therapies, such as omalizumab (an anti-IgE monoclonal antibody), target key pathways involved in systemic allergic responses and have demonstrated efficacy in raising the reactivity threshold to food allergens, particularly when used alongside oral immunotherapy. In 2024, the FDA approved omalizumab for the treatment of food allergies. Additional biologics are currently under investigation to evaluate their safety and effectiveness.[34][35] (B3)

The American College of Allergy, Asthma & Immunology's 2023 Practice Parameter Update emphasizes the importance of eliminating food allergens from the diet, utilizing epinephrine, and the need for education and preparedness in managing allergic reactions in community settings. These evolving approaches—from allergen avoidance and emergency preparedness to immunotherapy and biological therapies—reflect a comprehensive and increasingly personalized approach to treating patients with food allergies.[28]

Differential Diagnosis

The differential diagnosis of food allergies includes both immune-mediated and nonallergic disorders that present with a range of symptoms similar to food allergies. Eosinophilic gastrointestinal disorders, such as eosinophilic esophagitis, eosinophilic gastroenteritis, and eosinophilic colitis, are chronic, immune-mediated conditions characterized by eosinophilic infiltration of the gastrointestinal tract. These disorders are associated with Th2 cell activity and are often triggered by food allergens.[36] Eosinophilic esophagitis, the most common of these disorders, typically presents in school-age children to midlife and is frequently observed in individuals with a personal or family history of atopic conditions, including asthma, eczema, rhinitis, and IgE-mediated food allergies. Patients commonly experience dysphagia, vomiting, and reflux-like symptoms.

Mast cell activation syndrome is an immune-mediated condition characterized by the inappropriate activation of mast cells, leading to the release of mediators such as histamine and tryptase. This release causes a variety of symptoms across multiple organ systems. The symptoms can resemble those of food allergies, including gastrointestinal distress, rashes, and anaphylaxis.[28]

Patients with celiac disease experience an autoimmune reaction to gluten. Symptoms often include abdominal pain after gluten ingestion, chronic diarrhea, weight loss, fatigue, and anemia. Celiac disease is typically diagnosed through serological testing or a small bowel biopsy. Clinicians must also differentiate allergic reactions from non-food causes, such as medications or insect stings, which can produce symptoms coinciding with food ingestion.

Nonallergic conditions that present with symptoms similar to those of food allergies include lactose intolerance, fructose malabsorption, gastroesophageal reflux disease (GERD), irritable bowel syndrome, histamine intolerance, and panic or anxiety-related reactions. For instance, lactose intolerance may cause bloating and diarrhea after consuming dairy products, while GERD-induced regurgitation may be mistaken for food allergy-related vomiting. Infants with symptoms such as vomiting, lethargy, and poor weight gain may have inborn errors of metabolism, such as galactosemia. Panic attacks can lead to throat tightness, dizziness, and hyperventilation, further complicating the differential diagnosis.

Histamine intolerance, a less common condition, can mimic the symptoms of food allergy reactions. Affected individuals may experience headache, flushing, and urticaria after consuming histamine-rich foods such as aged cheeses, processed meats, fermented products, and alcohol. Additionally, the ingestion of foods containing additives or spices can lead to irritant or vasomotor responses that resemble food allergy symptoms, including flushing, nasal congestion, headache, and a burning sensation in the mouth.

Other nonallergic conditions that can cause urticaria include infections, such as viral illnesses or reactions to enterotoxins produced by Staphylococcus aureus. Foodborne gastroenteritis from pathogens such as Salmonella or norovirus may be mistaken for food allergies, as symptoms such as vomiting and diarrhea can follow ingestion of contaminated food. Because both immune-mediated and nonallergic conditions can mimic food allergies, thorough history-taking and diagnostic evaluation are essential. Important differential diagnoses include eosinophilic gastrointestinal disorders, mast cell activation syndrome, celiac disease, food intolerances, infections, and anxiety-related symptoms.

Prognosis

The prognosis for patients with food allergies varies based on several factors, including the specific allergen, age of onset, reaction severity, and the presence of comorbid conditions such as asthma or atopic dermatitis. Children with soy, wheat, milk, and egg allergies often outgrow these allergies. Most develop tolerance to soy and wheat by school age, and approximately 80% outgrow milk and egg allergies by adolescence. Notably, about 75% can tolerate these foods in baked form, even among those who remain allergic to milk and egg. In contrast, allergies to peanuts, tree nuts, fish, and shellfish are more likely to persist into adulthood. Only about 20% of individuals with a peanut allergy eventually outgrow it, and the likelihood is even lower for those with tree nut or shellfish allergies, which are typically lifelong.[8] Non-IgE–mediated food allergies usually resolve within the first few years of life.

Patients at increased risk for persistent or severe food allergies include those with elevated allergen-specific IgE levels, a history of anaphylaxis or severe systemic reactions, and children with delayed introduction of allergenic foods. The presence of asthma—especially when combined with a history of anaphylaxis—further increases the risk of life-threatening reactions. Importantly, individuals who have previously experienced only mild reactions may still develop systemic responses or anaphylaxis upon future exposures, underscoring the unpredictable nature of food allergy severity.

Reports reveal significant disparities in food allergy outcomes, with racial and ethnic minorities and individuals living in high-poverty areas experiencing higher rates of emergency department visits, hospitalizations, and fatalities due to food-induced anaphylaxis. Multiple studies have documented increased diagnostic coding for food-induced anaphylaxis among Black, Hispanic, and Asian children compared to White children. Black individuals, in particular, are disproportionately affected by comorbid asthma—a known risk factor for fatal anaphylaxis. Mortality data further reveal a greater burden of fatal reactions among Black individuals, especially males.[37] These findings underscore the urgent need for targeted public health strategies to address inequities in food allergy diagnosis, management, and outcomes.

With strict avoidance of known food allergens and appropriate emergency preparedness, most individuals with food allergies can lead full, healthy lives. For those who do not outgrow their allergies, immunotherapy and emerging biological treatments offer promising options for desensitization. However, food-related anxiety and overly restrictive diets can adversely affect a child’s prognosis, leading to poor nutrition, impaired growth, and diminished quality of life. Elimination of foods based on unconfirmed allergies may deprive children of essential nutrients. Moreover, anxiety surrounding food can contribute to social isolation and emotional distress for both children and their families, underscoring the importance of psychosocial support in improving long-term outcomes.

Complications

Complications of food allergies are diverse and can significantly impact health and development. The most severe complication of IgE-mediated food allergy is life-threatening anaphylaxis, which requires prompt intramuscular administration of epinephrine. Peanuts are the leading cause of food-induced anaphylaxis.[8] Risk factors for severe reactions include a history of systemic reactions, comorbid asthma, and delayed use of epinephrine. In infants with FPIES, severe vomiting and diarrhea can lead to hypovolemic shock. Food allergies may exacerbate atopic dermatitis, particularly in response to allergens such as milk, eggs, and peanuts. In patients with asthma, ingestion of food allergens can also trigger wheezing and other respiratory symptoms.

Children with multiple food allergies are at increased risk for nutritional deficiencies, growth delays, and feeding challenges due to the dietary restrictions required to avoid allergens. These limitations can also contribute to heightened food-related anxiety, diminished quality of life, and social isolation in both children and adults. Adolescents, in particular, may be vulnerable to developing selective eating patterns or eating disorders. Early intervention with psychosocial and nutritional support is critical to promoting healthy development and preventing long-term complications.