Peanut allergy

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Peanut allergy
Nut warning 1.jpg
A peanut allergy warning
Classification and external resources
ICD-10 T78.4
ICD-9-CM 995.61, V15.01
DiseasesDB 29154
MeSH D021183

Peanut allergy is a type of food allergy due to peanuts. It is different from nut allergies. Physical symptoms of allergic reaction can include itchiness, urticaria, swelling, eczema, sneezing, asthma, abdominal pain, drop in blood pressure, diarrhea and cardiac arrest.[1] Anaphylaxis may occur.[1]

It is a type one hypersensitivity reaction to dietary substances from peanuts that causes an overreaction of the immune system.[2] It is recognized "as one of the most severe food allergies due to its prevalence, persistency and potential severity of allergic reaction."[1]

In the United States peanut allergies are present in 0.6% of the population.[3] In Western cultures peanut allergy is the most common cause of food-related anaphylaxis death.

Signs and symptoms[edit]

Symptoms of peanut allergy are related to the action of Immunoglobulin E (IgE) 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. At least 11 peanut allergens have been described.[citation needed]

Symptoms can include mild itchiness, urticaria, angiodema, facial swelling, rhinitis, vomiting, diarrhea, acute abdominal pain, exacerbation of atopic eczema, asthma, and cardiac arrest.[1] Anaphylaxis may occur.[1][4]


The exact cause of someone developing a peanut allergy is unknown. A study did find a positive correlation between the amount of time a child is breastfed and odds that the child would develop peanut allergy.[5] The study also indicated that exposure to soy milk or soy products was positively correlated with peanut allergies.[5] However, an analysis of a larger group in Australia found no linkage to consumption of soy milk, and said that the appearance of any linkage is likely due to preference to using soy milk among families with known milk allergies.[6]

Food allergies seem less common in developing countries.[7] The hygiene hypothesis is an attempt to understand why this is the case.[8] Proponents of the hypothesis say that the relatively low incidence of childhood infections in developed countries contribute to an increased incidence of allergic diseases.[8] The hypothesis may also explain why first-born children are more likely to have an allergic disease.[8] The method used in cooking peanuts may result in the different incidence of allergies in developed nations in the west and undeveloped areas, as peanuts are much more frequently roasted in the west, whereas in other parts of the world peanuts are most frequently boiled, fried, or eaten raw.[9]

Timing of exposure[edit]

There is tentative evidence that eating peanuts early in life may decrease later allergies.[10][11]

A British study has found that consuming peanuts in infancy lowers the risk that a child will develop peanut allergies,[12] and the American Academy of Pediatrics, in response to ongoing studies that showed no reduction in risk of atopic disease, rescinded their recommendation to delay exposure to peanuts along with other foods. The academy also found no reason to avoid peanuts during pregnancy or while breastfeeding.[13] A study conducted jointly in Israel and United Kingdom noted a nearly tenfold increase in incidence of peanut allergy among British children compared to Israeli children. The study also found that Israeli children consumed peanuts at a much younger age than their British counterparts, whose parents delayed peanut consumption upon the recommendation of British pediatricians.[14] Pediatric associations in Britain and Australia recommend delaying introduction until age 3 and have not changed their recommendations as of 2009.[15]

Diet during pregnancy[edit]

A 2014 study found that peanut consumption by pregnant women without peanut allergies was associated with a decreased likelihood that their children would develop peanut allergies.[16] A 2003 study found no link to maternal exposure to peanuts during pregnancy or during breast-feeding.[5]

Routes of exposure[edit]

While the most obvious route for an allergic exposure is unintentional ingestion, some reactions are possible through external exposure. Airborne particles in a farm- or factory-scale shelling or crushing environment, or from cooking, can produce respiratory effects in exposed allergic individuals.[17] 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. In The Peanut Allergy Answer Book, Harvard pediatrician Michael Young characterizes this secondary contact risk to allergic individuals as rare and limited to minor symptoms.[17] Some reactions have been noted to be psychogenic in nature, the result of conditioning and belief rather than a true chemical reaction. Blinded, placebo-controlled studies by Sicherer et al. were unable to produce any reactions using the odor of peanut butter or its mere proximity.[17]


Diagnosis of food allergies, including peanut allergy, begins with a medical history and physical examination.[2][18] 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 demonstrate 50% to 90% of presumed food allergies are not allergies."[18]

Skin prick testing[edit]

Skin prick tests can be used to confirm specific food allergies.[1][2][18] Skin prick tests are designed to identify specific IgE bound to cutaneous mast cells.[1] During the test, a glycerninated allergen extract drop is placed on the patient's skin.[2] The patient's skin is then pricked through the drop.[2] 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.[2] The wheal that develops from the glycerinated extract drop is compared against the saline control.[2] A positive allergic test is one in which the extract wheal is 3mm larger than the saline wheal.[2] A positive skin prick test is about 50% accurate, so a positive skin prick test alone is not diagnostic of food allergies.[1][2][18]

Oral food challenge[edit]

The "gold standard" of diagnostic tests is a double-blind placebo-controlled oral food challenge.[2][18] At least two weeks prior to an oral food challenge, the person is placed on an elimination diet where the suspected allergen is avoided.[19] During the oral food challenge, they are administered a full age-appropriate serving of a suspected allergen in escalating size increments.[19] They are continuously monitored for allergic reaction during the test, and the challenge is stopped and treatment administered at the first objective sign of allergic reaction.[19]

Oral food challenges pose risks.[20] In a study of 584 oral food challenges administered to 382 patients, 48% (253) of challenges resulted in allergic reactions.[20] 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.[20] Double-blind placebo-controlled oral food challenges are also time consuming and require close medical supervision.[2] 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.[19] Open food challenges are those in which a patient is fed an age-appropriate serving of a suspected food allergen in its natural form.[19] 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.[18]


Currently there is no confirmed treatment to prevent or cure allergic reactions to peanuts and strict avoidance of peanuts is the only way to avoid an allergic reaction.[2] The principal treatment for anaphylaxis is epinephrine as an injection.[2]


The percentage of people with peanut allergies is 0.6% in the United States.[3] In a 2008 study, self-reported incidence of peanut allergy was estimated to affect 1.4% of the population of the United States, triple the 0.4-0.6% rate found in a 1997 study.[21] In England, an estimated 4,000 people are newly diagnosed with peanut allergy per year (11 per day); 25,700 having been diagnosed with peanut allergy by a clinician at some point in their lives.[22] Peanut allergy is one of the most dangerous food allergies, and one of the least likely to be outgrown.[21]

It is one of the most common causes of food-related death.[23] However, there is an increasing body of medical opinion that the measures taken in response to the threat may be an over-reaction out of proportion to the level of danger:[24] "About 3.3 million Americans are allergic to nuts, and even more—6.9 million—are allergic to seafood. However, all told, serious allergic reactions to foods cause just 2,000 hospitalisations a year (out of more than 30 million hospitalisations nationwide). And only 150 people (children and adults) die each year from all food allergies combined." Media sensationalism has also been blamed.[25]

Frequency among adults and children is similar—around 1%—but at a study shows self-reports of peanut allergy are on the rise in children in the United States.[26] The number of young children self-reporting the allergy doubled between 1997 and 2002.[27] Studies have found that self-reported rates of food allergies is higher than clinically-observed rates of food allergies.[2]

In 2013, Miranda Waggoner reported that the rates in self-reported incidence of the allergy, previously thought to be rare, could not be correlated with medical data confirming the self-reported incidence.[28][29]

Society and culture[edit]

Hypoallergenic peanuts[edit]

North Carolina Agricultural and Technical State University received a patent in 2012 for a process to reduce allergens in peanuts 98 percent or more. The process treats roasted peanuts, removed from the shell and skin, with food-grade enzymes commonly used in food processing. The treatment consists of soaking the peanuts in an enzymatic solution. The treatment reduces two key allergens, Ara h 1 to undetectable levels and Ara h 2 by up to 98%. The resulting peanuts look and taste like roasted peanuts. The peanuts are not genetically modified.

The effectiveness of the process was demonstrated in human clinical trials at the University of North Carolina at Chapel Hill, using skin-prick tests.[30]

N.C. A&T has signed an exclusive license for the process with Alrgn Bio. The company announced in October 2014 that batches of peanuts were available to food processing companies for evaluation. It said it would work with food processors and manufacturers to establish the process as “the industry standard for peanuts and peanut-derived ingredients.”[31]


Nicholas Christakis has said that measures taken (especially in schools) to ensure allergic children are not exposed to peanut allergens are disproportional to the actual risk of such exposure.[24][32] Dr. Christakis has also said that popular responses to the danger of peanut allergies "bear many of the hallmarks of mass psychogenic illness."[24]


Immunotherapy, while being studied, is not ready for use in people outside of trials.[33]

In those with mild peanut allergies, gradually eating more and more peanuts resulted in at least some short-term benefits.[34] Due to the amount of evidence being small and the high rate of adverse effects, this is not currently recommended as treatment.[34]

Sublingual immunotherapy involves putting gradually increasing doses of an allergy extract under a person's tongue.[33] The extract is then either spat or swallowed.[33] It is not currently recommended as treatment; however, it is being studied.[33]

Epicutaneous immunotherapy involves giving the allergen through a patch.[33] Trials look promising and are ongoing.[33]

An early trial of injecting escalating doses of peanut allergen was conducted in 1996. However, one participant died seconds after injection from laryngospasm due to a pharmacy error in calculating the dose. The death abruptly ended one of the only studies on injected allergen desensitization to peanut allergies.[35][not in citation given]

In 2011, a study was able to "turn off" peanut allergy in mice by attaching peanut protein to the mice's blood and injecting that into them. It has been successfully used in human studies of multiple sclerosis.[36]


  1. ^ a b c d e f g h C. LOZA; J. BROSTOFF (1995). "REVIEW Peanut allergy" 25. Clinical and Experimental Allergy. pp. 493–502. 
  2. ^ a b c d e f g h i j k l m n Saleh Al-Muhsen; Ann E. Clarke; Rhoda S. Kagan (2003). "Peanut allergy: an overview" 168 (10). Canadian Medical Association Journal. pp. 1279–85. 
  3. ^ a b "Food Allergy Quick Facts". National Institute of Allergy and Infectious Diseases. 2012-02-24. Archived from the original on 2010-04-07. Retrieved 2015-09-15. 
  4. ^
  5. ^ a b c Lack, Gideon; Fox, Deborah; Northstone, Kate; Golding, Jean; Avon Longitudinal Study of Parents Children Study Team (2003). "Factors Associated with the Development of Peanut Allergy in Childhood". New England Journal of Medicine 348 (11): 977–85. doi:10.1056/NEJMoa013536. PMID 12637607. [non-primary source needed]
  6. ^ Koplin, Jennifer; Dharmage, Shyamali C.; Gurrin, Lyle; Osborne, Nicholas; Tang, Mimi L.K.; Lowe, Adrian J.; Hosking, Cliff; Hill, David; Allen, Katrina J. (2008). "Soy consumption is not a risk factor for peanut sensitization". Journal of Allergy and Clinical Immunology 121 (6): 1455–9. doi:10.1016/j.jaci.2008.03.017. PMID 18436294. 
  7. ^ "Peanut Paste Saves Starving African Children - ABC News."
  8. ^ a b c Maria Yazdanbakhsh; Peter G. Kremsner; Ronald van Ree (19 April 2002). "Allergy, Parasites, and the Hygiene Hypothesis". Science. pp. 490–494. 
  9. ^ "Dry roasting enhances peanut-induced allergic sensitization across mucosal and cutaneous routes in mice". Journal of Allergy and Clinical Immunology 134: 1453–1456. doi:10.1016/j.jaci.2014.07.032. 
  10. ^ Du Toit, G; Roberts, G; Sayre, PH; Bahnson, HT; Radulovic, S; Santos, AF; Brough, HA; Phippard, D; Basting, M; Feeney, M; Turcanu, V; Sever, ML; Gomez Lorenzo, M; Plaut, M; Lack, G; the LEAP Study, Team (23 February 2015). "Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy.". The New England Journal of Medicine 372: 803–13. doi:10.1056/NEJMoa1414850. PMID 25705822. 
  11. ^ Gruchalla, RS; Sampson, HA (23 February 2015). "Preventing Peanut Allergy through Early Consumption - Ready for Prime Time?". The New England Journal of Medicine 372: 875–7. doi:10.1056/NEJMe1500186. PMID 25705823. 
  12. ^ "Food allergy advice may be peanuts". Science News 174 (2). Dec 6, 2008. 
  13. ^ Greer, F. R.; Sicherer, S. H.; Burks, A. W.; American Academy of Pediatrics Committee on Nutrition; American Academy of Pediatrics Section on Allergy Immunology (2008). "Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Timing of Introduction of Complementary Foods, and Hydrolyzed Formulas". Pediatrics 121 (1): 183–91. doi:10.1542/peds.2007-3022. PMID 18166574. 
  14. ^ Du Toit, G; Katz, Y; Sasieni, P; Mesher, D; Maleki, SJ; Fisher, HR; Fox, AT; Turcanu, V; Amir, T; Zadik-Mnuhin, Galia; Cohen, Adi; Livne, Irit; Lack, Gideon (2008). "Early consumption of peanuts in infancy is associated with a low prevalence of peanut allergy". The Journal of allergy and clinical immunology 122 (5): 984–91. doi:10.1016/j.jaci.2008.08.039. PMID 19000582. 
  15. ^ "News Medical". Retrieved 11 March 2013. 
  16. ^ Frazier A; Camargo CA, Jr; Malspeis S; Willett WC; Young MC (2014). "Prospective Study of Peripregnancy Consumption of Peanuts or Tree Nuts by Mothers and the Risk of Peanut or Tree Nut Allergy in Their Offspring" 168 (2). JAMA Pediatr. pp. 156–162. doi:10.1001/jamapediatrics.2013.4139. 
  17. ^ a b c Young, Michael C. The Peanut Allergy Answer Book: 2nd Edition. Fair Winds Press. ISBN 1-59233-233-1. [page needed]
  18. ^ a b c d e f Boyce, Joshua A. (December 2010). "Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAID Sponsored Expert Panel Report". J Allergy Clin Immunol. 
  19. ^ a b c d e Kirsi M. Järvinen; Scott H. Sicherer (2012). "Diagnostic oral food challenges: Procedures and biomarkers" 383. Journal of Immunological Methods. pp. 30–38. 
  20. ^ a b c Tamara T. Perry, MD; Elizabeth C. Matsui, MD; Mary K. Conover-Walker, CRNP; Robert A. Wood, MD (November 2004). "Risk of oral food challenges". J Allergy Clin Immunol. 
  21. ^ a b "Peanut Allergies in Kids on the Rise". WebMD. Retrieved 2013-12-29. 
  22. ^ Kotz, Daniel; Simpson, Colin R.; Sheikh, Aziz (2011). "Incidence, prevalence, and trends of general practitioner–recorded diagnosis of peanut allergy in England, 2001 to 2005". Journal of Allergy and Clinical Immunology f (3): 623–30.e1. doi:10.1016/j.jaci.2010.11.021. PMID 21236479. 
  23. ^ "Allergy Facts and Figures", Asthma and Allergy Foundation of America
  24. ^ a b c Christakis, Nicholas A. (2008-12-13). "This Allergies Hysteria Is Just Nuts" (PDF). British Medical Journal 337 (1384): a2880. doi:10.1136/bmj.a2880. PMID 19073662. Retrieved 2014-01-30. 
  25. ^ Colver, A. (2006). "Are the dangers of childhood food allergy exaggerated?". BMJ 333 (7566): 494–6. doi:10.1136/bmj.333.7566.494. PMC 1557974. PMID 16946341. 
  26. ^ Sicherer, SH; Muñoz-Furlong, A; Sampson, HA (December 2003). "Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study.". The Journal of allergy and clinical immunology 112 (6): 1203–7. doi:10.1016/s0091-6749(03)02026-8. PMID 14657884.  open access publication - free to read
  27. ^ Burks, A Wesley (2008). "Peanut allergy". The Lancet 371 (9623): 1538–46. doi:10.1016/S0140-6736(08)60659-5. PMID 18456104. 
  28. ^ Hotchkiss, Michael (2013-07-25). "Princeton researcher digs into the contested peanut-allergy epidemic". Princeton University. Retrieved 2014-01-09. 
  29. ^ Waggoner, Miranda (August 2013). "Parsing the peanut panic: The social life of a contested food allergy epidemic". Social Science & Medicine 90: 49–55. doi:10.1016/j.socscimed.2013.04.031. 
  30. ^ "A&T Signs Agreement to Commercialize Hypoallergenic Peanut". Retrieved 2014-12-09. 
  31. ^ "N.C. A&T, Xemerge launch spin-off peanut company; 1st hypoallergenic peanuts ready for food industry". Retrieved 2014-12-09. 
  32. ^ Alice Park (26 February 2009). "Why We're Going Nuts Over Nut Allergies". Time. Retrieved 6 April 2014. 
  33. ^ a b c d e f Jones, SM; Burks, AW; Dupont, C (February 2014). "State of the art on food allergen immunotherapy: oral, sublingual, and epicutaneous.". The Journal of allergy and clinical immunology 133 (2): 318–23. doi:10.1016/j.jaci.2013.12.1040. PMID 24636471. 
  34. ^ a b Nurmatov, U; Venderbosch, I; Devereux, G; Simons, FE; Sheikh, A (12 September 2012). "Allergen-specific oral immunotherapy for peanut allergy.". The Cochrane database of systematic reviews 9: CD009014. doi:10.1002/14651858.CD009014.pub2. PMID 22972130. 
  35. ^ Nelson, H; Lahr, J; Rule, R; Bock, A; Leung, D (1997). "Treatment of anaphylactic sensitivity to peanuts by immunotherapy with injections of aqueous peanut extract1". Journal of Allergy and Clinical Immunology 99 (6): 744–51. doi:10.1016/S0091-6749(97)80006-1. PMID 9215240. 
  36. ^ Smarr, Charles; Hsu, Chia-Lin; Byrne, Adam; Miller, Stephen; Bryce, Paul (October 5, 2011). "Antigen-Fixed Leukocytes Tolerize Th2 Responses in Mouse Models of Allergy". The Journal of Immunology. doi:10.4049/jimmunol.1100608. 
  1. ^ Basic Pathology - Robbins et al - 9th edition