What accounts for the increase in peanut allergies in the past decade

What accounts for the increase in peanut allergies in the past decade

Diagnosis of food allergies, including peanut allergy, begins with a medical history and physical examination.[3][33]National Institute of Allergy and Infectious Diseases guidelines recommend that parent and patient reports of food allergy be confirmed by a doctor because «multiple studies protest 50% to 90% of presumed food allergies are not allergies.»[33]

Skin prick testing

Skin prick tests can be used to confirm specific food allergies.[2][3][33] Skin prick tests are designed to identify specific IgE bound to cutaneous mast cells.[2] During the test, a glycerinated allergen extract drop is placed on the patient’s skin.[3] The patient’s skin is then pricked through the drop.[3] This procedure is repeated with two controls: a histamine drop designed to elicit an allergic response, and a saline drop designed to elicit no allergic response.[3] The wheal that develops from the glycerinated extract drop is compared against the saline control.[3] A positive allergic test is one in which the extract wheal is 3mm larger than the saline wheal.[3] A positive skin prick test is about 50% precise, so a positive skin prick test alone is not diagnostic of food allergies.[2][3][33]

Oral food challenge

The «gold standard» of diagnostic tests is a double-blindplacebo-controlled oral food challenge.[3][33] At least two weeks prior to an oral food challenge, the person is placed on an elimination diet where the suspected allergen is avoided.[34] During the oral food challenge, they are istered a full age-appropriate serving of a suspected allergen in escalating size increments.[34] They are continuously monitored for allergic reaction during the test, and the challenge is stopped and treatment istered at the first objective sign of allergic reaction.[34]

Oral food challenges pose risks.[35] In a study of 584 oral food challenges istered to 382 patients, 48% (253) of challenges resulted in allergic reactions.[35] 28% (72) of these challenges resulted in «severe» reactions, which were defined by the study as a patient having: lower respiratory symptoms; cardiovascular symptoms; or any four other, more minor, symptoms.[35] Double-blind placebo-controlled oral food challenges are also time consuming and require shut medical supervision.[3] Because of these drawbacks to the double-blind placebo-controlled oral food challenge, open food challenges are the most commonly used form of food challenge.[34] Open food challenges are those in which a patient is fed an age-appropriate serving of a suspected food allergen in its natural form.[34] The observation of objective symptoms resulting from ingestion of the food, such as vomiting or wheezing, is considered diagnostic of food allergy if the symptoms correlate with findings from the patient’s medical history and laboratory testing such as the skin prick test.[33]

Signs and symptoms

Most symptoms of peanut allergy are related to the action of immunoglobulin E (IgE)[10] and other anaphylatoxins which act to release histamine and other mediator substances from mast cells (degranulation).

In addition to other effects, histamine induces vasodilation of arterioles and constriction of bronchioles in the lungs, also known as bronchospasm. Symptoms can also include mild itchiness, hives, angioedema, facial swelling, rhinitis, vomiting, diarrhea, acute abdominal pain, exacerbation of atopic eczema, asthma, and cardiac arrest.[2]Anaphylaxis may occur.[2][11]

Tree nuts and soy

People with confirmed peanut allergy may own cross-reactivity to tree nut, soy, and other legumes, such as peas and lentils and lupinus.[12][13][14][15] The cause of cross-reactivity results from similarity in the structures of storage proteins between the food sources.[12] Allergenic proteins are grouped by protein families: cupins, prolamins, profilin and others.

What accounts for the increase in peanut allergies in the past decade

Peanuts and soybeans own proteins in the cupin, prolamin, and profilin families, while lentils contain cupin proteins.[12] Reviews of human clinical trials report that 6–40% of people with a confirmed peanut allergy will own allergic symptoms when challenged with tree nuts or legumes.[14][16]


As of 2020, there is no cure for peanut allergy other than strict avoidance of peanuts and peanut-containing foods. Additional care is needed for food consumed at or purchased from restaurants.[3]

Total avoidance is complicated because the declaration of the presence of trace amounts of allergens in foods is not mandatory (see regulation of labelling).


Immunotherapy involves attempts to reduce allergic sensitivity by repeated exposure to little amounts of peanut products.[38][39] Evidence as of 2019, however, has found that it increases rather than decreases the risk of serious allergies.[40] None of these are considered ready for use in people exterior of carefully conducted trials.[41] A 2012 Cochrane Review concluded that more research was needed.[42] Sublingual immunotherapy involves putting gradually increasing doses of an allergy extract under a person’s tongue.[41] The extract is then either spat or swallowed.[41] As of 2014, the evidence did not show that this was safe or effective.[41] Epicutaneous immunotherapy involves giving the allergen through a patch and has also been researched.[41]

In September 2014, the U.S.

What accounts for the increase in peanut allergies in the past decade

Food and Drug istration (FDA) granted quick track designation, and in June 2015, granted breakthrough therapy designation to AR101 for peanut allergy in ages 4–17.[43] AR101 was studied in the PALISADE international, multicenter, randomized, double-blind, placebo-controlled study.[44][45]

In September 2019, the Allergenic Products Advisory Committee (APAC) of the Middle for Biologics Evaluation and Research (CBER) voted to support the use of Palforzia (formerly AR101) for peanut allergy.[46][47][48] The price has not been set as of September 2019 but is proposed to be between $US3,000 and 20,000 per year.[49]


In 2017, the US National Institute of Allergy and Infectious Diseases (NIAID) published revised guidelines for lowering the risk or preventing peanut allergies by creating separate ways to assess childhood allergies and guide parents with infants at high, moderate or low risk.[7][36][37] The guidelines discussed how to introduce peanut foods to infants as early as 4 to 6 months of age, with the goal of preventing peanut allergy.[5][20][37]

For high-risk children, the guide recommended that an allergy specialist assess a child’s susceptibility, possibly involving peanut allergy testing, followed by gradual introduction of peanut foods under the supervision of an allergy specialist.[5][37] Peanut allergy is confirmed only if there is a history of reactions to peanut consumption and by a positive allergy test.[37] Moderate-risk children – who display an allergic reaction to peanut products with mild to moderate eczema – are typically not assessed in a clinic, but rather own peanut foods gradually provided to them at home by their parents, beginning at around age 6 months.[5][10][37] The Learning Early About Peanut Allergy (LEAP) study supported by NIAID established that early introduction of peanut products into a child’s diet can prevent – rather than only delay – the development of childhood peanut allergies, and that the effect is beneficial and lifelong.[5][10][20]


The cause of peanut allergy is unclear and at least 11 peanut allergens own been described.[17][18] The condition is associated with several specific proteins categorized according to four common food allergysuperfamilies: Cupin (Ara h 1), Prolamin (Ara h 2, 6, 7, 9), Profilim (Ara h 5), and Bet v-1-related proteins (Ara h 8).[19] Among these peanut allergens, Ara h 1, Ara h 2, Ara h 3 and Ara h 6 are considered to be major allergens which means that they trigger an immunological response in more than 50% of the allergic population.[19] These peanut allergens mediate an immune response via release of Immunoglobulin E (IgE) antibody as part of the allergic reaction.[19]

Some of the peanut allergens can undergo enzymatic and non-enzymatic modifications which makes them more likely to bind to ligands on antigen-presenting cells.

Ara h 1 can undergo glycosylation modifications which own been shown to induce immunomodulatory responses; it stimulates lectin receptors MR and DC-SIGN on dendritic cells which further propagate cytokines and bias the immune system towards a Th2 type response.[19] Peanut proteins that undergo non-enzymatic changes through Maillard reactions when cooked or exposed to room temperature own an increase in AGE modifications on their structure.[19] These changes own been shown to stimulate RAGE receptors and SR-AI/II on dendritic cells and thus lead to an increase in IL-4 and IL-5-releasing Th2 cells.

What accounts for the increase in peanut allergies in the past decade

Peanut allergies are unusual in children of undeveloped countries[20] where peanut products own been used to relieve malnutrition.[21] The hygiene hypothesis proposes that the relatively low incidence of childhood peanut allergies in undeveloped countries is a result of exposure to diverse food sources early in life, increasing immune capability, whereas food selection by children in developed countries is more limited, reducing immune capability.[20][22] A possibility of cross-reaction to soy was dismissed by an analysis finding no linkage to consumption of soy protein, and indicated that appearance of any linkage is likely due to preference to using soy milk among families with known milk allergies.[23]

Timing of exposure

When infants consume peanut proteins while 4 to 11 months ancient, the risk of developing peanut allergy before the age of 5 years decreases by 11-25%, specifically in children with higher allergy risk via their parents with peanut allergy.[24] From these results, the American Academy of Pediatrics rescinded their recommendation to delay exposure to peanuts in children, also stating there is no reason to avoid peanuts during pregnancy or breastfeeding.[25][26]

Diet during pregnancy

There is conflicting evidence on whether maternal diet during pregnancy has any effect on development of allergies due to a lack of excellent studies.[27] A 2010 systematic review of clinical research indicated that there is insufficient evidence for whether maternal peanut exposure, or early consumption of peanuts by children, affects sensitivity for peanut allergy.[28]

Routes of exposure

While the most obvious route for an allergic exposure is unintentional ingestion, some reactions are possible through external exposure.

Peanut allergies are much more common in infants who had oozing and crusted skin rashes as infants.[29] Sensitive children may react via ingestion, inhalation, or skin contact to peanut allergens which own persistence in the environment, possibly lasting over months.[30]

Airborne particles in a farm- or factory-scale shelling or crushing environment, or from cooking, can produce respiratory effects in exposed allergic individuals.[31] Empirical testing has discredited some reports of this type and shown some to be exaggerated. Residue on surfaces has been known to cause minor skin rashes, though not anaphylaxis.

What accounts for the increase in peanut allergies in the past decade

In The Peanut Allergy Answer Book, Harvard pediatrician Michael Young characterized this secondary contact risk to allergic individuals as rare and limited to minor symptoms.[31] Some reactions own been noted to be psychogenic in nature, the result of conditioning, and belief rather than a true chemical reaction. Blinded, placebo-controlled studies were unable to produce any reactions using the odor of peanut butter or its mere proximity.[31]


The allergy arises due to dendritic cells recognizing peanut allergens as foreign pathogens.[32] They present the antigens on MHC class II receptors and these antigens are recognized by cell receptors on T cells.

The contact along with the release of the cytokine IL-4 induces their differentiation into CD4+Th2 cells.[32] The Th2 cells proliferate and release pro-inflammatory cytokines, such as IL-4, IL-5, and IL-13, which can be bound to receptors on undifferentiated B cells or B cells of the IgM subtype.[32] The receptor-cytokine binding causes their differentiation into IgE which can then be bound onto FcεRI on mast cells, eosinophils and basophils.[32] This elicits degranulation of the aforementioned cells which release potent cytokines and chemokines, thus triggering inflammation and causing the symptoms characteristic of allergy.[32]


What accounts for the increase in peanut allergies in the past decade