Food allergy

Common agents associated with anaphylactic reactions.

Hospital missions for food induced anaphylaxis have had an increasing trend in the US.

IgE mediated food allergies affect an estimated 7.6% of children and 10.8% of adults.

An adverse immune response to a food protein.

Distinct from other adverse responses to food, such as food intolerance, pharmacological reactions, and toxin-mediated reactions.

Food intolerances are not mediated by immunologic mechanisms and can occur by metabolic, pharmacological, toxic, or undefined mechanisms.

Genetic susceptibility, microbiome alterations, exposure to detergents, and pollutants, can contribute to the risk of IgE mediated food sensitization and allergy.

There is no uniform minimum dose across all food allergens that induces allergic symptoms, as some individuals may react to trace amounts of food allergens, whereas others may tolerate higher amounts before experiencing symptoms.

Infantile eczema is the strongest risk factor for food allergy, as  an inflamed, impaired skin barrier promotes allergic sensitization when exposed to ambient food proteins.

Infants of families with atopic conditions, such as allergic rhinitis, asthma, or eczema, had a higher risk for IgE mediated food allergy.

The protein in the food is the most common allergic component.

Food allergy reactions can be mediated by IgE or non IgE mediated mechanisms.

Both mechanisms of allergy requiring immunologic sensitization to the food antigen.

The development of food allergy begins with sensitization, in a phase which a susceptible individual develops food, specific IgE antibody after food protein antigen contacts gut, respiratory tract, or skin.

A second phase of food allergy development occurs when sensitized individuals are reexposed to a food allergen, and it binds simultaneously to multiple food specific IgE  receptor complexes, cross-linking these complexes on basophils and mast cells.

This cross linkage causes rapid release of inflammatory mediators – histamine and proteases, including tryptase, allergic and inflammatory cytokines (IL-4, IL-6, and tumor necrosis factor), platelet activating factor, leukotrienes, and prostaglandins.

As a result of the release of these inflammatory mediators, there is increased vascular permeability, mucosal, and submucosal edema, smooth muscle hyperactivity, which drive the development of urticarial/angioedema, wheezing, bronchoconstriction, nasal hyperactivity, intestinal spasms, abdominal pain, and anaphylactic shock.

Immune system mistakenly identifies a protein as harmful.

Initiated by allergen cross-linking IgE immunoglobulin bound to intestinal mast cells, mast cell degranulation and release of mast cell products that act directly on intestinal epithelium, or indirectly via enteric nerves, causing intestinal ion secretion and barrier function alterations.

IgE reaction is to a specific allergen after exposure to the skin or to a mucosal surface of the body, which is typically the gastrointestinal tract.

Symptoms of classic IgE mediated food allergy varies in severity and includes: a combination of laryngeal edema, wheezing, nausea, vomiting, diarrhea, urticaria, angioedema, and hypotension.

Most immunologic reactions due to food allergies are IgE mediated and target one more proteins within the food called epitopes.

Epitopes are the binding site for specific IgE or T cells.

Most food allergens are comprised of several epitopes.

Allergic responses include dermatitis, gastrointestinal and respiratory distress, including such life-threatening anaphylactic responses as biphasic anaphylaxis and vasodilation.

Food allergic reactions can cause hives, red eyes, nasal congestion, oral, pharyngeal, swelling, shortness of breath, and anaphylaxis, which can occur within seconds of anllergen exposure.

Hospital admissions for food induced anaphylaxis have shown increasing trends.

Attribute to several processes including genetic predisposition and environmental exposure.

Prevalence of positive IgE reactions to food allergens is 18% age 18-29 years to 20.2% in those 60 to 69 years and 20% of those 70- 79 years.

Affects in estimated 8% of children.

1% to 2% of the population suffer from food allergy.

In adults, peanuts, tree nuts, finned fish, crustaceans, fruit, and vegetables account for 85% of the food-allergic reactions.

Wheat, crustacea, egg, fish, peanut, soybean, milk, and tree nuts, are generally considered to cause over 90% of food-induced allergic reactions in most regions.

In the US nine foods account from within 90% of symptomatic IgE mediated food protein allergies:prevalence in adults and children, respectively; for crustacean shellfish is 2.9% and 1.3%; for dairy 1.9% and 1.9%; for peanut 1.8 and 2.2%, for tree nuts 1.2 and 1.2%, for fin fish 0.9 and 0.6%, for egg 0.8% in 0.9%,  for wheat 0.8 and 0.5%, for soy 0.6 and 0.5% and for sesame 0.2%, and 0.2%.

Infants less than one year have a higher rates of symptomatic egg allergy at 8.9%.

The rate of symptomatic cows milk protein allergy are approximately 2 to 3% in children three years or younger.

Observational studies suggested patients with cow’s milk protein allergy have resolution in 19% by age 4 years and 79% by 16 years.
Studies suggest allergy to eggs resolve and 89% by age 6.
Peanut and tree nut allergies and more durable than egg and milk, allergies.
Peanut allergy resolves in less than 15 to 30% by age six through 10 years and tree nut allergy resolves in 9% by a median age of 10 years.

Peanut allergy is one of the most common causes of food-related deaths.

The leading food related causes of fatal and near fatal anaphylaxis, are due to allergies to peanut, tree nuts, crustacean, shellfish, and cow’s  milk with regional variability.

A meta-analysis found that death due to overall food-induced anaphylaxis was 1.8 per million person-years in people having food allergies, with peanut as the most common allergen.

Cells-reporting or parental reporting of food allergy overestimates the prevalence of the disease.

About 6% of US children under age 3 and 3.5–4% of the overall US population have food allergy.

NHANES suggest self reporting food allergy prevalence almost 9% with the prevalence of 6.5% in children and 9.7 % in adults.

Estimates of food allergy indicate that more than 2%, but less than 10% of the population have a food allergy, and rates tend to be higher in children-3 to 4% versus 1 to 2% in adults.

Increasing incidence

1.1% of general population estimated to be allergic to peanuts and tree nuts.

Incidence in atopic dermatitis about 20% in children and 10% in adults.

Risks: atopic dermatitis, family history of atop you, family history of asthma are primary risk factors for the development of food allergy.

Breakdown of skin barrier in atopic dermatitis can cause epicutaneous sensitization to foods resulting in allergy.

Almost 40% of children with food allergy have severe reactions that if not treated immediately can lead to hospitalization or death.

High risk children who regularly consumed peanut protein are less likely by 70-86% reduction to develop peanut allergy (Du Toit G et al).

Most common foods include peanuts, tree nuts, shellfish, milk, eggs, soy and wheat.

Peanut allergies have tripled in the last 15 years.

Subcutaneous immunotherapy used to treat allergic rhinitis and asthma is not an option for food allergies because introduction of subcutaneous allergens frequently induce anaphylaxis.

Presently, individuals with food allergy must simply try to avoid exposure to such foods.

Approximately 30,000 cases of food allergy anaphylaxis and 100-200 deaths occur each year in the United States (NIH-2006).

80-85% of children with allergies to milk, eggs, wheat, or so, outgrow those allergies before adulthood.

Peanut and tree nut allergy can occur during childhood or adulthood, and are less likely to be outgrown, and tend to cause more fatal reactions.

Higher incidence in males.

Milk is the most common allergen in infancy.

Peanut allergies more common in children between the ages of one and five years.

Seafood allergy is the most common allergy in adults.

20% of children with allergies to peanuts, tree nuts, shellfish, or fish develop permanent tolerance to the foods.

While many foods can induce an allergic reaction the most commonly implicated foods are:cow’s milk, egg, peanut, tree nut, soy, wheat, fish, and shellfish.

A wide variety of foods can cause allergic reactions, but 90% of allergic responses to foods are caused by cow’s milk, soy, eggs, wheat, peanuts, tree nuts, fish, and shellfish.

Eight food groups: wheat, crustacea, egg, fish, peanut, soybean, milk, and tree nut  are generally considered to cause over 90% of food-induced allergic reactions in most regions.

The highest risk of anaphylaxis from food allergens are peanut, tree nuts, and shellfish.

All allergenic foods can cause life-threatening respiratory, cardiovascular reactions along with hives, abdominal pain and diarrhea.

Respiratory symptoms may include sneezing, congestion, wheezing, laryngeal edema, and rhinorrhea.

Gastrointestinal symptoms include nausea, vomiting, abdominal pain, and diarrhea.

Cutaneous findings include urticaria, flushing, pruritus, and angioedema.

Cardiovascular manifestations include tachycardia, hypertension, or syncope.

Symptoms usually are seen within minutes of food ingestion but not it may not appear for up to two hours.

Reactions can vary in severity from priritus to anaphylaxis.

Diagnosis of food allergy includes skin prick testing, serum IgE testing, and oral food challenges.

The standard for the diagnosis of IgE food allergy is the oral food challenge.

A convincing clinical history, along with a positive skin prick test, and/or food allergen specific IgE  in serum confirm allergic sensitization allows to obviate the need for diagnostic food challenges.

In general. , comorbid allergenic conditions, such as allergic rhinitis, allergic asthma, and the topic dermatitis are. not indications to do test for food specific allergic sensitization.

In contrast to food protein allergy, allergic reactions to red meat in the alpha-gal syndrome are associated with IgE to the carbohydrate, galactose-alpha-1,3 -galactose (alpha-gal).

In the US, the development of alpha-gal specific IgE is associated with exposure to alpha-gal in tick saliva from Lonestar tick bites.

The presence of alpha – gal specific IgE  supports a diagnosis of alpha-gal syndrome in patients with allergic symptoms after meat  ingestion.

Oral immunotherapy can sensitize people with food allergies but such treatment is associated with high adverse reaction rates(alpha-gal, IGE concentration of 0.1 KU per liter, is suggestive.

Management includes avoidance of allergenic and cross-reacting foods and early recognition and the immediate treatment of reactions.

Injectable epinephrine is the first line treatment of severe allergic reactions and/or anaphylaxis.

Anti-histamines, corticosteroids, and mast cell stabilizers such as cromolyn are commonly prescribed in the acute setting, as they may mitigate symptoms of allergic reactions of pruritus, urticaria, and abdominal discomfort.

The primary management of IgE mediated food allergy is avoidance of culprit food allergens.

The top nine food allergens are disclosed onall food packaging labels by federal statute.

immunotherapy can increase the minimum amount of food allergen consumed that elicits a clinical allergic reaction.

Sublingual immunotherapy minimizes the risk of adverse reactions compared to oral immunotherapy because the dose of allergens given to increase tolerance or small: only micrograms-milligrams of allergen extract or given under the tongue versus milligrams or grams of allergy and consumed with oral immunotherapy..

Sublingual immunotherapy does not result in allergen tolerance levels as high as oral immunotherapy.

Oral immunotherapy will desensitize children to food allergies 70-80% of the time, but not permanently.

Allergic reactions associated with oral immunotherapy is the inherent risk of desensitization therapy and can increase after exercise, sleep deprivation, illness, fever, and the use of medications such as nonsteroidal anti-inflammatory drugs.

Peanut allergen powder is the only food allergy immunotherapy presently approved and is used for peanut allergy.

The traditional subcutaneous immunotherapy, effective against certain aeroallergens, is unsafe for the treatment of food allergy.

In a double-blind, randomized, and placebo-controlled study of 55 children ages 5 to 11 years with egg allergy receiving oral immunotherapy or placebo, it was shown that oral immunotherapy can desensitize a high proportion of children with such allergies and induce sustained unresponsiveness in the clinically significant subset (Burks AW et al).

Exposure of peanuts, eggs and cow’s milk early in infancy associated with much lower rates of food allergy suggesting the presence of oral tolerance.

Food processing may increase food allergy, as chinese eat as much peanuts per capita, but have virtually no peanut allergy eating their nuts boiled or fried as opposed to dry roasted.

3 million Americans allergic to peanuts or tree nuts.

Allergies to cow’s milk, egg wheat and soy have increased.

About 2.5% of newborn infants experience reactions to cow’s milk in the first year of life and 60% of these reactions are IgE mediated.

Hypersensitivity to eggs occurs in about 1.3% of children and hypersensitivity to peanuts in about 0.5%.

In the US 4% of children have food allergies.

Egg allergy has a cumulative prevalence of approximately 2.6% by 2.5 years of age.

Egg allergy reactions vary from mild urticaria to systemic anaphylaxis.

Severe allergic reactions occur with a single bite of cooked egg.

Children with egg allergy are treated on an egg free diet, but total avoidance of eggs is difficult.

There is an association between persistently low gut Bacteroides abundance throughout infancy and sensitization to peanuts in childhood.


Infants born by caesarean section or with low intestinal microbiota are at an increased risk of developing food allergies.

The  risk of food allergies increased in infants born to mothers of Asian ethnicity.

Birth mode and ethnicity influence developmental trajectories of gut microbiota. 

Persistently low Bacteroides abundance and high Enterobacteriaceae/Bacteroidaceae ratio increases the associations of food sensitivity. 

A deficiency of sphingolipid metabolism and persistent Clostridioides difficile colonization are characteristics of increased foos sensitivity trajectory.

The increased risk of food sensitivity for infants with this trajectory was especially significant for peanut sensitivity, with a 3-fold risk at age 3 years.

This peanut sensitivity risk was further increased in infants born with this trajectory to Asian mothers.

Most children outgrow milk allergy by 3 years.

Increased risk of food allergy may be due to delayed introduction of potentially allergenic foods in infants by exclusively breast feeding

Recommended that children allergic to peanuts, tree nuts, fish and shellfish should continue to avoid them as they get older.

Some medications may prevent, minimize or treat protein allergy reactions and treatment consists of oral immunotherapy .

Avoiding food allergens in pregnancy and during breast feeding does not reduce food allergies in children.

In children as young as  one year of age with multiple food,allergies, omalizumab treatment for 16 weeks was superior to placebo in increasing the reaction threshold for peanut andother common food allergies including cashews, eggs, and milk (Wood RA).

Omalizumab possible protection from food, allergies will most likely disappear when the treatment is stopped.

Timely and consistent and feedings of allergenic foods, such as peanuts and eggs during infancy, and into early childhood, is an effective primary prevention strategy against the development of food allergy in infants with eczema.

The dietary introduction of peanuts in infancy reduces the risk of peanut allergy 71%.

Diet introduction of hen’s eggs in infancy reduces the risk of egg allergy by 44%.

For peanut allergy, the greatest reduction in peanut allergy is when peanuts are introduced at an early age of 4 to 6 months.reduces the risk of egg allergy by 44%.

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