Everything You’ve Always Wanted to Know About Peanut Allergy (And Possibly More)

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Peanut is botanically classified as a legume but is often grouped with tree nuts because it looks like them and provokes the same kinds of reactions. Those reactions can be quite severe, partly because, like some nuts, peanut is capable of activating the immune system independently of allergic responses.

Peanuts cause more problems for people who are born in the West, possibly because the nuts we eat tend to be roasted rather than boiled or pickled, and this makes them more allergenic. There are two main types of peanut-allergic individual; the person who developed their allergy in childhood, often at the same time as egg allergy and/or eczema, and tends to suffer from relatively severe reactions, and the person who experienced their first, typically mild, symptoms in adulthood, often in their 30s, and often after developing an allergy to birch pollen.

Even though it’s not a nut, up to half of the peanut-allergic will experience cross reactions with one or more tree nuts. But peanut is also cross-reactive with sesame seeds and other legumes like lupin and fenugreek, which is why the peanut-allergic really need to know what’s in their baked goods and in their curries.

Although it can be difficult to avoid peanuts in our food, the vast majority of people are unlikely to react to contact with peanut butter or to inhaled peanut proteins, and air travel is not as hazardous as you might think. FFor those with severe peanut allergies, however, there is now a treatment that can minimise or even prevent reactions, although it will probably mean that you have to eat a small amount of peanut every day for the foreseeable future.

And now for the details, which include:

What is an allergy to peanuts?

Peanut (Arachis hypogea) belongs to the Fabaceae (or Leguminosae)—the legume, bean or pea—family, which also includes lupin, soy and fenugreek. Thus, the peanut is not a nut, but a legume. However, although peanuts and tree nuts have several botanical differences, they tend to be grouped together because of their similar dietary uses, nutritional profiles and tendency to cause allergic reactions.

Peanuts, or ‘groundnuts’ as they are known in some parts of the world, are the seeds of a legume grown for its edible seeds and oil production. The typical peanut seed pod usually contains two seeds which mature underground, hence the name ‘groundnut’.

The nutrient-rich peanut is an important food crop that is now cultivated in more than 100 countries throughout the tropics and sub-tropics. The plant is linked to the savannah-like Cerrado of South America and probably originated in Brazil or Peru, although there are no fossil records to confirm this. But we do have about 3,500 years worth of bits of South American jars shaped like peanuts and decorated with peanuts, and archaeologists have also found graves of ancient Incas buried with filled jars to provide them with food in the afterlife.

The peanut was taken back to Spain by the Spanish Conquistadors as part of their loot and, from there, to Asia and Africa, where it became a common crop in the western tropical region. African slaves, in turn, introduced the peanut to the US (the word goober comes from ‘nguba’, the Congo name for peanuts) and it was eventually grown throughout the southern United States, where it owes its popularity to the remarkable George Washington Carver, who began life as a slave and ended it as an internationally renowned botanist, agronomist, inventor and ‘father of the peanut industry’, responsible for developing over 300 peanut-containing products (but not peanut butter). Today, the world’s top producers are China, India, Nigeria and the US.

There are over 70 species in the Arachis genus and thousands of peanut cultivars are grown around the world, with the four most popular being the Runner (subsp. hypogaea var. hypogaea), Virginia (subsp. hypogaea var. hypogaea), Spanish (subsp. fastigiata var. vulgaris), and Valencia (subsp. fastigiata var. fastigiata).

Certain cultivars groups are preferred for particular uses because of differences in flavour, size, shape, oil content and disease resistance. For instance, most peanuts sold in their shells are of the Virginia type, as well as Valencias that are selected for large size and the attractive appearance of their shells. Runner cultivars produce smaller peanuts with a stronger flavour that are used to make peanut butter, along with some Spanish peanuts which are also used to make salted nuts and peanut-containing candy.

Peanuts are omnipresent. Apart from being put in snacks, they are also used to make oil (mainly consumed in the Asian subcontinent, notably in India), pastes and sauces, and peanut in flour form is used extensively to add flavour, nutrients and the right texture to processed foods like soup, curries, meat products, breads, cookies and desserts. Peanut is also used to make beverages (like tea and cocktails), cheese alternatives and milk (surprisingly unpopular considering the rise of plant-based milk, but useful in cases of malnutrition).

In the English-speaking world, peanuts tend to be consumed in roasted form; in the shell, or blanched and oven roasted, or ground to make peanut butter—which, incidentally, was created in (its modern form) as a group effort. First, Canadian Marcellus Gilmore Edson patented a method to make peanut paste in 1884 so that he could make peanut candy, although he apparently never sold any. Then, 11 years later, Dr. John Harvey Kellogg (yes, he of cereal fame) patented a process to make a peanut blend which he wanted to market as a protein-rich alternative for people who were unable to chew through steak (the actual recipe didn’t specify peanuts, but they were cheaper than tree nuts, so they won, and anything was better than that ‘sinful sexual stimulant’, meat). In 1903, another American, Dr. Ambrose Straub, patented a machine that could actually make peanut butter and finally, in 1922, the American chemist Joseph Rosefield created a way to make a peanut butter from which the oil wouldn’t separate and spoil. He ended up founding Skippy, one of the world’s major the peanut butter brands.

In other parts of the world (and the southern United States), peanuts are more commonly used as raw ingredients and boiled, fried or pickled.

The consumption of peanuts has increased during past few decades because of their health benefits, low cost and versatility. They are highly nutritious, energy-dense seeds, made up of around 50% oil and 25% protein. They are also rich in insoluble and soluble dietary fibre and multiple micronutrients including B vitamins, vitamin E, minerals (e.g. magnesium, iron, zinc and potassium) and antioxidant minerals (e.g. selenium, manganese and copper), healthy fats (monounsaturated fatty acids, polyunsaturated fatty acids) and antioxidants such as polyphenols, isoflavones, phytosterols and resveratrol (many of which are in the skins).

Research has found that the regular consumptions of peanuts is associated with lower blood blood pressure, a healthier lipid profile and better cardiovascular health, improved blood sugar regulation and a smaller risk of getting type 2 diabetes, a smaller chance of getting gallbladder disease and having gallstones, a lower risk of getting certain types of cancers (gastric, colorectal, prostate, breast) and a smaller likelihood of cancer spreading to other parts of the body, a lower risk of developing Alzheimer’s, increased satiety, a lower body mass index (BMI) and reduced likelihood of being overweight or obese and a smaller risk of death due to any factor.

Unfortunately, peanut can cause allergic reactions in a small percentage people. This happens because their body’s immune system mistakes one or more harmless peanut proteins for toxic invaders and creates IgE antibodies against them. The next time they eat peanut, the antibodies recognise the proteins and prompt a response from immune system cells. These, in turn, release a variety of chemicals into the bloodstream, including histamine, the chemical that is primarily responsible for the symptoms of allergy.

Identified allergens

The proteins (and occasionally carbohydrates) in a food that are capable of provoking allergic reactions are called allergens. Allergens are named using the first three letters of the genus—Arachis—the first letter of the species—hypogaea—and a number reflecting the order in which they were identified.

As of March 2026, 20 peanut allergens have been added to the WHO/IUIS allergen database (the official, peer-reviewed database of allergens maintained by the World Health Organisation and International Union of Immunological Societies):

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How common is peanut allergy?

A definitive diagnosis of allergy can currently only be established with a food challenge, but challenges are costly in terms of both time and resources, as well as potentially risky. So many prevalence studies measure sensitisation—using skin or blood test data—but sensitisation is not allergy. Being sensitised to something simply means that your immune system recognises it, but you may not actually react to it; in fact, many people don’t react to whatever it is they are sensitised to. Studies that use sensitisation data therefore tend to produce allergy prevalence numbers that are larger than they should be.

In a similar vein, studies that estimate allergy prevalence using questionnaires usually produce somewhat inflated numbers as people can self-report allergies that they do not actually have, although robust studies will use certain criteria to evaluate respondents’ answers and determine whether their symptoms suggest an allergy or not.

IgE-mediated allergy

The prevalence of peanut allergy worldwide varies widely between 1% and 2% in Western nations, notably the UK, the US, Canada and Australia, to much lower rates in Asian countries and Africa (based on the little data we have from those regions).

These variations in prevalence numbers around the world can be explained by differences in the age of the population under study and the geographical region in which the study is carried out, as well as the way that peanuts are consumed—e.g. boiled versus roasted—and when they are introduced into a child’s diet.

In 2023, a team of researchers investigating the prevalence of the 8 biggest food allergens in Europe reviewed 68 peanut-related studies carried out in the region and calculated that around 0.9% of Europeans had been diagnosed with an allergy to peanuts during their lifetimes.

There are, of course, regional differences. The Pronuts study, designed to examine the rate of co-allergy to peanuts and nuts in children under 16 in 3 European centres—London, Geneva and Valencia—reported that, although peanut allergy was the most common type of allergy overall, it was primarily driven by high numbers of children eating and being allergic to peanuts in London, where around two thirds of the nut-allergic children in that centre were allergic to peanuts. By contrast, in Valencia, only 1 in 5 nut-allergic children were allergic to peanuts, walnut and pecan allergies were more common.

Other Europe-wide studies (in the EuroPrevall project) have revealed that, in 2020, doctor-diagnosed peanut allergy affected around 1.8% of the children in Southampton (the UK), 1.6% in Madrid (Spain), 1.4% in Reykjavik (Iceland), 1.2% in Berlin (Germany) and Lodz (Poland), 0.8% in Amsterdam (the Netherlands), 0.6% in Vilnius (Lithuania) and 0.4% in Athens (Greece). Among adults, probable peanut allergy affected 0.45% in Madrid, 0.37% in Zurich (Switzerland) 0.35% in Lodz, 0.05% in Utrecht (the Netherlands), 0.02% in Athens and none in Reykjavik.

A 2004 survey of 1488 Swedish adolescents revealed peanut to be the 3^rd most common trigger of allergic reactions to food, reporting with a self-reported prevalence of peanut allergy of 5.9%.

In Denmark, a series of studies carried out between 2005 and 2008 estimated the prevalence of peanut allergy in the Danish population to be between 0.5% and 1.2% in the under 6s, 0.5% in adolescents, 0.6% in young adults (22-year-olds) and 0.4% in adults. It appeared around the age of 1 and a half and became the no.1 food trigger by the time food-allergic reached adulthood.

In the UK, a series of studies put the prevalence of peanut allergy at around 1.5% among 6- to 8-year-olds and adolescents living on the Isle of Wight.

In France, a 2005 study estimated peanut allergy prevalence of 0.3% to 0.75% in the general population.

In the Eastern Mediterranean region, namely Turkey, food-challenge proven peanut allergy among schoolchildren in the Ankara province has been calculated to be 0.05%.

In the US, multiple studies have been carried out in food allergic children and adults. The most recent analyses of detailed survey data collected between October 2015 and September 2016 put the prevalence of peanut allergy at 2.2% in children (affecting around 1.6 million) and 1.8% in adults (affecting around 4.5 million). The highest prevalence rates were noted among 2-year-old children (between 1.6% and 3.6%) and 30- to 39-year-old adults (between 2.5% and 3.3%), and the lowest among the over 60s (between 0.7% and 1%).

In Canada, the most recent study (using 2005 to 2007 data) involving Montreal schoolchildren aged between 5 and 9 put the prevalence of confirmed peanut allergy at 1.62%.

In Australia, the SchoolNuts population-based study reported that peanut was the most common trigger food among Australian children and adolescents, 2.7% of whom had clinic-defined peanut allergy. The HealthNuts study, a population-based study that followed 5276 children from the age of 1 till the age of 6, reported a challenge-confirmed peanut allergy prevalence of 1.9% in 4-year-old children down from the 3.0% of challenge-confirmed allergy reported in the same group of children when they were 1 year old. The second study found 12 cases of late onset peanut allergy in their group of 4 year-olds who had previously been tolerant of peanut at the age of 1, and more children must have acquired a new peanut allergy between the age of 4 and 14 when the prevalence was found to be at its highest.

Data on food allergy is more scarce in much of the rest of the world.

In Cuba, a 2017 study reported a prevalence of peanut sensitisation in the general adult population of 4.6%. The prevalence was higher in people with allergies; 18.6% in atopic adults and 25.6% in atopic children. That said, despite the relatively high sensitisation, allergy to peanut was not perceived as a frequent or serious health problem by Cuban doctors.

In South America, research from Mexico based on a structured questionnaire has calculated a prevalence of probably peanut allergy among children aged between 6 and 7 of 1.8%, and a rate of convincing allergy at 1.1%. In Colombia, a questionnaire-based study that asked 3099 random people living in Cartagena to report any self-perceived food allergies revealed that no-one thought that they were allergic to peanut. In Honduras, the challenge-proven prevalence of peanut allergy in 365 children was reported to be 0.8%. A study of 457 children in Brazil reported a prevalence of peanut sensitisation among children with allergies to be 14.7% and among those without known allergies to be 4.8%.

In Egypt, a recent questionnaire-based study reported that, of 2140 schoolchildren aged between 6 and 15, 8 (0.37%) had a convincing history of symptoms after eating peanuts. In South Africa, a multicentre study reported a prevalence of peanut allergy of 0.8% in South African children based on skin tests and oral food challenges. The study examined children who lived in urban area and in rural areas and revealed that, although some were sensitised to peanut, children who lived in rural areas did not seem to be affected by peanut allergy.

A cross‐sectional study of Kuwaiti schoolchildren aged between 11 and 14 years reported a peanut allergy prevalence of 1.3% based on clinical history.

Peanut allergy is generally regarded as less of a problem in Asia, and peanut is often not found on the list of the most common trigger foods, although the prevalence may have been increasing in recent years because of a shift in consumption from boiled peanuts (a less allergenic form of peanut) to processed peanut butter (made from roasted peanuts, which are more allergenic).

In Northern Thailand, allergy to peanut is rare.A 2019 survey of the parents of 561 preschoolers revealed that only 1 parent reported that their child had ‘ever had’ peanut allergy (and that child has apparently outgrown it).

By contrast, a nationwide survey of people in Taiwan in 2012 reported that peanut was one of the most commonly reported food allergens in the general population, behind seafood and alongside mango, milk and egg.

A 2015 study which surveyed the parents of 29,842 children Korean schoolchildren reported that peanut was the top trigger of immediate allergic reactions to food among 9- to 10-year-olds, the second most common among the 12- to 13-years-olds and the third most common among the 14- to 15-years-olds, estimating a prevalence of peanut allergy of 0.22%.

A 2010 study involving Singaporean and Filipino schoolchildren reported a similar prevalence of convincing peanut allergy in both 14–16-year-old Singaporeans (0.47%) and Filipinos (0.43%).

Prevalence rates differ greatly in China, which is a very large country. Whereas 12.3% of rural populations have been found to be sensitised to peanut, the second most common sensitising food, no-one seems to report convincing peanut allergy. In Hong Kong, however, the prevalence rate of peanut allergy has been reported as being comparable to those in Western countries, with peanut reported as being the third most common allergen to affect preschoolers.

A large 2024 study noted that peanut was still an uncommon food allergen in the country, although the prevalence of peanut allergy seemed to be rising in Chinese megacities (those with a population of over 10 million people). In Shanghai, the most populous region of China, peanuts ranked as the sixth most common food allergen, with a prevalence of 8.4% as confirmed by positive sensitisation and OFCs among children younger than 14 years old. In 2016, peanuts were the third most common food allergen to be reported in the cities of Shenzhen and Guangzhou, the third and fourth biggest cities in China. Basically, the prevalence of peanut allergy seems to be increasing in the regions of China which have experienced rapid economic development and urbanisation in recent decades, although it still remains lower than in Western countries.

Finally, as part of the EuroPrevall-INCO project, 37,000 schoolchildren were recruited from from urban and rural regions of China, Russia and India and screened for allergies. A 2020 study reported a prevalence of ‘probable’ peanut allergy (defined as reported immediate allergic symptoms and positive blood or skin prick test result) in Hong Kong, Guangzhou and Shaoguan (China), Tomsk (Russia) and India as 0.10%, 0.00%, 0.00%, 0.08% and 0.03%, respectively.

Peanut allergy is thought to be on the increase in some countries, namely the US, the UK and Australia. In the US, surveys of Americans around the whole country have reported higher prevalence rates of allergy in children in recent years, climbing from 0.4% in 1997 to 0.8% in 2002, 1.4% in 2008 and 2.2% in 2017.

In 2014, researchers examining a group of several hundred children born in the northeast of the US calculated several different prevalence numbers based on different definitions of allergy, and compared them with the numbers reported by previous studies which had used the same definitions; for example, a prevalence of 1.4 reported in a 2008 study in using the criteria of self-reported allergy plus certain symptoms became 4.6% in this study and a prevalence of 2.7% reported by a 2010 study based on certain levels of IgE antibodies in the blood became 5.0%.

All of which goes to show that definitions are important and, by whatever measure, the prevalence of peanut allergy does seem to be increasing in the US. The higher numbers corroborate those reported in a more recent analysis of data in a US healthcare claims database reported that the annual incidence of peanut allergy in 1-year-old children had increased from 1.7% in 2001 to 5.2% in 2017.

In the UK, a birth cohort set up on the Isle of Wight allowed researchers to examine the prevalence of food allergy over a period of several years. This project showed that the prevalence of peanut allergy initially increased during the 1990s (from 0.5% to 1.2%) before seeming to stabilise in the early 2000s.

More recently, a review of 15 years’ worth of medical records in a nationwide database study found that the point prevalence of peanut allergy in the entire population had risen from 31 to 202 per 100,000 and, in the under 18s, from 116 to 635 per 100,000 between 2000 and 2015. Additionally, the study found that number of new cases reported each year in the whole population had more than doubled during that time (from 8.6 to 18.2 per 100, 000), with the large majority (89%) being reported in children under 4 years old.

In Australia, the number of children under the age of five diagnosed with food allergy, most commonly to peanut, increased 12-fold between 1995 and 2006. A study that looked specifically at diagnoses of peanut allergy revealed that the estimated proportion of children diagnosed with peanut allergy in the Australian Capital Territory rose from 0.73% among children born in 2001 to 1.15% among those born in 2004.

Increases in sensitisation to peanut and to parent-reported allergy at the turn of the century were also reported in the Netherlands and Sweden, respectively, while the latter country also reported fewer reactions to other common allergens (namely milk, egg, fish and wheat).

However, a stable prevalence of peanut allergy has been reported in two Canadian studies. A study that compared the results of 2 surveys of parents of Montreal schoolchildren carried out between 2000-2002 and 2005-2007 reported that the prevalence of peanut allergy had remained relatively stable over time (estimated at 1.34% during the first period and 1.62% during the second).

The authors of the study speculated that the prevalence increase seen in other studies could be due to the methods used to calculate probable peanut allergy and imprecise results that ‘precluded definitive conclusions’.

Another Canadian study reported that, although prevalence of self-reported food allergy had increased from 7.1% to 9.3% between 2010 and 2016, the prevalence of doctor-diagnosed food allergy remained stable (5.9% vs 6.1%), implying that rates of self-reported allergy probably overestimated true rates of allergy, and this could probably be explained by increasing awareness of food allergy in general.

Notably, a study of clinician‐diagnosed peanut allergy registered in a national database in Britain revealed that the prevalence of peanut allergy in the UK had doubled at the turn of the century from 2001 (0.24 per 1000 patients) to 2005 (0.51 per 1000 patients). This increase was highest in boys and in the age group 10 to 14 years. However, the incidence—the number of new cases of allergy—had not increased over the years, implying that the increase in the overall number of people with peanut allergy was due to a trend of fewer children outgrowing their allergy.

Whether there is a global increase in prevalence of peanut allergy or whether it just affects a few populations and, if so, what could be behind it remains a matter of debate.

Non IgE-mediated and mixed allergies

Specific prevalence information for non-IgE-mediated conditions is more hard to come by.

One type of mixed allergy that’s associated with sesame is atopic dermatitis (AD), aka allergic eczema, which I shall now just call eczema (although, strictly-speaking, AD is the most common subtype of eczema).

About 2.6% of the global population is estimated to be affected by eczema, which is just over 204 million people. It’s a condition that’s more likely to affect young children and females, and food is thought to be a trigger in 20% to 30% of the cases, with the most common allergens being milk, egg, soy, wheat, peanut and fish.

Although food-triggered eczema affects children more than adults, quite a few adults still have the condition. The prevalence of food allergy in children with eczema is estimated to be somewhere in the range of 15% to 30% and the prevalence of food allergy in adults with eczema is thought by most experts to be between 1% and 3%, with between 9% and up to 24.5% of that number estimated to be new, adult-onset cases.

An international study which looked at the prevalence of food sensitisation in 2184 infants with eczema in 10 European countries, Australia and South Africa reported that peanut was the 3^rd most common food sensitisation, behind egg white and milk, with sensitisation to peanut being more common in Australia (45%), the Netherlands (38%) and the UK (36%) where infants were more likely to be exposed to peanut, and least common in Poland (10%) and Belgium (7%).

Separate research has reported that peanut is the third most common food sensitisation in Swiss children with eczema, and second in Swedish children with eczema, with sensitisation occurring before the age of 3 in 4 in 5 children. German research adds that, as with peanut allergic children who don’t have eczema, sensitisation to peanut seems to occur before it’s introduced into an infant’s diet.

In the US, peanut was identified as a common food allergy among people with eczema decades ago, with a 1999 study reporting it as the third most common food trigger in infants and children with eczema and the most common in adolescents and adults.

A 2016 review of the medical record of 298 American children with food allergy and eczema reported that, of the 183 children whose skin condition was likely triggered by food, 24 (13%) had flare-ups after eating peanuts.

In South Africa, peanut is reported to be the second most common trigger among food-allergic children with eczema, affecting around 1 in 4.

In Asia, peanut allergy is less common among children with eczema. According to Korean research (from around 2 decades ago), it doesn’t even crack the top 10, with food allergens such as seafood, meats and fruits more likely to cause problems for children and adolescents with eczema. A study of 266 young children reported that 43 (16,2%) were sensitised to peanut and around 8 (3%) may be allergic according to the levels of IgE antibodies in their blood (which is not very reliable). Sensitisation was higher in infants under 12 months old and in those who had moderate to severe eczema.

Not everyone with eczema and peanut allergy suffers from a worsening of their skin condition after eating peanuts.

A study of French children referred to an allergy clinic with suspected peanut allergy reported that, of the 177 children who failed a food challenge, 10 (5.6%) experienced an exacerbation of their eczema.

A 2011 Czech study which included 175 adolescents and adults with eczema reported that 41 (23.4%) were allergic to peanut, with 36 suffering from immediate allergic reactions to peanuts (including oral allergy syndrome—an ‘itchy mouth’—stomach pain and breathlessness) and 5 experiencing a worsening of their skin condition after eating peanuts. A second study carried out about a decade later examined the medical data of another 100 adolescents and adults with eczema and reported that 49 had a history of reactions to peanut. Of these, 8 experienced a worsening of their skin condition after eating peanuts.

A review of the medical records of 713 peanut-allergic children seen at 3 medical centres reported that only 8 (1.1%) experienced isolated eczema flares after eating peanuts.

Experts do not know the exact prevalence of food protein–induced enterocolitis syndrome (FPIES) but it’s estimated to occur in the general population at a prevalence ranging from 0.015% in Australia to 0.7% in Spain and reports of cases have been on the increase in recent years, either because of an increase in new cases or because of an increased awareness of the condition among doctors.

The most commonly identified triggers of FPIES among children are the ones that they first encounter in their diets. In English-speaking countries, that’s often milk, soy, grains (especially rice, oats and wheat) and egg, whereas in Spain, foods like fish and legumes are more frequently identified as trigger foods. Among adults, the most common trigger is seafood. Globally, peanut is infrequently reported as a trigger.

However, in the past decade or so, peanuts have been more frequently reported as an emerging trigger for FPIES, at least in Western countries such as the US and Australia.

Some study authors have suggested that guidelines advising the early introduction of peanut into children’s diets could be responsible for this increase.

However, early introduction is important for preventing the development of the potentially worse, IgE-mediated (‘classic’) form of allergy, and other experts point out that the assumption that the new guidelines are responsible for the increase in cases of FPIES to peanuts assumes that parents have been following them, which has not been proven. What has been proven is that the early introduction of peanuts did not lead to a rise in IgE-mediated allergy to peanuts. This suggests that other factors are responsible for the rise of allergy in general and in FPIES cases in particular, which have been reported to a whole range of foods and could be at least partly due to the fact that doctors are better able to recognise the condition now and are therefore reporting it more often.

Therefore, the advice to introduce peanut to children as early as possible still stands.

Cases of eosinophilic oesophagitis (EoE) have (also) been reported to be on the increase since the turn of the century, probably because the condition is better recognised. EoE is now thought to affect 1 or 2 people in 2000 but, in people who have food allergies, the number is more like 1 in 20. EoE to a food often develops in someone who already has a standard, IgE-mediated allergy to that food.

Eosinophilic oesophagitis is more common in males and can occur at any age, but it becomes more common as people get older, peaking in adults aged between 30 and 50.

According to a 2018 review, the few studies that report numbers of people with the condition reveal that between 1% and 16.7% of people of with eosinophilic oesophagitis have a condition that’s triggered by peanut- and/or tree nuts.

A 2019 study of children with EoE attending 26 European pediatric gastroenterology centres in 13 European countries reported that peanut was the 4^th most common trigger, affecting 1 in 10 (9.9%) of all the patients.

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Will it go away?

IgE-mediated allergy

Peanut allergy usually appears during childhood with the first allergic reactions to peanut typically occurring before the age of 2, sometimes as early as 4 months old. The appearance of symptoms is different in different areas of the world, depending on when peanut is introduced into a child’s diet; symptoms in American children, for example, can appear about a year earlier than those in Spanish or Swedish children, probably because Americans are introduced to peanut products—notably peanut butter—very early in their childhood. In Turkey, children are reported to have an earlier onset of symptoms to peanuts than many of their counterparts living in Western countries; typically around 12 months old.

Around three quarters of people with childhood peanut allergy experience reactions to peanuts during their first known exposure to them.

Because of this, there has been a few decades’ worth of debate over whether or not infants can be sensitised to peanuts via their mother’s breast milk. The authors of a 1980s study that involved 8 infants who had symptoms after eating certain foods, including peanut, for the first time were the first to speculate that breast milk was the most likely route of sensitisation. Since then, studies have detected the presence of peanut allergens in breast milk between 2 and 6 hours after the mother eats the relevant food. Research has also detected the presence of a major peanut allergen (Ara h 6) in breast milk within 10 minutes of the mother eating peanuts.

However, animal research has also shown that the ingestion of small amounts of these allergens via breast milk promotes tolerance to peanuts, rather than sensitisation. And we now also known that peanut dust in the environment, which is present when mothers eat peanuts in the home, is also a possible route of sensitisation (see Risk factors later). Which of the two is (most) to blame, if indeed either are the problem, is still unknown.

A peanut allergy is often a lifelong disorder. Around 1 in 5 children will outgrow their peanut allergy, according to data from several longitudinal studies carried out in the UK (where a resolution rate of 18% was reported in 1998), the US (where a resolution rate of 21.5% was reported in 2001 and updated to a possible 23.3% in 2003) and Australia, where the HealthNuts project reported in 2015 that 22% of children outgrew their allergy by the age of 4.

Unlike the previous British and American studies which diagnosed peanut allergy based on medical history and skin prick and/or blood tests, the HealthNuts studies were the first to prospectively monitor the status of food allergy in children by using standardised questionnaires, skin prick tests and oral food challenges, so their data is probably more reliable.

A child may have a 1 in 3 chance of outgrowing their peanut allergy by the time they are in primary school. A 2007 study from Australia used the medical records of 267 under-2s diagnosed with peanut allergy during a 5-year period to calculate an estimated resolution of peanut allergy of 13.2% by the age of 3, 21.4% by the age of 5 and 34.2% by the age of 7, which concurred with the results of the population-based HealthNuts study published in 2022 that reported that, by the age of 6, 29% of the children they were following had outgrown their peanut allergy. Similarly, an analysis of the medical data of children handled by 3 Korean hospitals estimated that by the age of 10, 32.8% % of peanut-allergic children would outgrow their allergy.

That said, a 12-year study of Canadian children pours water on this idea, calculating a remission rate of 10% by 4 years, 18% by 6 years, 22% by 8 years, 26% by 10 years and 27% by 12 years of age. The authors of this study point out that the previous calculations may have been too optimistic, based as they are on a bit of guesswork as people get older and are lost to the study. This study lost very few subjects (14 of 202) and most were also given food challenges to check their allergic status. Or there may be something different about a Canadian child’s environment that makes it less likely that they will outgrow their peanut allergy at an earlier age.

Researchers have identified a few factors that may indicate that a person’s peanut allergy is less likely to resolve.

One sign may be atopy—the tendency to get allergies— and a persistent allergy to other foods in particular. An early British study that compared the characteristics of 15 children whose allergy resolved with 15 children’s whose allergy was persistent noted that although several things were similar about the two groups—similar age of onset, similar symptoms—one thing that was different about the children whose allergy persisted was the fact that they were more likely to be allergic to other foods.

An early American study noted something similar. In this study, researchers followed the fortunes of 223 children diagnosed with peanut allergy between the age of 2 months and 15 years and found that those whose allergy resolved were significantly less likely to have current allergies to other foods, notably egg (many of the children in both groups had an ongoing tree nut allergy). The study also noted that the children who failed their challenges were more likely to have eczema.

Data from the Australian HealthNuts study also supports this idea, finding that both sensitisation to multiple food allergens and early-onset severe eczema were associated with an increased risk of persistent peanut allergy.

This could reflect the fact that the people with an ‘overactive’ immune system are less likely to outgrow their food allergies, or at least to outgrow them quickly. However, of all the markers of a possibly persistent allergy, atopy and food allergies in particular, is the weakest. Not only do most children who get food allergies also have other allergic conditions, a 2003 review of the medical charts of 84 peanut-allergic American children noted that having other food allergies (which just over half of them did) did not make a child more or less likely to pass their challenge after all.

By far a more more reliable indicator of a persistent peanut allergy is the level of specific IgE antibodies that a person has to peanut. Australian studies carried out in 2007, 2015 and 2022 have all mentioned that a person’s skin test response was quite a good indicator of whether or not their allergy might resolve, finding that larger weals were more likely to indicate allergies that would not be outgrown, and that people whose weal diameter increased between the ages of 1 and 4 were less likely to outgrow their allergy than those who saw the magnitude of their skin response diminish.

Similarly, among children with peanut allergy and eczema, those whose allergy resolved tended to have low levels of IgE antibodies to peanut which decreased over time, as well as somewhat milder forms eczema and milder reactions when accidentally exposed to peanut.

Even this is not a foolproof indicator, however; the authors of a 2015 study noted that among children whose skin test response decreased between the ages of 1 and 4, 53% did not outgrow their allergy. However, among the children whose skin test response either did not change or increased 90% remained allergic to peanut. So, no change in IgE levels or an increase is almost certainly bad news. The 2022 study identified weal size thresholds at the age of 1 above which a person could be fairly sure that they would not outgrow their allergy by the age of 6, but they came with the caveat that they were not very sensitive and would only correctly identify very few children with allergy.

Specific IgE antibody levels as measured by blood test have proven to be more reliable indicators of persistence and have been noted by studies carried out in America in 2001 and 2003, in Australia in 2007 and 2015, in Canada in 2013 and in Korea in 2021. As a general rule, lower initial levels of specific IgE to peanut at diagnosis, or falling levels after being diagnosed and relatively low levels when challenged are a promising sign that the allergy will be overcome, and the opposite is not. Even then, people with really low levels can suffer from a persistent allergy, and people with very high initial levels can outgrow their allergy, but it’s generally a rare occurrence.

That said, the general validity of these measures is why it’s common practice for doctors to monitor an allergic patient’s IgE levels to their trigger allergen periodically and to recommend a food challenge if the levels decrease to below a certain value so that they can check whether or not the allergy has resolved.

Childhood allergies are most likely to resolve if a child’s first reaction is relatively early—under the age of 2. However, even if you’ve not developed a peanut allergy as an infant or a toddler, you could still be at risk of becoming allergic to them; the 2022 HealthNuts study revealed that the peanut allergy prevalence at the age of 6 (3.1%) was similar to that found at the age of 1 (3%) in their birth cohort, largely owing to new cases of peanut allergy occurring in 0.7% of the children after the age of 1.

You can also become allergic to peanut for the first time as an adult. Currently all of the research on adults with peanut allergy seems to come from America, where almost 2 in 5 (17.5%) of the 4.5 million adults with peanut allergy experienced their first reaction in adulthood, around the age of 33.

American adults with adult-onset peanut allergy are more likely to be women than men, to be white than other ethnicities and to have other allergic conditions such as asthma, eczema and environmental allergies (e.g. pollen or house dust mite allergy). They are also more likely to be allergic to insects stings and latex and to have allergies to other foods, notably tree nuts and shellfish.

Environmental allergies in particular could be responsible for adult-onset food allergy. An adult’s new allergy to food is often a so-called secondary allergy, brought because their immune system mistakes the proteins in the food for proteins in the airborne allergen that they are allergic to; this is what happens, for example, in people allergic to birch pollen and peanut. And then, what starts off as an allergy to one food becomes an allergy to another new food as the person’s immune system is primed to start recognising and becoming reactive to more foods in some form of domino effect that’s not yet properly understood.

There seems to be two main types of peanut allergy; there’s the kind you can get as a young child which is often accompanied by systemic reactions—generalised reactions that can affect multiple organs around the whole body—that tend to occur on first exposure to peanut, and there’s the kind you can get in later childhood or adulthood, which can appear after years of eating peanuts without problem and is often associated with and allergy to birch pollen and milder reactions, notably oral allergy syndrome (predominantly an itchy mouth).

Both types are associated with different peanut allergens; the early childhood allergy is linked with a sensitisation to Ara h 2, a major storage protein associated with severe reactions, and the one you develop later (anytime after the age of 4) is associated with Ara h 8, an allergen that is similar in structure to and causes cross-reactions with an equivalent allergen in birch pollen, and which is linked to milder (or no) symptoms.

Unfortunately, whether you become sensitised to peanut during early childhood or have your first reactions to peanut during adolescence or adulthood, your allergy is unlikely to resolve.

Non-IgE-mediated and mixed allergies

Children with eczema and peanut allergy are less likely to outgrow either condition than people with allergies to other foods, with one American study finding that children with AD and peanut allergies were likely to keep their skin condition beyond school age and another reporting that just 1 in 4 children with eczema and allergies to egg, milk, soy, wheat or peanut outgrew their food allergy, compared to around 2 in 3 who were allergic to another food.

These results was corroborated by those of a Swedish study that followed 58 children with eczema until the age of 7 and found that children were less likely to lose their allergy to peanut (4 of 37 allergic to peanut) than children who were allergic to egg or milk.

A South African study that followed 19 children with peanut allergy and moderate to severe eczema for around 5 years after their diagnosis reported that only 3 outgrew their allergy around the age of 8 and a half years old.

Children with food protein–induced enterocolitis syndrome (FPIES) are also relatively unlikely to outgrow their condition according to an American study of 210 children with FPIES which reported that, of the 21 children with peanut-induced FPIES, only 5 became tolerant to peanut (which, at 23%, is actually quite similar to the resolution rates for children with IgE-mediated allergy, but this is one small study).

If by the age of 10 you’ve not outgrown your allergy, your chances of doing so get much smaller according to Canadian researchers, who revealed that the spontaneous resolution of childhood peanut allergy normally occurs before the age of 10 and rarely after the age of 10, a result supported by data from a 2007 study of Australian children that found that no further remissions in their study cohort occurred after the age of 7.

Image by David Rama on Pexels

Risk factors for peanut allergy

There are several things which can increase a person’s chances of developing peanut allergy.

An infant with egg allergy and/or eczema has a high chance of developing an allergy to peanuts. Other allergic conditions including asthma and hay fever (allergic rhinitis) as well as allergies to other foods are very common in people allergic to peanuts. Multiple studies from around the world have reported that at least half of their peanut-allergic paediatric patients have at least one of those conditions. Sometimes that number is around 9 in 10.

Asthma itself is not just common among children with food allergies, it’s been closely linked to peanut sensitisation and peanut allergy in particular, with children with asthma more likely to get peanut allergy and vice versa. Asthma is also more likely to be found among black children, who may be more likely to suffer from peanut allergy (see later).

A recent study that used machine-learning models to comb through large swathes of medical data looking for patterns relating to peanut allergy revealed that peanut-allergic children were more likely to have doctor‐diagnosed asthma characterised by persistent wheeze, more likely to have made unscheduled visit to GPs and emergency departments because of it, and more likely to receive asthma medication. Among asthmatics, however, peanut allergy was not associated with more severe asthma.

The data also showed that cat ownership during pregnancy/early life was associated with a threefold increased risk of a child developing peanut allergy, and that being allergic to peanuts was also associated with a bigger risk of becoming sensitised to inhalant allergens and developing hay fever, a risk that increased as the child got older. The authors of the study hypothesised that being exposed to cat dander very early in life may promote the development of early inhalant sensitisation which, in turn, creates ‘a permissive milieu’—i.e. the right conditions—to develop multiple allergies.

Peanut-allergic children and adults are often allergic to other foods, but whereas adults are more likely to be allergic to tree nuts, the most common sensitisation or allergy among peanut-allergic children is one to egg, an association that has been reported in multiple studies over the past few decades, including research focussed on children with  eczema, It was a study designed to identify infants with the highest risk of being allergic to peanuts as part of the British and American LEAP (Learning Early About Peanut Allergy) project that first explicitly linked egg allergy to a higher risk of developing an allergy to peanut.

Their conclusion was backed up by data from the American Consortium for Food Allergy Research (CoFAR), which found that, among the 512 infants with likely egg or milk allergy and no known peanut allergy recruited for their studies, 40% ended up with a diagnosis of peanut allergy.

A separate study into the prevalence and characteristics of egg allergy in a large, nationally representative sample of American children reported that, among those who reacted to egg within their first year of life, just over a fifth (21.5%) developed an allergy to peanuts, too (a 10-fold increase in risk over those who didn’t have reactions to egg), and that an early reaction to wheat and to soy may be similarly predictive of subsequent peanut allergy development, with 26.1% and 18.9% of those children, respectively, also developing an allergy to peanut.

Research carried out all over the world has also found a clear link between peanut allergy and eczema. For example, (relatively old) Taiwanese research reported that children with eczema were more likely to be sensitised to peanut (and egg yolk and soybean) than children without the skin condition or those allergic to other foods. More recently, an Australian study found that infants with eczema were 11 times more likely to develop peanut allergy (and 6 times more likely to have egg allergy) by the age of 1 than infants without the skin condition.

An international, multi-centre study revealed that infants who developed eczema in their first 3 months of life were more likely to develop a sensitisation to peanut (and egg and milk), and that those with severe eczema were at higher risk, a result backed up by the findings of a Czech study involving adolescents and adults with eczema which reported that those with peanut allergy were more likely to be suffering from a moderate or severe skin condition. (And, actually, children with early-onset and/or severe eczema seem to be at a higher risk of developing an allergy to any food).

Interestingly, and probably accurately, the researchers from the LEAP project speculated that the association between egg allergy and peanut sensitisation in children was probably due to the fact that both types of allergy shared the same risk factors, such as severe eczema.

More recently, British researchers used artificial intelligence to look for meaningful patterns in data from multiple sources—parental and doctor reports and prescribed medication, environmental exposures and genetic information—about more than a 1000 children with eczema who had been followed from birth up to the age of 11. They published their results in a 2022 study which reported that the children with persistent eczema—which is often severe—had a 9 to 11 times greater chance of developing peanut allergy (and asthma and hay fever) than did the other children.

Another study that used machine learning-derived models showed that the risk of getting peanut allergy was greatest in children who had early-onset (in the first year of life), persistent eczema.

Infants—notably those with damaged skin barriers—are at higher risk of developing peanut allergy if there are peanut allergens in their environment. The reason so many children with eczema seem to be vulnerable to developing peanut allergy is probably due to all the peanut allergens that surround them in their day-to-day lives.

A British study that reported a link between household consumption of peanut and the amount of peanut protein in household dust in the infant’s home environment (bed, crib rail and play area) was also able to show that the peanut protein in the dust was biologically active; it was able to provoke a reaction from the basophils—histamine-containing white blood cells—in the blood of several peanut-allergic children.

Multiple studies have measured the presence of peanut protein and specific peanut allergens in house dust (and classrooms and school cafeterias in inner cities) and their results unfortunately imply that complete peanut avoidance may be impossible.

For example, a Norwegian study found peanut allergens in mattresses, especially those belonging to little girls, whose tendency to put teddies and decorative pillows on their beds—aka ‘dust and allergen reservoirs’—may help to explain why they had more peanut allergen in their beds than boys. Other risk factors for more peanut allergen in mattresses included the size of the home, having bedrooms and kitchens on the same floor, and the frequency of cleaning. However, although vacuuming the bedroom once a week was associated with less peanut allergen in mattresses, homes with hard floors that were mopped were associated with more peanut dust, possibly because the mopping caused air turbulence that just moved the peanut dust around.

You might think that households that restrict peanuts have a lower amount of peanut allergens in them than homes without peanut restriction. That’s what a team of American researchers hypothesised when they carried out a study to detect the levels of Ara h 2, a major and potent peanut allergen, in 85 American homes, some of which belonged to families with peanut-allergic members who did not allow peanuts or peanut-containing products into their homes, and some of which belonged to families with no allergic household members who regularly ate peanuts.

Much to their surprise, they found that the levels of peanut allergen in both homes that banned peanuts and homes that did not were similar. This, they reasoned, could be due to several factors;

• it may be that the people they interviewed had a different definition of ‘peanut restriction’ than the researchers did
• although an individual with peanut allergy may avoid eating peanuts, the rest of their household may keep doing so (that said, most household containing a peanut-allergic individual tended to ban peanuts from the home, but that would not stop non-allergic members from eating peanuts outside of the home and bringing allergens back in on their hands and clothes)
• or, most likely, the eating practices of family members changed only after a diagnosis was reached, and they could not say for sure how long peanut allergens still hung around in the environment (for an as yet unknown amount of time) after people in the household stopped eating them

Another British study reported that peanut protein is spread around the home by hand transfer and saliva (but probably not by means of aerosolisation, except briefly after shelling peanuts) and is difficult to clean off; vigorous cleaning with detergent did not remove peanut protein from laminate and wooden table surfaces and, although machine washing significantly reduced peanut protein levels from the dust of sofa covers and pillows, some was left over. That said, the level of peanut protein left after cleaning was 1000 times lower than that required to elicit an allergic reaction, although it might be enough to sensitise a young child.

By contrast, a previous American study reported that a major peanut protein (Ara h 1) was relatively easily cleaned from desks, cafeteria tabletops and water fountains in schools using common cleaning agents (except dishwashing liquid which left protein behind on some surfaces) and hand washing with liquid soap, bar soap, or commercial wipes was also effective, although washing with just water and hand sanitiser was not.

The different conclusions between the studies may have been caused by the use of different detection methods and standards. The comforting thought, however, is that the researchers behind both studies concluded that the amount of protein left after cleaning would be unlikely to cause any reactions.

The reason that all of this is important is that, in the past couple of decades, scientists have built up a convincing body of evidence showing that sensitisation to foods can happen via the skin. The first study to mention this in connection with peanut allergy was a British birth cohort study which noted that a common denominator among the young children who ended up developing peanut allergy was that they had had creams containing peanut oil applied to their skin when they were infants to treat nappy rash and other skin problems.

Another British study was the first to highlight a possible connection between a high weekly household peanut consumption during a high-risk child’s (defined, in this case, as a child with egg allergy) first year of life and an increased risk of that child developing peanut allergy, presumably due to levels of peanut allergen in the child’s home environment.

The researchers compared the levels of peanut consumptions in households of high-risk infants (before it was known—or even suspected—that they had peanut allergy) and healthy controls and found that the average weekly peanut consumption in households where an infant went on to develop peanut allergy was significantly higher than that in households where an infant did not become allergic to peanuts. In fact, the average consumption in households with a newly peanut-allergic child was about 3 times higher than the average consumption in households with healthy controls and over 10 times higher than that in households with high-risk but peanut-allergy free children (18.8 g vs 6.9 g vs 1.9 g, respectively).

They also noted that the most hazardous form of peanut consumed by families seems to be peanut butter, at least when compared to whole peanuts and peanut-containing chocolate (the latter of which did not seem to pose a risk, probably because the peanut is surrounded by chocolate). They posited that peanut butter may be the most dangerous form of peanut-based food because it’s extremely high in peanut protein which is exposed to the environment, and very sticky, meaning that the peanut protein can be more easily transferred from the hands of someone who has eaten it to a baby’s skin.

The researchers also highlighted the presence of a group of high-risk children who did not develop peanut allergy, despite relatively high levels of environmental peanut exposure and similar levels of eczema. A common denominator between these children was the fact that many of them had eaten peanuts during their infancy, which suggested that early peanut consumption may have protected them against developing peanut allergy, a surprising conclusion because, at the time, the standard advice was that infants at risk of developing peanut allergy should avoid eating peanuts for the first few years of their lives, advice that has since been reversed.

Finally, another interesting nugget of information from this study was the fact that the mother’s consumption of peanuts during pregnancy (and lactation) was not significant when the researchers took into account the amount of allergen in the environment; in other words, although the maternal consumption of peanuts had been linked to infant peanut sensitisation in previous research, what seemed to make the difference was whether or not the household as a whole consumed a lot of peanuts (in which case, the mother-to-be was also likely to consume a relatively large amount) thus ensuring a lot of peanut protein in the house. Theoretically, then, if a mother-to-be consumes her peanuts outside of the home, her infant should not be at higher risk of developing peanut allergy. The debate continues.

Nine years later, another British study confirmed a link between environmental exposure to peanut in the first few months of life and a subsequent sensitisation to peanut in 8-year-old atopic children (with atopic in this case being defined as children with sensitisation to egg and atopic parents).

Children with damaged skin barriers are most at risk from environmental peanut allergens. The most common (and obvious) sign of a damaged skin barrier is eczema. An American study that examined the link between peanut dust exposure on peanut allergy concluded that the risk was much higher for children with eczema, with the risk increasing as the severity of the skin condition increased.

The study also backed up the idea that the link between maternal peanut consumption and peanut allergy is probably due to levels of peanut protein in the living environment, rather than in the mother herself.

Loss-of-function mutations in the filaggrin gene (FLG), which plays a key role in the correct formation and function of the skin barrier, have also been shown to represent a significant risk factor for peanut allergy.

In an international study, a group of peanut-allergic English, Dutch and Irish children had their DNA tested to see whether it contained null mutations in the filaggrin gene; the researchers reported that these mutations represented both a highly significant genetic risk factor for eczema and ‘the single most significant genetic risk for peanut allergy that has been identified to date.’ The results were then replicated in a population of peanut-allergic Canadian children.

In a subsequent study, British researchers revealed that children with filaggrin loss of function mutations who were exposed to peanut protein in household dust during their first year of life were were 3 times more likely to develop peanut allergy by the time they were school-aged age (8 to 11 years old) than those without filaggrin mutations.

A recent study that used machine-learning models to comb through large swathes of medical data looking for patterns reported that filaggrin mutations were significantly associated with peanut allergy among children without eczema, with those children being around 8 times more likely to develop peanut allergy than children without the genetic mutations (although, due to the small number of children with peanut allergy who did not have early-onset eczema, this result needs ‘to be interpreted with caution’), but that these mutations did not increase the risk of developing peanut allergy among children with eczema (i.e. whose skin barriers were already damaged).

Although scientists have not definitively proven a causal relationship between exposure to environmental peanut allergens and the development of allergy—this would involve intentionally exposing infants to peanut allergens just to see what happens, which is ethically dubious—the observational evidence gathered so far strongly suggests that, while eating peanuts during infancy protects against allergy, exposing the skin to peanut allergens during infancy promotes the development of peanut allergy.

In good news, a letter to the editor published in a 2015 journal suggests that limiting household consumption of peanut may be worth trying if you have an ‘at risk’ infant with eczema or you are atopic and may have passes this characteristic onto your child. The letter describes the work of a Spanish team of researchers who found a clear relationship between nut consumption by people living in the same as house a very young child and that child’s likelihood of becoming sensitised to the type of nuts that their relatives were eating.

The study included 96 children between the ages of 3 and 18 months who had never eaten peanuts or tree nuts and were not known to be sensitised or allergic to them and focused on households consuming almond, walnut and peanut. The relatives of the children were given questionnaires about their nut consumption and the children were then tested for nut allergies.

Analysis of the data revealed that the sensitisation rate among children living in homes where nuts were consumed ‘very often’ was higher than those living in home in which nuts were consumed ‘often’ or ‘not often’, showing a dose-dependent relationship between the amount of nut the family ate and the likelihood that the child would become sensitised to that nut. None of the children who lived in homes were nuts were not consumed were found to be sensitised.

Some studies have reported that race may be a risk factor for the development of peanut allergy. This finding comes predominantly from studies carried out in the US, which have reported that non-white infants (black, Asian and other non-white races) are at higher risk of being sensitised to peanuts than white infants, and that black children and men, in particular, have a greater chance than people of other ethnicities to develop food allergy in general, and peanut (and shrimp) allergy in particular.

This idea that race may be a risk factor in developing food allergy is supported by data from the HealthNuts study in Melbourne, Australia, that reported that, compared to infants with Australian-born parents, peanut allergy (and eczema) was more common among infants with parent/s born in East Asia but not among those with parent/s born in the UK or Europe.

However, not all the results on this topic are straightforward. An analysis of data from 3 facilities in Indiana, America, has reported that peanut sensitisation and allergy was more common among Caucasians, and an analysis of American national survey data has similarly reported that peanut allergy was reported most often among white children. This may just say something about the type of Americans who are more likely to visit allergists or reply to surveys.

In the UK, one of the Learning Early About Peanut Allergy (LEAP) studies involving children from Manchester reported that black children were more likely to have a positive blood test to peanut than children of other ethnicities, but that they were also more likely to have a negative skin test, suggesting that they may actually be less likely to develop an allergy to peanut, if skin test are to be considered more reliable (which is, in itself, debatable).

Interestingly, a South African study focussing on children with eczema noted that the black subjects had a similar rate of sensitisation but a lower rate of allergy than their mixed race counterparts, which was especially evident when it came to peanut allergy, with 15% of their black children being allergic to peanut versus 37% of their mixed race children.

The jury is still out as far as race as a factor in peanut allergy is concerned.

Siblings of children with peanut allergy may have a slightly higher risk of reacting to peanut when it is introduced into their diet. Food—including peanut—allergy is known to have a genetic component. An American study carried out among 58 pairs of monozygotic (identical) and dizygotic (fraternal) twins calculated that the probability of inheriting peanut allergy was 81. 6%, similar to other allergic diseases like asthma (87%), hay fever (74-82%) and eczema (74%).

Their study revealed that 9 of 14 (64%) of the identical twins (who share all of their genes) both had peanut allergy, but only 3 of 44 (6.8%) of the fraternal twins (who share about half of their genes) did. 35 pairs of twins had other siblings, none of whom had peanut allergy, and 4 of the twins’ parent did have peanut allergy, all of which backed up the idea of a strong genetic component involved in the development of peanut allergy.

The potential risk for siblings of children with peanut allergy to develop peanut allergy themselves was first mentioned in a 1996 study carried out in Britain. In this study, 622 adults and children with reported, suspected or known peanut allergy answered a questionnaire about their disease. 50 children from Southampton also underwent skin prick testing.

Peanut allergy was reported by 3 of 2409 (0.1%) of the grandparents, 7 of 1213 (0.6%) of the aunts and uncles, 19 of 1218 (1.6%) of the parents and 42 of 610 (6.9%) of the siblings. Taking into account the rate of peanut allergy in the general population (1.3%), this meant that the sibling of a child with peanut allergy had about a 7-fold higher risk of developing the same condition.

A Canadian study that looked at the data of children born into 514 households in 1995 found that if the children had an older peanut-allergic sibling, the risk that they also developed a peanut allergy was almost 7-fold greater than it was for children who did not have a peanut-allergic sibling. If the children themselves had a peanut allergy, the risk that a younger sibling also developed a peanut allergy was almost 12-fold greater. The researchers recommended that children born into families with peanut-allergic children be assessed by an allergist before being introduced to peanut.

A more recent 2016 study from Canada repeated the advice, noting that this type of pre-emptive testing was very often negative and that, when it was, the chances were very high that the child was indeed tolerant of peanuts. The biggest benefit of the testing is that is gives many parents of peanut-allergic children peace of mind when it comes to introducing peanuts at home to a younger sibling.

Tellingly, the researchers also mentioned that the children in their study who had reacted to peanut upon introduction were significantly older than the other children in the study. This is important because the original research in this area did not take into account other environmental factors that we now know can contribute to the chances of a child developing peanut allergy, such as delaying the introduction of peanut into their diet.

Ultimately, the chances that a sibling of a child with peanut allergy will develop the same condition, although higher than those of a child without a peanut-allergic sibling, are still pretty low, and some experts think that testing for food allergy in children without a history of clinical reactivity is unjustified and could lead to the unnecessary avoidance of peanut.

Additionally, the risk also depends on the allergy status of the child themselves; siblings of children with peanut allergy who do not have eczema, asthma or other food allergies, should be able to have peanut cautiously introduced into their diet at home without any need for testing.

The choice is, in the end, up to the parent.

Image by Vanessa Loring on Pexels

Cross reactions to peanut

Technically-speaking, a person can be allergic to peanut and another food (or foods, or aeroallergen(s)) either by cross-reactivity—the immune system mistakes the proteinin one allergen for aprotein with a similar structure inthe other—or by an independent sensitisation to each food and/or aeroallergen(a co-sensitisation or co-allergy), in which case the immune system has developed specific IgE antibodies against each allergen. It can be difficult to determine whether reactions are caused by cross-reactions or co-allergies,but the end result is the same; problems, problems.

People with a peanut allergy may also have problems with other legumes, some random fruit and, most famously, tree nuts.

Even though peanuts are more closely related, botanically-speaking, to legumes than they are to tree nuts, people with peanut allergy are at a greater risk of developing tree nut allergies than the average person, and the average food-allergic person. In Australia, the population-based HealthNuts study, reported that children who had peanut allergy when they were 12 months old had a 27% chance of having a challenge-confirmed tree nut allergy at the age of 6, significantly more than the children who were allergic to egg at the age of 1 (and had a 14% chance) but less than those with both peanut and egg allergy (who had a 37% chance). By the age of 6, 45% of peanut-allergic children had allergies to one or more tree nuts.

However, if you look at studies carried out using the blood of the peanut-allergic (in vitro studies), the potential for cross-reactions with tree nuts is very high indeed, but if you look at a peanut-allergic patient’s history of reactions or have them undergo a challenge to different tree nuts, the picture is rather different.

A good example of this an American study which looked at the medical records of patients referred to 2 different allergy centres, 234 of whom a convincing history of reactions to peanuts. Although 86% of them were sensitised to at least one tree nut, only 34% had a documented clinical allergy to any type of nut.

This rate of documented allergy is similar to the proportion of Americans who have reported allergies to peanuts and tree nuts in a survey of patients with convincing histories of reactions to peanut and/or tree nuts taken in 1998 (about a third) and among members of a registry for people allergic to peanut and/or tree nut allergy taken in 2001 (23%)

However, a more recent, 2015 review of the medical records of nut-allergic children and adults seen at a centre in New York reported that 30 of the 59 (51%) patients with peanut allergy had a documented clinical allergy to tree nuts.

In the UK, research from the 1990s put the prevalence of people with peanut and tree nut allergies at around 20%. A review of the medical records of 145 British children diagnosed as nut-allergic at a single medical centre during a 5-year period from 2006 put the prevalence even lower, reporting that, among the 94 children with peanut allergies, only 7 (7.4%) actually failed a challenge with a tree nut (almond, Brazil nut, cashew nut, hazelnut and walnut), despite 22 (31%) being sensitised to at least one.

By contrast, an Australian study reported a rate of clinic-defined peanut and tree nut allergy in 41.5% of peanut-allergic children aged between the ages of 10 and 14.

This helps to illustrate the different prevalence rates of allergies in different populations and the effect that cultural eating habits might have on allergy. No study better demonstrates this than the one that helped to kick start the new guidelines for introducing peanuts into a child’s diet at an earlier age than was previously advised. In it, researchers revealed that 43 of 73 (58.9%) of the British study subjects with peanut allergy were also allergic to tree nuts, whereas, among the Israeli subjects, that number was 4 of 8 (50%).

They speculated that the low prevalence of (peanut and) tree nut allergy could be due to the fact that Israeli infants were introduced to peanuts at an earlier age, which induced ‘cross-tolerance’ to tree nuts, too.

The different rates of co-allergies or cross sensitisations reported in different studies may also have something to do with the study population itself. For example, a 2017 study that examined the results of tree nut challenges carried out at one American referral centre reported that, of the 68 challenges undergone by peanut-allergic patients with a sensitisation to tree nuts, 65 produced no symptoms, a passage rate of 96%. The 3 failed challenges occurred in 3 different people (to walnut, hazelnut and pistachio).

These are the kinds of numbers that might make a person want to run off and get (their child) tested. But these challenges were given to children who were likely to pass them (i.e. who had low levels of IgE antibodies in their blood or who had never demonstrated any symptoms to any kind of tree nut), which is standard policy when it comes to carrying out food challenges in places that are not hospitals, especially when it comes to potentially dangerous foods and especially when a parent does not want their child to run any risks.

Among the general population (i.e. people not attending allergy clinics) the rate of allergies to both peanuts and tree nuts is, naturally, even lower, with an American population survey reporting (self-reported) co-allergy rates of 0.3% in children and 0.2% in adults.

The tree nut allergic seem to have a greater chance of also being allergic to peanut than the other way around. One American study of 278 children with tree nut allergy, for example, reported that 190 (68%) were allergic to peanut, and only 29 (10%) had outgrown a peanut allergy (and those who had were also more likely to outgrow their tree nut allergy).

One thing that seems pretty universal among peanut-allergic individuals is that those who are allergic to tree nuts are likely to develop allergies to more nuts over time. This has been shown in multiple studies, such as a British study of nut and/or seed-sensitised or allergic children younger than 6 that reported that just over a third (36.4%) developed a new nut allergy over the next 2 to 4 years, and an Australian one that reported that 4.7% of peanut-allergic children under 2 were also allergic to at least one tree nut, a number which increased to 45% in adult patients over the age of 40.

This could be because the (often unnecessary) elimination of tree nuts from the diets of children with multiple foods allergies eventually leads to the development of sensitisation and allergy to tree nuts.

Or it could be because people tend to try new nuts as they get older and that’s when they notice that some of them provoke reactions. This theory was put forwards in the 1990s by British researchers who noticed that allergies to specific types of nuts did not seem to depend on personal characteristics like age or sex but rather on how much and which type of nut a person ate. A later study of British children noted that they tended to eat more types of nuts as they got older, and this coincided with a rise in sensitisation and allergy to multiple nuts.

Recent data from Turkey has revealed that children in the Eastern Mediterranean region, where children are introduced to a more varied diet of nuts at an earlier age than their Western counterparts, also develop peanut and tree nut allergies at an earlier age. They develop allergies to more different types of nuts until about the age of 10, at which point the number of nut allergies tends to stabilise then decrease. By the age of 5, only 5 of the 227 (2.2%) children in this study were allergic to peanut alone.

Or people could develop allergies to more nuts over time because of something else that has not been specified yet. For example, data provided by theEuropean Pronuts study, in which children with at least 1 confirmed nut or sesame seed allergy were given food challenges to other nuts in 3 different centres (London, England, Geneva, Switzerland and Valencia, Spain) is less clear. Results showed that the children with the highest chances of having an allergy to multiple nuts were those who were older than 3 and those who lived in Valencia.

The children tested in Valencia were both older than those in the other 2 centres and more likely to eat a bigger variety of nuts. This could imply, again, that the more nuts you eat as you grow up, the more allergies you develop. But it could also have been that the Spanish children had started eating a variety of nuts just before entering the study, but not during their first year of life, when the effect might have been protective.

The data also showed that if a child was already eating cashews, peanuts, walnuts or pecans before entering the study, they were likely to be allergic to fewer nuts. Which could imply that eating nuts during early childhood is good. Or perhaps it’s something about those particular nuts. Who knows? No-one, yet.

(The good news for the peanut-allergic is that peanut was the most common allergy in children with a single nut allergy.)

What does seem clearer is that peanut-allergic children with eczema are more likely to develop allergies to other nuts (but, note, the Spanish children in the former study were less likely to have eczema than the other children). And to legumes. (And, if you consider allergy research in general, any food). This was revealed in a 2017 study, when French researchers attempted to pinpoint characteristics that would identify peanut-allergic children with a greater risk of developing tree nut allergies.

They examined the records of 317 children with peanut allergy and grouped them into 3 clusters according to their shared characteristics. The group with no cross-allergies to tree nuts (or legumes) was mainly made up of boys with mild peanut allergy, as well as low levels of asthma and eczema, who required relatively high doses of peanuts before showing symptoms.

The group with the highest chance of developing cross-allergies to tree nuts (or legumes) was mainly made up of children who had eczema (94.7% of them had it, to be precise) and other allergies (to other foods, hay fever, asthma) and required relatively small doses of peanuts before showing symptoms; 74.3% had a cross-allergy to tree nuts (in order of frequency: hazelnut, pistachio, cashew, walnut, almond and pecan) and/or other legumes (in order of frequency: pea, lentil, soy, lupin and chickpea).

In between was a group of comprised mostly girls with severe peanut allergy, most of whom had asthma and/or hay fever and who reacted to the smallest doses of peanuts. 31.9% had cross-reactions to tree nuts and/or legumes.

All in all, 137 of the 317 (43.2%) peanut-allergic children were found to have cross-allergies (38.8% to at least one tree nut and 7.9% to at least one other legume) and eczema was identified as the leading risk factors for developing cross-allergies. The researchers speculated that the children with eczema, a skin barrier defect, had probably had skin contact with tree nuts and/or legumes early in their lives and had thus developed sensitisations and then allergies to these foods.

Finally, researchers also tells us that peanut-allergic children who are also sensitised or allergic to tree nuts are less likely to outgrow their peanut allergy.

The peanut- (and tree nut-) allergic also need to be wary of sesame seeds, because their storage proteins (vicilins/7S globulins and 11S globulins) also have very similar structures, giving them the potential to cross-react.

Several studies have reported that a significant proportion of children with peanut and tree nut allergy are sensitised or allergic to sesame seed. A study that looked at the medical records of peanut sensitised Australian children, for example, found that 60% of the under-2-year olds were also sensitised to sesame, which was greater than the number that were also sensitised to tree nuts. An 11-month old infant was reported to have developed facial swelling, hives and wheezing after their first taste of tahini, which their mother had eaten throughout her pregnancy and while breastfeeding.

Another study of Australian children with peanut allergies reported that children who remained allergic to peanuts were more likely to develop an allergy to sesame than those who outgrew their allergy, despite strict instructions to avoid sesame, suggesting that cross-reactivity might have had something to do with it.

Prevalence numbers of sesame allergy reported within the (pea)nut-allergic population are not unanimously high, with an old British study finding that, among 55 people with peanut or tree nut sensitisation, only 4 (7%) had a positive skin prick test to sesame, and a more recent American one (2) reporting that, among the peanut-allergic children seen in one centre between July 2000 and April 2006, 6% were sensitised or allergic to sesame.

Another American study designed to determine the potential problems that sesame or coconut could pose to the (pea)nut-allergic population looked at the results of skin prick tests given to (mostly) children between December 2006 and March 2008 and reported that 53.3% of the 40 peanut-sensitised patients and 57.7% of the tree nut sensitised patients were allergic to sesame, and 68.9% of those sensitised to both peanuts and tree nuts were sensitised to sesame.

The picture was the same amongst those with allergies; 13.2% of the peanut allergic children were also allergic to sesame, 14.8% of those with tree nut allergies were also allergic to sesame, and half of those with allergies to peanuts and tree nuts were also allergic to sesame. Basically, people who are sensitised or allergic to both peanuts and tree nuts are quite likely to also be sensitised or allergic to sesame. Furthermore, children with a history of allergic reactions to either peanuts or tree nuts were not more likely to have an allergic reaction to sesame, but those with a history of reactions to both peanuts and tree nuts, were. There was, however, no link found between sensitisation or allergy to peanuts or tree nuts and coconut.

The different rates of sensitisation and allergy in different populations might have something to do with cultural eating habits. As part of the Pronuts study, researchers at three European centres (London, Geneva and Valencia) gave 122 children aged between 0 and 16 years with at least 1 confirmed nut or sesame seed allergy food challenges to other nuts and sesame. Researchers reported an average rate of co-existent peanut/tree nut or sesame seed allergy in 74 (60.7%) of the children.

They also revealed that, among the nuts and seeds, sesame was most frequently consumed by the children in all of the countries. However, whereas only 40% and 46% of the children in Geneva and London, respectively, had already eaten some before entering the study, 93% already ate sesame seeds in Valencia, which was the only centre not to report any allergy to sesame.

The idea that early introduction to seeds and peanuts may be protective against developing nut allergy was backed up by research carried out by another group of scientists who found a higher prevalence of both peanut and sesame allergy in the UK (1.85% and 0.79%, respectively) than in Israel (0.17% and 0.13%, respectively). They also found that Israeli infants ate both more peanuts and more sesame than British infants. Taking into account the potential for cross-sensitisation between the two plant foods, they proposed that the lower rates of allergy in Israeli children ‘could be due to cross-tolerance induced through the early, high, and frequent consumption of peanut in Israel.’

Finally, an American report of 3 children who outgrew their allergy to peanut but subsequently had reactions to tree nuts and sesame highlighted the fact that an allergy to tree nuts or sesame can already exist in or be developed by people whose peanut allergy has resolved, the point being that people who are newly tolerant to peanut should not assume that they can suddenly stop avoiding tree nuts and/or sesame without consequences.

Another category of plant food that contains the same problematic storage proteins is legumes. Although lab (in vitro) tests done using the blood of peanut-allergic patients tend to show extensive cross-reactivity between peanuts and other legumes, which initially led to the advice that people allergic to peanut should avoid all other legumes, when people are given food challenges to a legume that they are sensitised too, only a tiny minority actually react.

This was demonstrated in an early study which submitted 69 American children with at least one positive skin prick tests to legumes to challenges with peanut, soybean, pea, green bean, and lima bean reported 43 positive results in 41 children, meaning that only 2 (5%) of the children were actually allergic to more than one legume. The authors then carried out tests on the blood of the same children to show that they were all sensitised to a number of legumes even though they did not have problems eating them, and concluded that the elimination of all legumes from the diets of people who were allergic to one legume was unwarranted, even if skin or blood tests found that they were sensitised to multiple legumes.

Similarly, another American study from the 1980s which tested 32 peanut-allergic children reported that 17 had a positive skin test to soy, 15 to pea, and 10 to both pea and soy, but only of 2 of the peanut-allergic children had a positive food challenge to another legume, one to soy and one to pea. 

And in an early British study, in which an allergist describes 47 cases of peanut-allergic children he saw during a one-year period, only 3 of the peanut-allergic children were reported as being allergic to other legumes, and their reactions to the legumes were milder than their reactions to peanuts.

People who are allergic to certain legumes seem to be more likely to suffer from cross-reactions than others. A Dutch study carried out on legume-allergic adults determined that people with peanut allergy were less likely to suffer from reactions to other legumes than people allergic to peas, lupin, lentil and bean in whom, by contrast, ‘peanut was almost inevitable’ and co-allergy with other legumes were common. People with soy allergy were unlikely to have allergies to other legumes except for peanut, which was quite common.

Like other studies, researchers noticed a high degree of co-sensitisation to different legumes among the adults, but they were, for the most part, not associated with clinical symptoms (for example, 70% of those with peanut allergy were sensitised to lupin but only 16.7% of them were actually allergic).

The potential of cross-reactions between also affects different populations differently; those who eat more legumes are more likely to have symptomatic cross-sensitisations, like Spanish children who are, on average, allergic to around 3 legumes.

In France, a 2022 study of peanut-allergic children noted that, of the 191 children for whom they had sensitisation data, almost two thirds (63.9%) were sensitised to another legume. Among those children, 8 of 38 (21.0%) were allergic to lentil, 12 of 63 (19.0%) were allergic to lupin, 8 of 52 (15.4%) were allergic to pea, 6 of 61 (9.8%) were allergic to fenugreek, 5 of 61 (8.2%) were allergic to soy, and 2 of 27 (7.4%) were allergic to chickpea. Most had a history of anaphylactic reactions, including 100% for soy, 62.5% for lentil, 50% for lupin, 50% for chickpea, and 50% for pea, and 33.3% for fenugreek.

In much of the research literature, the legume that is the most frequently mentioned as a potential problem for people with peanut allergy is soybean. Studies have shown similarities between the peanut and soy allergens Ara h 1, Ara h 3, and Ara h 8 with Gly m 5, Gly m 6, and Gly m 4, respectively. Gly m 5, in fact, is the closest known homologue of Ara h 1.

However, early American research reported a low chance of soy allergy among the peanut-allergic. A 1989 study which tested 69 children for allergy to more than one legume reported that, of the 31 children with severe peanut allergy, only 2 (6.5%) reacted to soy. Their reactions were relatively mild (skin symptoms and nausea). Both children outgrew their soybean allergy within 1 to 3 years of the challenge while on a peanut and soybean elimination diet.

A 2001 study carried out to see how many children with peanut allergy eventually outgrew it reported that, of 223 children, 34 (15%) were also allergic to soy. And in 2007, a retrospective study of the medical records of 140 peanut-allergic children seen at one centre over a period of 6 years reported that 10 (7%) of them were sensitised or allergic to soy, which they determined using a combination of medical history, skin and blood test results and the result of oral challenges.

But higher numbers have been reported since. A 2008 Dutch study involving 39 peanut-sensitised adults, for example, reported that 87% were sensitised to soy and that a third had a history of reactions to it. The researchers concluded that ‘clinically relevant’ sensitisation—i.e. allergy—to soy occurs frequently.

And peanut allergy among people allergic to soy is also quite high; one American study reported that, among 122 with spy allergy, 107 (88%) were also allergic to peanuts (based on either having a history of allergic reactions to peanuts or a high level of peanut-specific IgE antibodies in the blood).

Reactions to soy were initially considered to be uncomfortable rather than dangerous, until a study from Sweden investigating severe reactions to food was published in 1999. In it, the authors reported that four people with peanut allergies but no known allergy to soy, had had fatal asthmatic reactions to food containing soy. The study was widely criticised with other experts suggesting that the food may have been contaminated with peanut, although it did not show up in the victims’ stomach contents. Since then, however, there have been no more reports of fatal reactions to soy.

In 2018, a team of British researchers tested the cross-reactivity between peanut and soy by challenging 64 children with peanut allergy, some severe, with roasted soy in the form of WOW butter. None of them were actively avoiding soy in their diet, and almost half (31, 46%) reported eating it regularly. Only 2 of them had objective symptoms to the roasted soy, and they were mild.

So it would seem that many of the peanut-allergic have little to fear from soy, although a recent study of peanut-allergic French children did find that, although few of their subjects (8.2%) were allergic to soy, the ones that were had a history of severe reactions to it.

Finally, it may be good to know that, according to a Finnish study that followed 170 milk-allergic infants until the age of 4, the use of a soy formula during the first 2 years of life does not increase the infants’ risk of developing peanut sensitisation or allergy.

Their data was corroborated a couple of years later by that of an Australian study which was designed specifically to investigate whether using soy formula could lead to a peanut allergy as some previous research had suggested. In it, researchers recruited 620 babies with a family history of allergies and then telephoned their parents to ask them about their infant’s diets and allergies once a month for 15 month, and then again at 18 months and 2 years old. They also gave the infants skin prick tests to peanut, milk, and egg when they were 6, 12, and 24 months old.

They discovered that children who were given soy formula or soy milk were indeed more likely to be sensitised to peanuts by the age of 2, but this was entirely due to the fact that children who were sensitised to cow’s milk and/or had siblings who were allergic to milk were the ones who were given the soy formula and they, in turn, were more likely to become sensitised to (other foods and) peanut in the first place. The relationship between soy formula and peanut allergy was therefore not causal. They concluded: ‘There is no evidence to suggest that avoidance of soy can be recommended as a strategy for peanut allergy prevention in infants of atopic families.’

A much more problematic legume is lupin, which has a relatively high chance of producing symptoms in people with peanut allergy, and those symptoms can be quite severe. Peanut and lupin have a high degree of cross-reactivity, thanks to several allergens—β-conglutins, delta-conglutins, profilins and PR10 proteins—showing significant structural similarity.

The first study to mention a reaction to lupin in a peanut-allergic individual was a 1994 case report of a 5-year-old American girl who experienced hives and swelling after eating pasta fortified with sweet lupine seed flour.

The first to people point out the potential for cross-reactivity between lupin and peanut were a team of French researchers who reported that, of 24 peanut-allergic patients they’d examined, 11 (44%) were sensitised to lupin. 8 oral challenges were given, 7 to people sensitised to lupin and one to a control patient who had tested negative for lupin IgE antibodies. All of the patients who were sensitised to lupin failed their challenges; 6 had immediate symptoms and one had a delayed response. They researchers that ‘The risk of crossed peanut-lupine allergy is high, contrary to the risk with other legumes.’

Studies have since reported varying rates of sensitisation and allergy to lupin among the peanut-allergic. A large study involving 2,680 children and 2,686 adults in France and Belgium showed that 17.1 % of children and 14.6 % of adults with peanut allergy were also sensitised to lupin.

A small study carried out in the UK involving 47 peanut-allergic children and teenagers and 46 healthy controls showed that peanut-allergic children were much more likely to be sensitised to lupin (34%) than non-peanut-allergic children (4%). Of the 16 peanut-allergic children who were also sensitised to lupin, 9 were given oral challenges and 2 reacted, giving a minimum prevalence of lupin allergy in peanut-allergic children of 4%. Both children developed itchy mouths, 1 also got hives and the other had difficulty breathing.

A study of 39 Dutch peanut-sensitised adults reported that 32 (82%) were sensitised to lupin and 14 (35%) failed oral challenges, leading them to conclude that clinically relevant sensitisation to lupin occurs frequently.

In Italy, 12 children with a history of reactions to peanut were selected for a trial involving lupin-enriched pasta. 2 of them reacted, one to only 0.2g of the pasta, and one to 6.4g.

And a recent study in Chile involving 43 patients with peanut allergy confirmed that 19 (44%) were also allergic to lupin and reported that anaphylaxis was the most frequent symptom recorded during the failed challenges, with 1g of lupin flour recorded as the minimum eliciting dose.

Another legume which is more likely to cause trouble than other members of the Fabaceae family is fenugreek. Fenugreek has been used as a medicinal plant for around 6,000 years and is used as a dietary supplement in Western countries. It is also a popular condiment; the leaves of the plant are used as a herb and the seeds as a spice, so it can often be found in spice mixes.

However, it also has toxic properties and, more pertinently, is quite likely to pose problems for people with peanut allergy because of the high cross-reactive potential between the two plants caused by the very similar structures of their storage proteins.

Reactions to fenugreek are frequently severe—involving anaphylaxis, although they can also be milder and provoke skin symptoms, stomach pain or vomiting—often require only small doses, and are regularly provoked by curries. Most of them are thought to be secondary reactions, that is, cross-reactions to fenugreek in people allergic to peanut.

In a recent study of peanut-allergic French children, around 1 in 10 who were sensitised to fenugreek were confirmed to be allergic to it and, although only a third of them had severe symptoms after eating it, they only required a small dose to provoke a reaction and half of them failed their challenge to the legume after eating it for the first time.

Unfortunately for the peanut-allergic who have picked up a cross-sensitisation to another legume, although successful immunotherapy treatments for peanuts are on the way, they have not been developed for other legumes or for tree nuts, and desensitisation to peanut does not seem to have an effect on legume cross-sensitisation.

Cross reactivity produced by storage seeds do not just cause cross-reactions in tree nuts, they have also been shown to cause cross-reactivity between peanut and kiwi fruit (seeds). A Swedish study investigating cross-reactions to kiwi fruit in adolescents and adults with peanut allergy reported that 23 out of the 59 subjects reported having symptoms after eating kiwi fruit and 15 (65%) of them were sensitised either to kiwi fruit extract or kiwi seed storage proteins (specifically the 11S globulins and 7S globulins, which have shown both structural similarities and the potential to cross react with peanut and tree nut allergens in test tube studies).

The authors of the study also mention another study in which more than half of the children with severe kiwi fruit allergy also reported peanut and tree nut allergies, several of whom had reacted to their first known exposure of kiwi fruit, indicating that they were primarily sensitised to a cross reacting allergen from another source like peanut and/or tree nuts.

Peanuts contain panallergens—allergens that can be found in all other, in this case, plants. One of these panallergens is the non-specific lipid transfer protein (Ara h 9), which shows a similar sequence identity to the equivalent protein in peach, and a weaker potency which implies that, in cases cross-reactions where have been found, peach is the primary sensitiser and peanut the secondary allergy.

Another panallergen in peanut is the PR-10 protein (Ara h 8) which is very similar in structure and function to the Bet v 1 birch protein and produces a secondary allergy to birch pollen in the peanut-allergic. Bet v 1 is highly potent which is why even people living in areas without many birch around can still be affected by it.

Population studies suggest that the high rates of sensitisation to peanut among the general public is due to the cross-reactivity between birch pollen and peanut allergens. For example, a screening of an unselected population of German children in 2011 revealed that almost 11% were sensitised to peanuts. However, this high rate of sensitisation did not translate into actual peanut allergy and was deemed to be caused by a (mostly) harmless, asymptomatic cross-reactivity to pollen.

In many cases, people who are exclusively sensitised to the peanut PR-10 protein are tolerant to peanuts, or have relatively mild symptoms often limited to the mouth (aka oral allergy syndrome (OAS)).

There’s also not a lot of Ara h 8 in peanuts and it’s vulnerable to digestion. However, it’s more allergenic after roasting and thus more likely to provoke reactions in people sensitised only to this allergen who live in Western countries and commonly eat peanuts in roasted form.

Not everyone who is sensitised to both birch pollen and peanuts will experience mild symptoms. In a study in which 20 Swiss and Dutch people allergic to both peanut and birch pollen were challenged with roasted peanut flour, 8 (40%) had more severe symptoms including nausea, stomach ache, hives and throat tightness.

There is also a greater risk of (more serious) reactions during birch pollen season, as demonstrated in a Swedish study in which children who were exclusively sensitised to Ara h 8 were given challenges with roasted peanuts. Although most of the children passed without having symptoms (and a quarter had symptoms confined to the mouth), one child suffered from a worsening of his hay fever symptoms and subjective breathing difficulties. When he was challenged again outside of the birch pollen season, he passed the test.

Finally, there is also a risk of more severe reactions if you eat a large amount of peanuts, which is what happened when a 16-year-old Swedish girl who had passed 2 oral challenges ate 300 g of roasted peanuts and had an anaphylactic reaction.

People who are allergic to peanuts can also be sensitised to the pollens of other trees, such as walnut and plane tree, although these potential cross-sensitisations do not seem to cause any symptoms.

Image by Joshua Chekov on Unsplash

Symptoms of peanut allergy

Peanut allergy can be IgE-mediated, non-IgE-mediated or mixed; a combination of both. These variations generally present different types of symptoms.

Immediate reactions to peanut

Immediate allergic reactions are caused by IgE antibodies. These antibodies bind to certain immune system cells—mast cells and basophils—and trigger the release of histamine and other inflammatory chemicals that cause the characteristic symptoms of allergy.

Immediate reactions are the most common type of allergic reaction to peanut and they range from rashes to life-threatening anaphylaxis. Reactions are different for different people, and they can also be different for the same person, varying in severity from episode to episode.

Symptoms can be grouped into categories, namely:

• Skin (cutaneous) symptoms
• Breathing (respiratory) symptoms
• Digestive (gastrointestinal, GI) symptoms
• Cardiovascular symptoms
• Neurological symptoms

Symptoms often occur within half an hour of eating the offending food—in one study, 95% of the first reactions to peanut happened within 20 minutes—but it’s not unusual for them to take longer to appear. In another study, the median time for a reaction to occur after a food challenge was 55 minutes, with a range of between 5 minutes to 210 minutes. 15 of the 63 children in this study experienced more severe reactions (wheeze, shortness of breath) but only 4 of them experienced their symptoms within 30 minutes of eating peanut.

Much of the research on peanut allergy comes from the US, where studies carried out on children report that skin symptoms are by far the most common reactions to peanuts, followed by digestive symptoms and respiratory symptoms. Cardiovascular and neurological symptoms are extremely rare.

A 2018 study which examined the medical records of 795 American children who underwent peanut food challenges reported that ‘adverse events related to skin were the most prevalent (48.9%), followed by GI events (36.7%) and respiratory (13.6%).’ Nobody experienced cardiovascular symptoms.

A French study published in 2002 reported that, of the 177 children who experienced symptoms during food challenges to peanut, just under three quarters (72.3%) had hives and just over a quarter (26.6%), GI symptoms, while 22 (12.4%) had asthmatic symptoms, 2 (1.1%) experienced throat swelling and 7 (4%) experienced anaphylactic shock.

Reactions to peanut often involve several organ systems at once. A 2014 study of 63 German children with severe peanut allergy reported that just under half (49%) of the children experienced objective symptoms affecting only one organ system, with 14% experiencing only skin systems, 19% experiencing only GI symptoms and only 6% experiencing only respiratory symptoms.

Subjective symptoms are difficult for young children to describe. Infants are not able to describe the experience of an allergic reaction and will often spit the food out and become upset instead. Breathing symptoms can be recognised by a change in voice pitch of their voice, hoarseness or a loss of voice, noisy, high pitched breathing, excessive drooling and breathlessness.

Skin (cutaneous) symptoms include:

• hives (urticaria)
• swelling of the face (angio-oedema) and/or tongue and/or throat and/or hands
• itchy skin (pruritus)
• redness (erythema)
• eczema (atopic dermatitis)

The skin is the organ most likely to be involved during reactions to peanut, and if a reaction involves only one organ, it’s also most likely to be the skin. Hives and angio-oedema tend to be the most common symptoms. Studies of American children often report facial oedema as the most common manifestation during a reaction to peanut, whereas studies of European children tend to report hives as the most common symptom.

Another constellation of skin symptoms that a peanut-allergic person can experience is Oral Allergy Syndrome (OAS). OAS is typically a mild reaction that occurs within minutes of eating the offending food and primarily consists of itching or a ’burning’ sensation and swelling in the mouth, tongue, lips and throat, and sometimes the ears.

Note that OAS is not the same thing as Pollen Food Syndrome (PFS). Whereas the latter is a secondary allergy caused by the immune system mistaking food allergens for pollen allergens, OAS is simply a set of symptoms mostly confined to the mouth. The symptoms of Pollen Food Syndrome are caused by plant food allergens that are often vulnerable to heating—therefore, raw fruit and veg—but OAS can be caused by any food, including egg, seafood and peanuts. If someone tries to tell you that you can’t be experiencing OAS because you’re eating cooked peanuts, feel free to tell them they are getting the symptoms of OAS confused with Pollen Food Syndrome. Not enough people (including health professionals) seem to know this.

Among the peanut-allergic, between around 1 in 10 and 1 in 4 children seem to experience OAS after eating peanuts. A Czech study reported that oral allergy syndrome was the most common symptom of peanut allergy among adolescents and adults with eczema, finding that 29 of the 36 patients who had an immediate allergy to peanuts experienced OAS after eating peanuts. A study that included mostly adult patients from allergy centres in 12 European countries reported that, of the 517 reporting immediate symptoms to peanut, 41% had isolated oral allergy symptoms. Many of these older patients were sensitised to birch pollen and probably suffering a mild cross-reaction to peanut.

Although people who experience OAS often have a mild version of peanut allergy, OAS can also be the first stage of a more serious reaction—for example, the throat can then swell up and block the airways. This type of reaction is described in a British study in which four adults experienced OAS as an initial reaction to eating peanuts which then progressed to severe respiratory difficulty and, in 2 cases, loss of consciousness and respiratory arrest.

Peanuts can also cause contact reactions. This often takes the form of contact urticaria, which is a localised weal-and-flare reaction (i.e. hives) that generally appears within minutes after contact with a peanut-containing substance.

A 2017 review of the medical records of 713 peanut-allergic American children reported that 203 (28.5%) had suffered from contact urticaria to peanuts. It was the most frequently reported type of skin reaction among this group of children. This relatively high number may have something to do with the popularity of peanut butter in America and the fact that peanut butter is both extremely high in peanut protein and very sticky, (see Risk factors section, earlier).

Contact with peanut butter can also be responsible for more generalised skin reactions in children who are very sensitive to peanut, as described in an early case series of contact reactions which reported a case in which a 9-month-old infant boy developed a general case of hives after his brother ate a peanut butter sandwich and then barely touched his younger sibling’s bare leg.

Digestive (GI) symptoms include:

• stomach pain
• vomiting
• nausea
• diarrhoea

Peanut seems more likely to provoke GI symptoms than other major allergens. A German study describing the reactions of 880 food-allergic children who failed food challenges reported that egg and peanut were more likely to provoke GI symptoms than milk, soy, wheat and hazelnut, with almost half (45.7%) of the peanut-allergic children developing GI symptoms after their challenge.

Their findings are supported by those of an American study that described the results of 1054 positive food challenges taken by 410 children and reported that food challenges with egg, peanut, sesame, cashew, and walnut were more likely to be associated with GI-related symptoms than hazelnut and milk.

Another German study reported that children who did not react to peanut by vomiting were almost twice as likely to develop immediate skin symptoms and/or lower respiratory symptoms (i.e. wheezing, chest tightness, coughing and shortness of breath).

Breathing (respiratory) symptoms include:

• blocked (nasal congestion) or runny nose (rhinorrhoea), itchy nose, sneezing, mucus draining from your nose into your throat (rhinitis)
• red, itchy eyes (conjunctivitis, not strictly-speaking a respiratory symptom but often associated with upper respiratory tract symptoms)
• wheezing
• high-pitched, noisy breathing (stridor)
• difficulty breathing/shortness of breath (dyspnoea)
• feeling of chest tightness
• persistent coughing
• hoarse voice

Respiratory symptoms may affect between 1 in 4 and 2 in 5 people with peanut allergy. A review of the medical records of 70 children with peanut and/or tree nut allergy seen at an American allergy clinic reported that around just over 1 in 4 (25.4%) reported respiratory issues after eating peanuts, including wheezing, difficulty breathing and laryngeal oedema (strictly speaking, a skin symptom, but it tightens your throat and affects breathing).

A report of the food challenges taken by 177 peanut-allergic French children found that just over 1 in 10 (12.4%) experienced an asthma attack, just under 1 in 10 (9%) developed hay fever-like symptoms (rhinoconjunctivitis) and 2 of the children (1.1%) experienced laryngeal oedema.

A study involving 880 German food-allergic children revealed that those who were allergic to peanut were more likely to develop respiratory symptoms after a challenge than children allergic to egg, milk, wheat, hazelnut or soy, at a rate of 41.3% versus 19.5%, 17.3%, 13.3%, 11.8% and 3.6%, respectively.

Another German study involving 1,013 pea/nut allergic children who undertook food challenges, reported that 1 in 3 developed lower respiratory symptoms (e.g., repetitive coughing and wheezing).

However, adolescents and adults are more likely to experience respiratory symptoms than younger children, who are, in turn, more likely to experience skin symptoms (especially eczema).

Some people with peanut allergy who react to inhaled peanut protein may be able to tolerate eating small amounts of peanut, according to one study. French researchers gave food challenges to 8 peanut-allergic children aged between 3 and 9 who had had inhalation reactions to peanuts but had never eaten any to see whether the children needed to strictly avoid peanuts. They found that all the children were able to eat some peanut without reacting and could therefore enjoy less restrictive diets.

Although there are reports of inhaled peanut proteins triggering allergic reactions in particularly sensitive individuals in places like restaurants, this is incredibly rare. When American researchers gave 30 peanut-allergic children an inhalation challenge which involved holding a cup containing 3 ounces (85 g) of peanut butter 12 inches (30 cms) away from each child’s nose for 10 minutes, none of the children reacted. The children were observed for an hour after the challenge and also given spirometry tests to see whether being exposed to the peanut butter had affected their ability to inhale or exhale, but the researchers detected no effect of any kind on any of the children.

Of course, this does not mean that it never happens. There is, for example, a report describing the case of a 5-year-old boy who, on one occasion, developed acute wheezing while taking a nap next to a friend whose clothes were smeared with peanut butter and, on another, started wheezing after entering the classroom of a teacher who had just eaten peanuts.

Anaphylaxis

Peanut has a fearsome reputation as one of the most dangerous food allergens, although its more likely to provoke anaphylaxis in children than other age groups; according to a meta-analysis of 65 studies carried out in 41 countries, milk and crustaceans are actually more likely to be the cause of severe anaphylaxis in adolescents and adults, at least in Europe and Asia. (That said, the food now thought most likely to provoke life-threatening reactions in the under-2s is milk.)

A 2021 global review of data concerning food-induced anaphylaxis calculated an incidence of anaphylaxis among peanut-allergic children of 2.74 cases per 100 person‐years—which means that there will be an average of 2.74 cases of anaphylaxis among 100 children with peanut allergy who are observed for one year.

An analysis of European Anaphylaxis Registry data (provided by centres in Germany, France, Switzerland, Ireland, Greece, Austria, Spain, Bulgaria, Italy and Poland) reported that, as a whole, peanut was the most common trigger for children and adolescents, accounting for 26.3% and 18.4% of food‐related anaphylaxis cases, respectively.

An analysis of anaphylaxis registry data covering emergencies reported in Germany, Austria, and Switzerland found that peanut was the second most common trigger reported for children, even though peanut has traditionally been regarded as less popular in those central European countries than in English-speaking ones.

Peanut has also been reported as the second most common trigger for anaphylaxis (after tree nuts) in Danish children and the second most common cause (after milk) of hospital admission for food-induced anaphylaxis in French children, responsible for just over a quarter (27.3%) of all cases of food-related anaphylaxis.

In the US, peanuts have been reported to provoke more severe reactions in both children and adults than any other trigger food. A study of urban minority children reported that anaphylaxis was the second most commonly reported reaction to peanut (and tree nuts and milk)

A 2008 study of the medical records of 778 Australian children with peanut allergy reported that 169 (just under a quarter, or 22%) experienced anaphylaxis on first exposure to peanuts and 95 (16%) progressed from milder reactions to anaphylaxis over time. The Australian SchoolNuts study, which included 547 adolescents aged 10–14 years, reported that peanut was the no.1 trigger of (suspected) anaphylaxis, causing almost 2 in 5 (38.6%) of all confirmed anaphylaxis episodes and just under 1 in 3 (30.6%) of unconfirmed anaphylaxis episodes.

Interestingly, recent research suggests that the common triggers of anaphylaxis in Asia may be changing, with a 2015 study of the medical records of 98 Singaporean children admitted to one hospital with anaphylaxis reporting that peanut was the most common trigger. This in stark contrast to a similar study carried out 15 years previously which did not report any cases of anaphylaxis to peanuts or nuts. The authors of the study suggested that this could in part be due to the fact that, while children’s first exposure to peanuts used to be to its boiled form in soup or porridge, they were now eating peanut butter instead. A 2017 nationwide study of Korean schoolchildren also reported peanut to be the most common trigger of anaphylaxis in those aged between 9 and 16.

Don’t panic: To be clear, the official definition of anaphylaxis is probably not what you think it is.

This means that many of the cases of anaphylaxis reported in medical studies are not actually life-threatening—when dealing with an emergency, however, since it’s impossible to predict which reactions will become life-threatening, every case of anaphylaxis should be treated as if it is potentially deadly.

Signs of the most severe types of reaction will involve the following cardiovascular & neurological symptoms:

• headaches
• dizziness
• blurred vision
• low blood pressure (hypotension)
• rapid heart rate (tachycardia)
• loss of consciousness (syncope)
• anxiety
• confusion
• seizures
• fatigue
• malaise (aka ‘a feeling of impending doom’, which can occur during anaphylactic reactions)

Anaphylaxis to peanuts has a higher chance of being biphasic than anaphylaxis to other foods, which essentially means that, even if treated correctly, the symptoms can come back anywhere up to 72 hours after they initially resolve, often within the first 8 hours. The second wave of symptoms is often milder, but not always, and may require a second dose of adrenaline (aka epinephrine).

Generally, anaphylaxis to peanut is unlikely to involve cardiovascular symptoms. When German researchers examined the results of food challenges given to 1,013 pea/nut-allergic children they found that, although two thirds were classified as multi-organ reactions, therefore qualifying as anaphylaxis according to the medical definition, only 6% involved cardiovascular symptoms.

Likewise, an analysis of the medical records of 76 self-reported peanut- and/or tree nut- allergic American children older than 3 found that, although anaphylaxis (involving more than one organ system) was reported in around a quarter (23.7%) of those allergic to peanuts, there were no reports of hypotensive (low blood pressure) symptoms such as dizziness or fainting.

Among adults, the story is similar. A Canadian study of 1,135 adults who had gone to various emergency departments across the country with anaphylactic reactions during a 12.5-year period reported that peanut was the most common food trigger, causing 13.5% of all food-related cases. However, peanut was also one of the triggers that was least likely to cause severe anaphylaxis, with that dubious privilege being reserved for drugs, venom and tree nuts.

That said, given the propensity of peanut to cause more severe symptoms than most other triggers and its intimidating reputation, it should come as no surprise to learn that anaphylaxis to peanut is associated with higher rates of visits to hospital emergency departments and of admissions than other food‐related and non‐food‐related causes of anaphylaxis.

A 10 year review of Swedish hospital data found that peanut and tree nuts accounted for half of the visits to the emergency department and were more frequently associated with adrenaline treatment and hospitalisation than other foods.

However, most of the data on around peanut allergy comes from the US, where an analysis of medical data in a large, nationally representative database reported that peanut was the most likely food to send American infants and toddlers (younger than 3) to the hospital emergency department, and peanut-allergic children have been found to be more likely to be admitted to hospital than children with allergies to others foods.

A retrospective review of 15-year’s worth of medical data including emergency department (ED) visits and hospital admissions performed in New York City identified peanuts as the most common allergen implicated in emergency department visits (20.2%) and hospitalisation (27.1%). Rates of both ED visits and hospitalisations were highest among children under 4 years old.

A 2019 analysis of data from a database covering much of North America identified peanut as the no. 1 identified trigger of anaphylaxis among paediatric intensive care unit (ICU) patients from 2010 to 2015 in North America (US and Canada) and Mexico, affecting almost half (45%) of the patients.

Data covering the US showed regional differences, with peanuts being the most important trigger (and tree nuts, the second most important) for children in the Western region of the country, whereas the most important triggers for American children from the Midwest were milk and crustaceans. Children living in the Northeastern US were more likely to be affected by eggs and milk, and children in the Southern regions had crustaceans as their no.1 trigger.

Another American study that used data from a national administrative health claims database reported that, between 2005 and 2014, emergency department visits for food-induced anaphylaxis more than doubled (a 214% increase), with peanuts accounting for the highest rates (5.85 per 100 000 cases in 2014).

These results are mirrored by those of an Australian study which examined medical data in a national mortality database and found that, between January 1997 through December 2005, food-induced anaphylaxis admissions increased by around 350%, with hospital admission rates increasing most quickly for peanut- and crustacean-induced anaphylaxis, especially among peanut-allergic children under 4 years old, although the number of deaths remained stable.

Peanut is often implicated in cases of fatal anaphylaxis. Analyses of national anaphylaxis data in the UK, the US and Canada have revealed it to be the most common trigger, where it’s responsible for between around a fifth to around 9 in 10 of the reported food-induced deaths, often because people ate baked goods or sweets containing hidden peanuts and, in at least one cases, because of a fatal cross-reaction to a tree nut.

In Canada, where an analysis of the Ontario Coroner’s database found that peanut was responsible for 16 of 40 (40%) food fatalities, at least one fatal reaction to peanut has been reported as a result of an in‐hospital food challenge, and a 2018 analysis of all children hospitalised for anaphylaxis in intensive care units in France between 2003 and 2013 reported that peanut was responsible for (the only) 3 reported deaths (one of which was also as a result of a food challenge.

Peanut is not the most important cause of deadly anaphylaxis everywhere; in Ireland and Italy, for example, it has been reported as just one of the several foods to cause fatalities, and in Australia it’s the second most common trigger food, behind seafood, responsible for 7 of 22 (18%) deaths. Within countries, the population affected is different (in Ireland, it has not been responsible for any deaths in the under 13s, but in Australia, it’s the most common trigger among people aged under 20) and in the US, there are regional differences, with crustaceans being the most important cause of death in New York and peanut ‘just’ being responsible for 4 of 24 (16.7%) deaths. (4)

In the UK, an analysis of national hospital data including cases of hospital admissions due to food anaphylaxis registered between 1998 and 2018 found that, although peanut was responsible for 14% of deaths in children under the age of 16 and 20% of deaths in everyone else, since 1992, there has been a downward trend in the proportion of deaths caused by peanut or tree nut (possibly as a consequence of heightened awareness of nut allergies by food businesses). Instead, (cow’s) milk seems to be becoming more deadly.

All that said, it pays to remember that the risk of fatal anaphylaxis to food, including peanut, is extremely low, with food-induced anaphylaxis generally being the least common cause of deadly reactions; a 2013 meta-analysis of fatal food anaphylaxis data found that the incidence of peanut‐induced deaths was 2.13 per million person‐years and stated that ‘Fatal food anaphylaxis for a food-allergic person is rarer than accidental death in the general population’.

It’s a common misconception that the people who have the highest risk of having an anaphylactic reaction are those who have a history of serious reactions; in fact, anaphylaxis, even fatal anaphylaxis, is often experienced by people who have previously suffered from relatively mild reactions. In the same vein, just because you’ve had anaphylaxis in the past does not mean that your next reaction will be as bad.

An analysis of medical data from 3 allergy centres in Indiana reported that anaphylaxis occurred on second exposure in around a third (38 of 112, 33.9%) of the peanut-allergic children who had had an initial reaction to peanut confined to the skin. Conversely, in 21 children with known anaphylaxis, the second peanut exposure resulted in anaphylaxis in only a third (7) of them.

Risk factors for more severe reactions to peanut include older age, co-existing asthma and other severe allergies. Age is a factor in severe reactions to any trigger, including peanuts. Studies of British, Danish, French, Belgian and Luxembourger patients have all noted that teenagers and adults have more severe symptoms than younger children.

One study that examined the results of oral food challenges to peanut carried out in hospitals in the UK, Ireland, and Australia reported that anaphylaxis was 3 times more common in teenagers than younger children, and that older children also tended to have lower thresholds to the allergen.

A British study reported that (pea)nut-allergic adults were 2 to 9 times more likely to develop severe reactions than children. Another British study revealed that peanut-allergic adults were around 2 and a half times more likely than children to experience dizziness and loss of consciousness and that older children were more likely to experience bronchospasm (a sudden tightening of the muscles in the small airways in the lungs) and pharyngeal oedema (a swollen throat).

People with a larger risk of bronchospasm were also more likely to have severe asthma requiring regular inhaled corticosteroids, which brings us neatly to our next risk factor for more severe reactions: asthma.

As with age, asthma is a known risk factor for more severe allergic reactions to any food. It has been highlighted as a risk factor for severe (and fatal) reactions to peanut in studies carried out in several European countries, as well as the US and Australia.

A 2018 meta‐analysis of 32 studies of food‐related anaphylaxis that found that peanut and tree nuts were the leading triggers of fatal anaphylaxis also reported that a history of asthma in young adults was an important risk factor for fatality.

Asthma as a risk factor for more severe reactions to food seems to makes sense because one of the main features in case of severe reactions to food is a person’s inability to breathe properly. Therefore it would seem logical to think that a history of asthma could influence a person’s risk of developing severe anaphylaxis.

However, there is some debate as to whether asthma is actually a valid risk factor for severe reactions; over half of people with food allergy also have asthma, and the vast majority of them will never have a severe reaction to food. A 2022 meta-analysis of 32 studies examining the relationship between asthma and reaction severity found no consistent evidence that asthma was associated with an increased risk of having a severe reaction. Instead, the key factor could be whether or not the asthma is under control. Even then, one American study into anaphylaxis fatalities specifically noted that asthma ‘was considered well controlled in all’  of the asthmatic fatalities, so even uncontrolled asthma may not be a valid risk factor for more severe reactions.

Other things that have been identified as potential risk factors for serious reactions to peanut include:

• having other severe allergic diseases such as eczema (associated with a 3-fold risk of becoming unconscious during an acute allergic reaction), hay fever (associated with a 4-fold risk of severe pharyngeal oedema) or asthma (associated with a 7-fold risk of acute bronchospasm)
• reacting to inhaled peanut proteins
• reacting to skin contact with peanut, or having an allergy to latex or house dust mites, or a family history of allergies
• having more frequent allergic reactions to peanuts

Although some studies have reported that eczema is associated with more severe reactions to peanut, others have reported that it may have a protective effect. A study of American children with peanut allergy, for example, reported that those who had eczema reported significantly fewer anaphylactic reactions than children who did not (19.7% versus 30%, respectively). Similarly, a Dutch study in which peanut-allergic children and young adults were given food challenges found that those who did not have eczema were more likely to react to lower doses of peanut. As with asthma, the key may be how severe the condition is and whether or not it is under control or the person is experiencing a flare-up at the time of the reaction.

The severity of a person’s symptoms may also have something to do with the amount of food allergen they eat; some people may experience initially mild symptoms, but develop anaphylaxis with further exposure.

A study of Slovenian 94 peanut-allergic children noted both an association between the amount of peanuts consumed and the severity of an allergic reaction, and an association between a higher number of previous allergic reactions and anaphylaxis. This led the authors of the study to suggest that ‘allergic reactions of different severities may occur in the same patient, depending also on the amount of peanuts consumed.’

A study of Cuban patients with peanut allergy noted that they did not seem to suffer from symptoms as severe as those experience by peanut-allergic individuals in other countries. The authors speculated that this may be because Cubans traditionally eat roasted seeds rather than processed products like peanut butter. Since roasting increases the allergenicity of peanuts, it’s probably not their cooking method that’s making the difference. But it’s possible that the average amount of peanut butter (also made from roasted peanuts) that a person consumes before noticing the beginnings of a reaction contains more peanut protein than the number of seeds that they would eat in the same time, thus putting the person eating the peanut butter more at risk of a severe reaction. Or maybe not. Who knows? Nobody, yet.

Other severe symptoms that can be caused by an allergy to food, including peanuts, include Kounis syndrome—a rare event whereby the histamine released during an allergic reaction acts on the coronary histamine receptors to trigger a coronary event such as a heart attack, something which is more likely to happen in someone with underlying coronary artery disease, but can also happen in people with no history of heart disease—and acute pancreatitis, a sudden inflammation of the pancreas which generally manifests as stomach pain and can normally be treated with no lasting damage.

Delayed reactions to peanut

Delayed allergic reactions can occur hours or even days after exposure to an allergen, unlike IgE-mediated reactions that often happen within minutes. These reactions either involve diseases that rely on cell-mediated mechanisms (immune responses that do not rely on the production of IgE antibodies but instead involve the activation of T cells and macrophages which leads to inflammation and tissue damage) or by ‘mixed’ diseases that rely on both IgE- and cell-mediated mechanisms.

The three most common forms of delayed reactions to peanut are eczema (atopic dermatitis, AD), food protein induced enterocolitis syndrome (FPIES) and eosinophilic oesophagitis (EoE).

Eczema is a chronically relapsing inflammatory allergic condition that specifically affects the skin and looks like this. It’s classified as a ‘mixed’ form of allergy that can produce either immediate or delayed reactions that can occur up to 48 hours after eating a trigger food.

Peanut allergy is associated with eczema that is more severe than it is in people with allergies to other foods, but that may be because severe eczema is a risk factor for peanut allergy, rather than because peanut allergy causes severe eczema.

Only a minority of people with eczema and peanut allergy seem to experience a worsening of their skin condition as a result of eating peanuts; for example, a Czech study revealed that only 5 of their 41 (12.2%) peanut-allergic patients with AD experienced a worsening of their eczema (along with skin reddening, papules, rash and itchy skin), which occurred 6 to 8 hours after they had eaten peanut-containing food.

Food Protein Induced Enterocolitis Syndrome (FPIES) is a delayed allergic reaction to food that affects the gastrointestinal (GI) tract. There are two main types of FPIES, chronic and acute.

Chronic FPIES is quite rare and occurs mostly in infants who eat the trigger food on a daily basis. It can be recognised by intermittent vomiting and diarrhoea and, occasionally, failure to thrive (which means that a child is not getting in enough calories to reach a similar weight and size to other children of the same age and sex). Cases of chronic FPIES in adults are vanishingly rare, but not unheard of.

Acute FPIES is by far the most common form. In children, symptoms often occur within 2 to 4 hours after eating the offending food and can include:

• vomiting
• pallor
• lethargy
• dehydration
• diarrhoea
• shock or hypotension (i.e. low blood pressure) which can manifest as dizziness, fainting or blurred vision (as well as pallor and lethargy)

Symptoms of peanut-induced FPIES in children tend to appear when solid foods are introduced into their diets, often between the ages of 5 and 8 months, often on first exposure, but sometimes after the child has already eaten peanut a few times.

Occasionally, a child may have been diagnosed with FPIES to other foods before discovering that peanut provokes symptoms, too. In fact, about half may have FPIES to other foods as well as peanut.

Sometime children with chronic FPIES end up developing acute FPIES and this form of FPIES can, in turn, develop into an IgE-mediated form of allergy.

In adults, the typical symptoms of acute FPIES are not the same as those seen in children. They can also appear faster. They include:

• stomach pain and cramps
• diarrhoea
• vomiting
• transient weakness and shivering (possibly hypothermia)
• lethargy
• weight loss

People who experience severe symptoms of acute FPIES may have a longer-lasting form of the disease.

Eosinophilic oesophagitis (EoE) is an inflammation of the oesophagus caused by a food allergy, environmental allergens or acid reflux. It is characterised by symptoms including:

• food impaction; this is when food becoming stuck in the oesophagus which can lead to a sensation of squeezing in the chest, and can be accompanied by excessive salivation (unlike choking, a person can still breathe and talk, but they cannot eat or drink any more)
• difficulty swallowing (dysphagia)
• reflux (the flow of liquid back from the stomach into the oesophagus)
• vomiting
• heartburn (pyrosis)
• stomach pain
• food refusal

Symptoms are variable and often age-dependent. In infants, EoE tends to provoke general symptoms of oesophageal difficulties such as gagging, vomiting, feeding difficulties and weight loss, or so-called ‘failure to thrive’. Young and school-age children have symptoms that are indistinguishable from those associated with gastroesophageal reflux, such as abdominal pain, vomiting and an unpleasant taste in the back of the mouth that comes from regurgitating sour or bitter liquid. Older children and adults are more likely to have trouble swallowing and to get food lodged in their oesophagus (food impaction) and, less commonly, to suffer from heartburn.

Because symptoms can be severe, if you do suspect that you’re allergic to peanut, it’s important that you see your GP/family doctor and get a referral to an allergy clinic for further testing.

Threshold for reactions

It does not take a lot of peanut to provoke a reaction.

VITAL®, the Australian initiative for voluntary incidental trace allergen labelling, put out recalculated threshold doses for the ‘Big 14’ allergenic foods in 2020. Using a database containing datasets from studies carried out worldwide that used double-blind, placebo-controlled food challenges (DBPCFC), they calculated that the lowest threshold dose of protein that was needed to produce a reaction in 1% of the population allergic to peanut is 0.2 mg. (Note: in this case, the ‘population allergic to peanut’ is 1306 people who were given a DBPCFC)

This is one of the lowest eliciting doses of the main allergenic foods. 7.1 mg was the dose needed to produce a response in 10% of the test subjects, and 165 mg was the dose needed to provoke a reaction in half of the test subjects.

Tiny doses of 100 µg (that’s 100 micrograms, or 0.1 milligrams, or 0.0001 grams)—of peanut protein have been shown to elicit subjective—i.e. invisible to others, such as an itchy mouth or a feeling of nausea—allergic reactions in some subjects in a couple of studies, and one study even reported 2 people who reacted with objective symptoms to a miniscule dose of 3 µg (or 0.000003 grams) of peanut protein.

Note: we’re talking about milligrams of peanut protein. A single peanut is composed of about 25% to 30% protein. The primary peanut varieties sold in Europe are Runner and Virginia peanuts. Virginia tend to be used for roasting and snacking. A single, large Virginia peanut typically weighs around 1 gram, meaning that it would contain about 250 to 300 mg of peanut protein.

Protein content varies according to how you eat your peanuts. Boiled peanuts tend to contain less protein—about half of the protein content of roasted peanut, 140 mg per gram—because some of the protein is lost in the cooking water. Peanut flour is partially defatted and is typically around 50% protein, so 500 mg per gram, and peanut butter (made from Runner peanuts) contains around 25% protein, or 250 mg per gram.

The Australian HealthNuts study used ‘real world’ measurements to report the results of their challenges of 156 4-year-olds who were diagnosed with peanut allergy when they were 1; 52% reacted to a smear of peanut butter inside the lip, 18% to 1/16th of a teaspoon, 17% to 1/8th of a teaspoon, 7% to a quarter of a teaspoon, 5% to half a teaspoon and 1% to 1 teaspoon.

An analysis of the data in the European Anaphylaxis Registry reported that just over two-thirds (67.6%) reacted to the equivalent of less than a teaspoon of peanut which they put at around 1 gram of protein, or 4 to 5 peanuts.

It’s important to remember that the vast majority of people who react after eating their threshold dose of peanut do not have an anaphylactic attack. Only 5% of the children with persistent allergy in the Australian HeathNuts study mentioned earlier, for example, had anaphylaxis. Most of the symptoms were skin symptoms; hives and facial swelling (angio-oedema). In general, people who experience anaphylaxis to a food trigger tend to be older children and young adults.

One study has reported that the eliciting dose seems to get smaller as a peanut-allergic child gets older, and that those who react to the lowest doses of peanut tend to be older than 10. The authors note that this may help to explain why older children (and adults) often have more severe reactions to food than young children.

However, having a low threshold is not necessarily linked to the severity of a person’s reactions to peanut; the results of studies on this issue are mixed. Some have found that people who have more severe reactions during food challenges and/or have had more numerous and more severe accidental reactions in the past tend to have lower threshold doses than people who normally experience mild symptoms.

Other studies, however, have found no relation between a person’s eliciting dose and the severity of their reactions to peanut either during an oral food challenge or during previous reactions at home, suggesting that people with histories of severe reactions to peanut-containing foods ‘do not appear to represent a distinct sub-population with greater sensitivity’.

Research suggests that most people’s eliciting dose stays relatively stable. One study that examined the medical data of 189 peanut-allergic patients who had between 2 and 4 food challenges found that 70% either saw their thresholds stay the same or increase, while 30% experienced a decrease.

A 2021 meta analysis of 19 studies covering 3151 peanut-allergic patients, 534 of whom had repeat challenges, got a similar result, reporting that 71.2% of the patients had a relatively stable threshold, with just small increases or decreases. About 20% of the patients experienced greater change, with a 10-fold shift one way or the other, and 10% experienced a far greater change. In some cases the change was around 1000-fold, which could represent a child outgrowing their allergy, but some people’s thresholds also became over 100 times smaller. The researchers calculated that around 4.5% of people who react to 5 mg or less of peanut would be expected to develop anaphylaxis.

The smaller a person’s eliciting dose, the less likely they were to be triggered by the same amount when they were challenged again. People who’d had objective symptoms triggered by 5 mg of peanut protein or less were more likely to experience their initial reaction at a higher dose the next time around. Around 2.4% of people who’d tolerated 5 mg of peanut protein the first time around reacted the second time around, but none experienced anaphylaxis.

Similarly, about three-quarters of the patients who’d experienced anaphylaxis during their first food challenge did not experience it when they were challenged again with the same (or a smaller) dose. However, when re-challenged, a small number of people did experience anaphylaxis to a dose that they had previously had a milder reaction to.

This type of research comes with several caveats. One is that study populations tend to differ, and different populations can have different average thresholds. For example, children who have more allergies (e.g. multiple food allergies and/or asthma and/or eczema and/or hay fever) will likely have lower thresholds than children who do not.

Study method matters, too. Sometimes patients are given 15 minutes between doses during a challenge, sometimes half an hour. But symptoms can take much longer to appear; researchers who were aware of this problem carried out a study involving 63 children with peanut allergy using a modified challenge procedure with doses scheduled 2 hours apart; they found that it took an average of 55 minutes before the children reacted.

So, it could be that, during the average food challenge, allergists are not waiting long enough for some of their patients to develop symptoms before giving them the next dose. In which case, the threshold doses being estimated for peanut allergy may be too high. Additionally, patients who have experienced anaphylaxis are often not offered food challenges and are generally excluded from these kinds of studies, meaning that people with severe allergies are not represented, which could also impact the average dosage amounts.

And since food challenges involve feeding a person one dose of their allergen after another, it’s difficult to determine whether a reaction has occurred to the last, discreet dose of the food, or whether it has occurred to the total amount consumed by the allergic patient at the time of their reaction. Meaning that the eliciting doses are currently being underestimated.

One team of researchers carried out a study designed to check this out. Taking the results of a previous study that found that it took 1.5 mg of peanut protein to provoke symptoms in 5% of people with peanut allergy, the researchers gave 378 peanut-allergic children from 3 centres in Ireland, Australia and the US one dose of 1.5 milligram’s worth of peanut protein to see how many visibly reacted. That number was 8; that is 2.1%, rather than the 5% that was predicted. Furthermore, none of those 8 children experienced more than a mild reaction. 4 were treated with antihistamines and 4 needed no treatment.

67 (18%) of the children experienced subjective symptoms and 58 (15%) experienced symptoms that were so mild and short-lived (e.g. 2 hives that came and went in 5 minutes, a single sneeze or cough) that they were not counted (if the cases of 3 or fewer transient hives had been included, the reaction rate would have been 5.5%, showing that definitions of what reactions to include in the official statistics matter, too). Some of the children who had subjective reactions also had lower

When it comes to the average peanut-allergic individual, the typical threshold dose for triggering objective symptoms is apparently equivalent to one to three peanuts.

Ultimately, the threshold dose needed to provoke symptoms varies widely between people. It also varies per person, depending on the circumstances around the meal.

Your threshold can be lowered and your allergic reactions worsened by things called ‘cofactors’. Cofactors include things like how much you eat and whether those ingredients have been cooked or processed, as well as exercise, anti-inflammatory drugs, alcohol, infection and stress.

Analyses of European anaphylaxis registry data have revealed that children and adolescents with peanut allergy are more likely to report the involvement of cofactors in their reactions than children with other food allergies, that infection is one of the most common cofactors affecting children and adolescents, and that exercise is the most common cofactor affecting the peanut-allergic of all ages.

Clinical immunotherapy trials have traditionally been a good source of data as far as cofactors are concerned because the people taking part are regularly taking the same dose of their trigger food and are better placed to notice when something else makes their reactions worse. These studies have specifically mentioned things exercise and infection (again, most commonly), suboptimally controlled asthma, menstruation, and tiredness; a 2023 trial reported a link between eating peanuts in the evening and a higher likelihood of having anaphylaxis requiring the administration of adrenaline in children undergoing peanut oral immunotherapy.

British research also suggests that a lack of sleep is an important cofactor in peanut allergy. Researchers designed a set of experiments to examine the impact of exercise or a lack of sleep on the thresholds of 73 and 71 peanut‐allergic adults, respectively, and reported that both exercise and sleep deprivation reduced the reaction threshold by 45%.

A separate analysis of the data found that sleep deprivation also increased the severity of the symptoms by 48%, whereas exercise had no effect.

Further analysis of raw data from the first experiment found that the effect of exercise on the reaction threshold was more modest than initially reported; in fact, only 12% of the participants saw a significant drop in their threshold, so, the impact of exercise does not seem to be as important as a lack of sleep in the majority of peanut‐allergic individuals.

You can experience more than one cofactor at the same time like, for example, exercise and menstruation, which probably work together to have a cumulative effect on lowering your threshold.

Cofactors are thought to play a role in about 14% to 30% of all anaphylactic reactions.

The amount of peanut needed to provoke a reaction says nothing about how severe the reaction will be. And, even if your reactions have been mild in the past, it does not mean that they will continue to be mild.

Food challenges are almost always stopped as soon as objective symptoms are noted. In a unique study, 27 peanut-allergic children were given challenges that were not stopped as soon as the first symptoms appeared, but were instead allowed to continue. This resulted in 21 of the children eventually experiencing anaphylaxis. 6 children did not experience anaphylaxis, even at the maximum dosage, and in only 3 children was anaphylaxis the initial reaction. A history of anaphylaxis was also not predictive of anaphylaxis during the food challenge.

In other words, while a food challenge enables a diagnosis of allergy to peanut, the dose at which a person first visibly reacts is not a reliable indicator of how severe their symptoms are likely to be. And their past reactions are not predictive of their future ones.

Image by Ivan Samkov on Pexels

Diagnosing peanut allergy

A diagnosis of peanut allergy will primarily be based on your clinical history—a record of consistent symptoms following the consumption of peanut or peanut-containing foods. This will require you to provide your allergist with answers to questions about your general medical background (including any other allergies you may have and relevant illnesses in your family) and your dietary history (what you ate to provoke your symptoms, what those symptoms were, how long they lasted, whether you had exercised or taken painkillers and many other details).

Your medical history determines what comes next; on the basis of your answers, the allergist will try to determine what type of allergy you have—a primary, immediate-type allergy, a cross-reactive allergy or a delayed-type allergy—or whether it could be something else, and this will determine the tests they ask for to come up with a diagnosis.

Diagnosing IgE-mediated reactions to peanut

Skin tests

An IgE-mediated sensitisation to peanut is typically confirmed by a skin prick test, which involves someone placing a small sample of peanut extract onto your skin (generally the forearm of an adult/older child or the upper back of a young child) and pushing it through the top layer of skin by pricking it with a lancet. It takes about 15 minutes to see a reaction (or not).

This test is often carried out first because it is quick and simple to perform and gives rapid results. It is often used to rule out an allergy rather than to confirm one, because it generally has good negative predictive value—if the skin weal is under a certain size, you are unlikely to have an allergy—but poor positive predictive value; the skin weal has to be very large before the allergist will say with any kind of confidence that you probably have an allergy.

Unfortunately, these tests are not always reliable. There are, for example, people who are allergic to peanuts and but whose skin prick test produces a 0 mm weal. This is partly because the tests can only be as good as the extracts they use, and those extracts aren’t perfect.

Commercial peanut extracts made by different manufacturers contain different amounts of peanuts allergens and, as a result, produce inconsistent results.

This is, in large part, due to the fact that peanut proteins do not have the same solubility and they also react differently to processing. Some proteins that are vulnerable to heat, like Ara h 8 and Ara h 5, will only be present in low amounts in peanut extracts, if at all, meaning that someone who actually is allergic to peanut could be wrongly told that they are not. Likewise, oleosins, that are often responsible for severe allergic reactions, are often missing from standard peanut extracts due to their insolubility in aqueous solutions.

One solution to this problem is the prick to prick test. This test is very similar to the skin prick test, except first the lancet is used to puncture fresh food and then it is used to prick your skin. When the food is in liquid form, such as peanut oil, the technique is actually the same as the one used for the skin prick test, and when the food is solid it is often ground down and put in saline solution.

The prick to prick test often produces superior results to commercial extracts because the fresh food used should contain all of the allergens that a person can react to. The lab used by the clinic can also prepare the extract their own way by, for example, boiling it, which may add to its efficacy.

Blood tests

Sometimes, the doctor may decide to order a blood test, aka an immunoassay. Perhaps the skin prick test was inconclusive, or the suspected allergen is not available for skin prick testing, or you’re unable to undergo the test for some reason.

A blood test involves having a small sample of blood drawn so that it can be sent to a lab where technicians will use allergen extracts to check whether there are IgE antibodies in your blood that react to them. It can take 1 or 2 weeks to get the results.

Blood tests can be less sensitive or specific than skin tests, but they have other advantages: they are perfect for people who cannot stop taking certain medications or have extensive skin disease or tattoos, and they can safely be used on infants, squirming toddlers and people who are at risk of suffering an anaphylactic reaction.

Blood test panels also typically include a whole range of potential allergen extracts including other foods or aeroallergens that the allergist may want to check your reaction to.

Blood tests that use whole peanut extract to diagnose peanut allergy may eliminate the need to perform up to 2 in 5 oral food challenges but they can generally only be used to confirm food allergies and not to exclude them.

This is because they tend to have a good positive predictive value—if your test result shows a high enough level of peanut-specific IgE antibodies in your blood, you’re quite likely to have a symptomatic allergy—but a poor negative predictive value—if the amount of peanut-specific IgE antibodies measured in your blood falls under a certain value, you could still be allergic to peanut.

As with the skin tests, blood tests can be unreliable; people who are allergic to peanuts can have blood test results showing very low levels of peanut-specific IgE. because peanut extracts made for blood tests also contain differing amounts of allergen and will produce inconsistent results.

Another way of getting around the missing allergen problem would be to perform a component blood test—aka Component Resolved Diagnosis (CRD)—which also enables the allergist to make a more refined diagnosis. Instead of using extracts of whole foods containing only heat-stable and soluble allergens, this test uses isolated, individual proteins.

CRD allows the allergist to see which molecular component(s) of an allergen you react to, which may affect how you manage your allergy. Having a positive test to just Ara h 8, for example, means that you will probably only suffer from mild symptoms and can eat foods that contain trace amounts of peanut, whereas being sensitised to Ara h 2 or Ara h 6 means that you will probably have a more severe form of peanut allergy and will need to avoid all peanut-containing products.

Unfortunately, although CRD could potentially reduce the need for oral food challenges and contribute to tailored management plans, it’s not yet considered a routine diagnostic method and it’s not comprehensive; the most widely used tests neither contain all of the identified allergens (which are also not all of the possible allergens), nor are they universally available. Testing for certain specific peanut allergens would require special preparation and is therefore only likely to be done for research purposes.

As with the skin and standard blood tests, CRD is better at confirming an allergy than at eliminating the possibility of one. And, because sensitisation patterns differ according to geography and populations, with different allergens being more important in different regions and in people of different ages, allergists need to understand their patient populations so that they interpret the results of the tests correctly.

After all those caveats, it should come as no surprise to find out that a positive skin or blood test does not mean that you are allergic to something. While lab tests do help with diagnosis, positive results only show sensitisation to specific allergens. Being sensitised to a food doesn’t mean that you’re allergic to it and that you will develop any symptoms.

The literature is littered with studies reporting that children who have been diagnosed with peanut allergy because of positive skin and/or blood tests can actually eat peanuts.

For example, in a British study, 79 children who had had a positive skin test to peanut underwent an oral food challenge but only 7 reacted and, in a Canadian study, 8 of 37 children who were sensitised to peanut were reported to routinely eat peanuts without problem.

In a German study, 61 peanut-sensitised infants and children were given oral challenges and 27 passed. Although 94% of the allergic children were sensitised to Ara h 2 (a major peanut allergen), so were 26% of the tolerant ones. 25 of the children had very high levels of IgE antibodies to Ara h 2, but 7 of them were able to eat peanut without symptoms.

A positive skin or blood test result simply means that your immune system is specifically aware of an allergen or allergens in that food. Why some people later develop an allergy to that food, and some do not, is not yet known.

In some cases, children pass an oral food challenge and successfully introduce peanuts into their diet only to develop higher levels of peanut-specific IgE antibodies in their blood over time while still being able to eat peanuts without problem. There’s no explanation for those cases, either.

A negative skin or blood test result doesn’t mean that you are tolerant to something, either. In one study, three quarters of the peanut-allergic children with ‘negative’ (actually very low or unmeasurable levels of IgE to peanut) blood test results failed their food challenges. In another study, 4 adults with early-onset peanut allergy and 3 with late-onset peanut allergy either failed their challenges or reported recent reactions despite having negative blood test results and, in 2 cases, negative skin test results, too.

In some cases, the test might have been measuring the wrong thing. For example, if the allergist has been focussing on Ara h 2 to diagnose peanut allergy in a child, and that child has a negative test result to that component but is actually allergic, it may well be that they are sensitised to another peanut allergen. Even if they live in a country in which Ara h 2 is considered a major allergen. There are always exceptions to the rules, they are just relatively rare. The wide variety of test results produced in different people is why the clinical history is so important.

Neither can the results of your skin or blood test, or even a component blood test, predict how severe your reaction to eating some peanut might be; having a large skin weal or a high level of IgE antibodies in your blood does not mean that you will have a serious allergic reaction if you accidentally eat a peanut-containing curry. Neither will a history of previous reactions to the offending legume.

That said, because nothing is straightforward when you’re dealing with allergy, some studies have found a correlation between the size of a person’s skin test response and/or their blood IgE level and their risk of having a serious reaction during a food challenge, or at home, even though the association may be weak or may require the measurement of IgE blood IgE levels to several different allergens (e.g. Ara h 1, 2/6 and 3) together.

So, somewhat encouraged by the latter studies, researchers are hard at work trying to find specific skin test weal sizes and IgE blood levels—so-called ‘cut-offs’—that could help allergists to reliably determine whether or not a patient has an allergy, so that they can avoid carrying out food challenges. Some teams have come up with cut-offs for skin prick tests and prick to prick tests, some have come up with cut-offs for IgE blood levels, to whole peanut extract or individual components, and some have come up with measurements that use a combination of both skin prick test and IgE blood levels that allow allergist to classify their patients with almost complete certainty. Some have tried to find cut-offs that can predict the likelihood of experiencing anaphylaxis during a food challenge.

A couple of teams of researchers are also using machine learning models to try and predict the outcome of food challenges, and another team has come up with a scoring system that involves the skin test response, the blood IgE level and the clinical history to try and predict the severity of the reaction.

Studies suggest that lab tests are more successful in predicting the outcome of the food challenge, and therefore the existence of an allergy, than the reaction severity or the amount of peanut needed to provoke symptoms.

While they can be useful, cut-off values differ depending on the extract and the method used and the population being tested, and the high cut-off values that are needed to provide an almost certain diagnosis make the test very insensitive and risk leaving up to half of patients with food allergy at risk of accidental exposure unless they have a clear history of reacting or are given a food challenge and thus diagnosed as allergic.

The fact is, no test is 100% accurate and lab tests alone can never be used to diagnose an allergy. At the very least, a person’s history of reactions must be taken into account in combination with their test results in order to have a pretty good idea of whether or not they are allergic to something.

Food challenge

The only way to get a definitive diagnosis of peanutallergy, and to have some idea of how severe your reactions may be and how much peanut is needed to provoke them,is to undergo an oral food challenge. This generally involves eating a very small amount of peanut, waiting for a reaction, and then doing it again, gradually increasing the dose until an objective—visible—reaction occurs or a maximum dosage is reached. It can take around 4 hours, depending on the type of challenge undertaken and the length of observation time needed.

You can read more about oral food challenges here.

Because of the risk of severe reactions, oral food challenges should only be done by an experienced consultant in a medical setting.

Oral food challenges with peanut can be risky—several studies have noted that they are more likely than other foods to produce severe reactions that involve several organ systems and need to be treated with adrenaline. 

But other research has also reported that peanut challenges are no more hazardous than challenges to other foods (in fact, wheat and milk seem to be more risky). It simply depends on the characteristics of the people taking them.

According to some research, people who react to very small amounts of peanut are more likely to have serious reactions during their OFC but, according to other research, this is not the case. Some research has even reported that the minimum eliciting dose for severe reactions to peanut tends to be higher than those needed to provoke mild or moderate reactions, but this could be due to the amount of time that was taken in between doses; it’s possible that the allergists did not wait long enough to see if one dose provoked a reaction before giving the next one.

The fact is, when it comes to allergic reactions, making any kind of prediction is tricky because there are all kinds of variables involved, including cofactors—like, for example, how well a person slept the night before or whether they had a painkiller earlier that day—and how much of their trigger good a person has eaten, and how long it takes a person to react to an allergen—so, if someone takes longer to react than the average person and is given their second dose of peanut before they had time to show symptoms to the first, it might look like they have a relatively high threshold.

Accordingly, during one study in which 27 patients aged between 4 and 19 years old were challenged with peanut twice, all but 2 of them reacted with different severity scores and/or different doses during each challenge. So it would seem that an oral food challenge can identify an allergy but cannot identify a person’s threshold.

Oral food challenges are often not carried out in practice; for the most part, allergists rely on a personal history of reactions and lab tests to diagnose their patients. Challenges are typically only carried out in cases of doubt when there are conflicting results and a person’s history of reactions does not agree with their lab test results—i.e. they have had reactions to peanut in the past but their lab tests are negative, or they have had no reactions but they have high levels of IgE antibodies to peanut, or they have a negative skin test response but a high level of IgE antibodies in their blood, or vice versa.

In cases where there is a strong suspicion of allergy, or a clear history of reactions to peanut, an oral food challenge will not be required, especially if someone has a history of severe symptoms.

Although food challenges help to diagnose food allergies and identify a suspect food, there are other reasons to undergo food challenges, namely:

• to identify culprit foods in cases of allergies to multiple unknown foods
• to determine a patient’s threshold—how much peanut they can eat without reacting—so that dietary advice based on the outcome of the challenge can be given
• to confirm the development of tolerance to a trigger food (although children who are allergic to peanut are likely to be offered food challenges to check for acquired tolerance less frequently than children with allergies to other foods that are more likely to be outgrown)
• to allow people who have excluded foods from their diets on the basis of skin sensitisation alone to reintroduce food into their diet after a negative test result

Diagnosing non IgE-mediated and mixed reactions to peanut

Non IgE-mediated diseases are difficult to diagnose for several reasons, not least of which is the fact that IgE testing is often of no use. This makes the clinical history especially important for the diagnosis of these types of conditions. Even then, the symptoms are not easy to connect to the actual meals because of the time delay, and the symptoms associated with digestive allergies lack the skin and respiratory signs that doctors usually associate with allergy.

Skin tests

Eczemais diagnosed based on personal and family history of allergy and a skin examination.. While there are no standard diagnostic criteria, there are certain features that a doctor can look for to diagnose it.

That said, these criteria are based on the characteristics of paediatric eczema, which is not the same as the manifestation of eczema in adolescents or adults, making diagnosis of eczema in older age groups more challenging. Sometimes people with eczema in these age groups will have to undergo additional tests to rule out other diseases first, and a skin biopsy may be needed before a diagnosis of eczema is made. However, these differences are now being taken into account and guidelines are being updated.

Once the diagnosis of eczema is made, efforts will first be made to try and get the skin condition under control using topical skin creams and drugs before any further testing is done. Generally, only if the skin is not getting any better will tests be carried out to see whether allergens, like food, could be aggravating the condition.

The identification of potential food allergens is generally done by looking for specific IgE antibodies to a food using skin prick tests or blood tests (the latter is often used if the skin condition is too bad for a skin test, or medications are being taken that will interfere with the results, or if the tests involve a young infant).

In cases of delayed symptoms, doctors may use the atopy patch test (APT). This test generally involves walking around with food (either fresh or in solution) contained in tiny aluminium capsules taped to your back for up to 3 days and having your skin checked for a reaction after 48 hours and 72 hours.

The atopy patch test has also been used to try and diagnose delayed digestive allergies, with mixed results; in the case of food protein–induced enterocolitis syndrome (FPIES), for example, it has proven itself to be both ‘a promising diagnostic tool for the diagnosis of FPIES’ and ‘not helpful in identifying the [trigger] foods’, while showing ‘poor utility in the follow-up prediction of outgrowing FPIES in children’, and with eosinophilic oesophagitis (EoE), it has shown that it can ‘identify potential causative foods’. For these diseases, it is not the diagnostic instrument of choice.

A skin application food test (SAFT) may be used instead for children under the age of 4. It’s basically the same thing, but the capsule of food is only applied to the skin for 10 to 30 minutes. It’s been described as reliable and child-friendly and as adding value in the diagnosis of peanut allergy.

Elimination diets and food challenges

While skin tests may provide an indication of sensitisation, they cannot diagnose a food allergy; that has to be done with a food challenge during which the doctor can see whether or not, in addition to any immediate reactions, the suspected food produces a worsening of the skin symptoms within the next 48 hours. If it does, the food can then be eliminated from a person’s diet and their skin condition will be monitored for the next few months to see if there is a persistent improvement. When more than one food is suspected, the next challenge will be done a few weeks after the first one.

The diagnosis of delayed digestive allergies generally starts with exclusion; first other possible causes of the symptoms are eliminated and only then will the suspected food(s) be excluded from a patient’s diet—and, if they are breastfeeding, from their mother’s diet, too.

If the symptoms disappear, a diagnosis can then be confirmed by re-introducing the foods one by one back into the diet and seeing if the symptoms return. If symptoms don’t disappear, it could be that the diet hasn’t been restricted enough and other foods may be considered for testing and elimination. Or it could be that something other than an allergy is responsible, in which case, the allergist’s job ends and another specialist’s begins.

The diagnosis of food protein induced enterocolitis syndrome (FPIES) mainly relies on a person’s clinical history and symptoms appearing when the offending food is reintroduced after an elimination diet.

In the case of chronic FPIES, an elimination diet should result in the symptoms going away within 3 to 19 days. Reintroducing the trigger food should produce the symptoms of acute FPIES—i.e. projectile vomiting—which should be enough confirmation.

In the case of acute FPIES, eating the offending food should be followed by symptoms that should fit specific diagnostic criteria including copious vomiting within 4 hours. Although confirmation of the diagnosis officially requires an oral food challenge, because it often produces nasty symptoms that the patient quite rightly has no wish to suffer through, in practice, this is rarely done and challenges for the diagnosis of chronic FPIES are more common.

However, since FPIES symptoms tend to be different for adults with acute FPIES and there are no strict diagnosis guidelines for them, oral food challenges are often necessary.

There are other reasons to undergo food challenges in cases of FPIES, including:

• identifying a culprit food in cases of allergies to multiple foods
• confirming the development of tolerance to a trigger food, which is often done between 12 to 18 months after the most recent reaction
• identifying alternative nuts that can be eaten without symptoms in order to avoid an unnecessarily restrictive diet

Many clinics will only carry out a food challenge in an infant to see whether they have outgrown their allergy.

Although the majority of people with FPIES will have negative skin or blood tests to their trigger food, in some cases people do have an IgE sensitisation too. This is called ‘atypical FPIES’ and it affects between 1 in 4 and 1 in 8 people with FPIES. According to American research, the foods most commonly associated with this type of FPIES are egg, milk and peanut, but this may just be because those are the foods most typically eaten by American children (who make up the bulk of these studies). A person can have atypical FPIES to several foods, and those foods can include anything, from shrimp to avocado.

Some children with atypical FPIES may take longer to outgrow their condition (if, indeed, this happens at all) or may develop a classic IgE-mediated food allergy with potentially more dangerous symptoms. As such, periodic testing for an IgE sensitisation is advised in children who also have an IgE-mediated food allergy to other foods or suspected food-induced eczema.

When diagnosing eosinophilic oesophagitis (EoE), other conditions that produce similar symptoms, like gastroesophageal reflux disease (GERD), are first eliminated as a possibility before any intrusive testing is done. Then, if eosinophilic oesophagitis is still suspected, an upper GI endoscopy (aka an oesophagogastroduodenoscopy) and biopsies are carried out to look for specific levels of eosinophils in the oesophageal tissue (15 or more eosinophils per high-powered field, to be precise).

Standard elimination diets for cases of EoE are often based on the most common causes of the disease, either ‘2 food diets’ (dairy and wheat), ‘4 food diets’ (dairy, wheat, egg, and legumes) or ‘6 food diets’ (dairy, wheat, egg, legumes peanuts/tree nuts and fish/shellfish). These are called ‘empiric’ diets, i.e. diets that are based on observation and experience. The diet can be made less cumbersome by starting small, first with one food (i.e. milk) or two foods and then eliminating more foods if the symptoms don’t disappear.

The empiric diet approach is not the only approach. Sometimes the foods to be eliminated are determined using lab tests—atopy patch test and SPT and/or blood test—first (a targetted approach). Both methods work equally well for both children and adults although the targetted approach has the advantage of often requiring the elimination of fewer foods. That said, a lot of people with EoE don’t have any measurable IgE antibodies to their trigger food, so the targetted approach can only help some.

The diet normally takes about 6 weeks. If the symptoms go away and the tissue samples look good, the trigger is assumed to be one or more of the foods that was eliminated. In order to pinpoint the trigger(s), each food is reintroduced back into the diet one by one. If a reintroduced food causes symptoms to return and/or biopsy specimens to look abnormal, then it is identified as a trigger food and must be eliminated from the diet indefinitely. (In the real world, children may balk at undergoing so many intrusive tests or there may not be the capacity to perform them, in which case, they will probably not be required for a diagnosis.)

Elimination diets are best performed under expert guidance, because there is a risk that excluding a food from your diet because you think that you may be allergic to it or because it causes mild or delayed symptoms can lead to you developing an IgE-mediated allergy to that food, often with severe—sometimes fatal—reactions.

The good news is that, when a delayed digestive allergy is diagnosed, excluding offending food(s) from the diet leads to the resolution of symptoms and the repair of the underlying tissue damage in most children and adults, and improves quality of life, even though it the diet may be difficult to stick to. When it comes to young children, if staple foods are being eliminated, dietary guidance may be needed to ensure normal growth and development.

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Good to know

Peanut is one of two foods (the other being egg) for which there is consistent evidence that introducing it into a child’s diet at an early age can help to prevent the development of allergy.

At the turn of the century, after allergists had noticed that peanut allergy was becoming more common around world and circumstantial evidence pointed to this being caused by mothers eating peanuts during pregnancy and introducing peanut products to their child at an early age, doctors recommended that children not be introduced to peanuts or tree nuts until the age of 3.

However, opinions began to change after a team of British researchers comparing the prevalence of peanut allergy in a population of Ashkenazi Jewish children living in the UK versus one living in Israel revealed that the children living in the UK had a much higher chance of being allergic to peanuts than did the ones in Israel. The main difference between the two populations was that the British children typically avoided peanut products during childhood, whereas the Israeli children were often given Bamba, a type of corn puff soaked in peanut butter, as an introduction to solid food.

This revelation led to other studies, notably the LEAP (Learning Early About Peanut Allergy) study, which showed that peanut-sensitised ‘at risk’ infants (those with eczema and/or egg allergy) who avoided peanuts until the age of 5 were more likely to be allergic than their counterparts who were introduced to peanuts from the age of 4 months (with a prevalence of peanut allergy of 35.3% in the former group versus 10.6% in the latter). This result was then repeated in the EAT (Enquiring About Tolerance) study among infants who were not considered at risk, with 7.3% of those who were not introduced to peanut early becoming allergic versus 2.4% of those who were.

Current guidelines from various (Western) allergy associations are heavily influenced by these findings, with the majority advising the introduction of peanut into the diet no later than 6 months:

• The European Academy of Allergy and Clinical Immunology (EAACI) advises that peanut be introduced between the age of 4 to 6 months in an age-appropriate form, for example, a heaped teaspoon of diluted peanut butter every week. They also recommend that peanut not be the first solid food to be introduced
• The British Society for Allergy & Clinical Immunology (BSACI) advises that infants at ’higher risk of developing food allergies’ be given peanut at the age of 4 months in an age-appropriate form after the baby has been introduced to pureed fruits and vegetables and egg
• The American Academy of Allergy, Asthma, and Immunology (and friends) recommend that both peanut and egg be introduced around the age of 6 months, and not before 4 months
• The Australasian Society of Clinical Immunology and Allergy advises that peanut and other solid foods be introduced to all infants, regardless of their allergy risk factors, before 12 months, but not before 4 months
• The Canadian Paediatric Society advises the introduction of peanut and other allergenic solid foods at around 6 months, but not before 4 months of age in high-risk infants, and at around 6 months of age in infants at low risk

Recent research involving over 300 American infants supports recommendations that peanut should be introduced ‘as soon as possible and earlier than age 6 months’ in infants with moderate to severe eczema who are the highest risk of developing peanut allergy.

Most guidelines do not suggest having your infant screened for allergies before introducing peanut. For one, a positive skin or blood test confirms only sensitisation and does not mean that an infant has peanut allergy (in fact, up to half of the positive tests in this age group are false positives), although a negative skin prick test generally does exclude immediate-type allergy. Second, peanut allergy does occurs in infants who do not test positive, so a test does not provide any certainty.

That said, the American National Institute of Allergy and Infectious Diseases guidelines does recommend an evaluation with a peanut skin prick or blood test prior to peanut introduction in infants at high risk of allergy (i.e. with severe eczema and/or egg allergy). But, the Australasian Society of Clinical Immunology and Allergy does not, and neither does the Canadian Paediatric Society. The European Academy of Allergy and Clinical Immunology (EAACI) makes no specific recommendation and the British Society for Allergy & Clinical Immunology recommends that parents of infants with other known food allergies and/or severe eczema ‘speak to a healthcare professional for advice’.

Basically, anyone with an infant with a known food allergy, severe eczema and/or asthma should speak to a healthcare professional for advice before introducing allergens into their diet. Infants who do not have any existing allergic conditions should be able to have peanut butter cautiously introduced into their diet at home.

Early introduction does not guarantee that your child will not develop an allergy to peanuts, as demonstrated by the infants in this American case series that describes 7 instances of children aged between 6 and 12 months old who were introduced to peanuts early and actually tolerated them for a few weeks, even months, before showing signs of immediate or delayed forms of peanut allergy after eating them. Importantly, none of the initial reactions were severe.

Although early introduction will not help everyone, research suggests that it should help the vast majority. A couple of follow-up studies were carried out on the children who were part up the original LEAP trial that further demonstrated the advantage of early peanut introduction.

The LEAP-On study was published in 2016 and involved 556 children from the original LEAP trial. Researchers asked half of the group to avoid eating peanut products from the age of 5 to the age of 6 while the others continued to consume peanuts regularly. They then tested the children again, and found that, even after 1 year of peanut avoidance, most of the children from the original peanut-consumption group remained protected from peanut allergy at the age of 6 (3 new cases of allergy developed in each group).

Finally, the LEAP-Trio study was published in 2024. It followed up with 508 of the original LEAP trial participants—around 80%—who were now around 12 years old and had been eating as much peanut as they wanted, whenever they wanted to (what scientists call ad libitum), from the age of 6. 255 had been in the LEAP peanut-consumption group and 253 in the LEAP peanut-avoidance group. The researchers wanted to see if the advantage gained from the early consumption of peanut products had lasted into adolescence. They found that 38 of 246 (15.4%) of participants from the early childhood peanut-avoidance group and 11 of 251 (4.4%) from the early childhood peanut-consumption group now had peanut allergy. (Complete data was unavailable for 11 of the 508 participants), results that show that regular, early peanut consumption until the age of 5 can reduce the risk of peanut allergy in adolescence by around 71% compared to early peanut avoidance, irrespective of whether a child continues to eat peanut.

You can reacquire a peanut allergy after you’ve outgrown it.

This was first reported by researchers about 20 years ago. In the first such case, 3 boys are described to have outgrown their peanut allergy only for it to come back again. After successfully passing a food challenge, the boys all ate small amounts of peanuts sporadically for the next year or so before they started to show symptoms again.

These boys were actually part of a large study examining the resolution of peanut allergy in children which found that only about half of the children who outgrew their peanut allergy had actually started eating them on a regular basis. This seems to be a problem.

The authors of a subsequent study evaluated 68 people between the age of 5 and 21 who had outgrown their childhood peanut allergy with questionnaires, skin tests and blood tests. Subjects whose status was uncertain were also invited to undergo a food challenge. When the questionnaire answers and test results were in, 3 of 15 people who consumed peanuts infrequently (specifically, ate ‘may contain peanut’ products) or not at all after outgrowing their allergy were found to have reacquired it, whereas all of the 23 people who ate peanut frequently were still tolerant.

The study suggested that children who eat concentrated forms of peanut frequently have a considerably lower chance of becoming allergic to peanuts again than children who eat peanuts infrequently or not at all.

The authors also calculated a rough 7.9% chance of reacquiring peanut allergy once it’s outgrown, but that number could have been either an overestimation or an underestimation because so many of the children in the study had either refused a food challenge (the only way to be certain of their allergy status) or had avoided peanuts since being declared tolerant.

In fact, trying to calculate the odds of a peanut (or any) allergy coming back is almost impossible due to the understandably high number of people who tend to avoid the foods that used to plague them, either because they don’t like the taste or because they are worried about having a(n even worse) reaction. One study that surveyed people previously allergic to peanut about their peanut consumption reported that around 1 in 5 (19%) ate peanuts about once a week and about 1 in 10 (9%) about once a day after being given the all-clear. The remaining 7 in 10 of those surveyed ate them about once a month or less.

Unfortunately,  the exact mechanism by which peanut allergy can recur is unknown and scientists can’t say for sure that eating peanuts on a regular basis will protect you from reacquiring your allergy because a small proportion of those who become allergic to peanuts again either seem to reacquire their allergy very quickly or ate significant amounts regularly.

As such, the best we can currently say is that people who have outgrown their peanut allergy are less likely to become allergic to peanuts again if they eat them on a regular basis but, either way, they should still carry their auto-injector around with them for a year or so after passing their food challenge, just in case.

You can also become allergic to peanuts if you are sensitised but tolerant to them and unnecessarily eliminate them from your diet.

This is what happened to a 50-year-old woman who, during an allergy evaluation, had a positive skin test result to peanut. Although she had always eaten them without problems, her doctor inexplicably* told her to avoid eating them, which she did for 3 years. She then underwent a food challenge and experienced asthmatic-like symptoms; she had lost her tolerance to peanuts and had become clinically allergic.

*This is inexplicable because this kind of thing is known to have happened with several different foods and the medical advice clearly states that if you are sensitised to a food allergen but you can actually eat it without (or with very mild) symptoms, you can (and, indeed, should) keep eating it.

The way peanuts are prepared affects their ability to provoke reactions.

Peanut allergens, like all food allergens, are affected by different processing methods and this, in turn, impacts their ability to provoke reactions.

The amount of fat in a peanut-containing food can affect a person’s reactions to peanut. In one study, 4 peanut-allergic patients undertook 2 peanut challenges, one to a high-fat recipe containing peanut, and a subsequent one to a low-fat recipe containing peanut. 3 of them reacted to much smaller doses of peanut (on average, about 23 times less) in the low-fat recipe. These three patients also had more severe symptoms to the higher-fat recipe during the first challenge.

This latter result was replicated in another study, in which the results of 210 food challenges taken by peanut-allergic children were analysed to see what effect a high-fat recipe (peanut cookies) had compared with a low-fat recipe (peanut in gingerbread). The data showed that the children who ate some of the peanut cookies had more severe reactions than those who ate some of the peanut in gingerbread.

A limitation of this study is that the children did not eat both types of snack. However, the low-fat recipe actually contained more peanut and still provoke a smaller reaction and, unlike the previous study, there was no difference found in the amount the children had to eat before having a reaction, so there does seem to be an aggravating effect of having more fat in a peanut-containing food.

The reasons for the discrepancies in the results between the studies are unknown. However, research has found that fat delays gastric emptying—that is, it stops the stomach from emptying its contents into the intestines so quickly. This means that there would be less peanut allergen initially available to irritate a peanut-allergic individual, so they would have to eat more food before having an obvious reaction, and if a person has eaten more food because it has taken longer for symptoms to appear, this could make their reaction worse than it otherwise would have been. Allergens spending a longer time in the stomach could also potentially aggravate it and increase gastrointestinal permeability, allowing more peanut allergen to enter the bloodstream and amplifying the reaction further.

Additionally, not all fatty foods are created equally. That also makes a difference. In an experiment designed to measure the effect of eating peanuts in a low fat chocolate dessert as to a high-fat cookie, the researchers found that the presence of fat, this time, made (some but) little difference to how likely to peanut was to cause a reaction. This, they thought, may have had something to do with the high temperatures involved in baking the cookie, which may have made two of the major peanut allergens more digestible.

Whatever the mechanics behind the whole thing, what this means is that, if you happen to notice a smaller reaction to peanuts after eating a high-fat dessert, you should not make the mistake of thinking that your allergy is not as bad as you thought it was.

On a side note, they also found that peanut-allergic individuals taking antacids are more likely to have an allergic reaction to peanuts in their food, because antacids raise the pH of the stomach acid and prevent the digestion of the peanut protein, thus increasing the likelihood of an allergic reaction, something that has been demonstrated in large populations of people allergic to all kinds of foods.

Boiled peanuts are also less allergenic, partly because many of the major allergens end up in the cooking water and partly because some of them are broken down ((denatured) and become less able to bind to IgE antibodies. Similarly, pickled peanuts—i.e. peanuts treated with vinegar—are less likely to provoke reactions, because three of the major allergens undergo structural changes that make them less likely to bind to IgE antibodies.

The difference in allergenicity between roasted, boiled and pickled peanuts has been a hot topic since experts noticed that the prevalence of peanut allergy in the West, where peanuts are commonly dry-roasted, is higher than it is in Eastern countries, where peanuts are commonly boiled, fried or pickled.

Research has shown that the lower prevalence of allergy in East Asians countries is not because the people who live there eat fewer peanuts—they are just as likely to be sensitised to peanuts as their Western counterparts—and nor is it due to a genetic advantage; Asian Americans adults, for example, account for 3.8% of the US population, but 6.3% of those with peanut allergies.

Environmental factors are probably involved, as evidenced by a survey on peanut and tree nut allergy in Singapore and the Philippines that found that children of either Asian or white ancestry who were born in Western nations had an increased risk of peanut allergy compared to those who were born in Asia. And one of these environmental factors is how peanuts are cooked before being eaten.

The potential of boiled peanut to actively induce tolerance in peanut-allergic children is currently being investigated. The idea is that a period of eating an increasing amount of boiled peanut—essentially a weakened version of a peanut with partially destroyed allergens—followed by a period of eating an increasing amount of roasted peanut could train a child’s immune system to handle eating peanuts, just like standard immunotherapy, but with a handier type of food.

The first people to float this idea was a team of British and Australian scientists in 2014 who were investigating the allerginicity of boiled peanut. As well as pointing out that many of the major allergens were leached out during cooking, they also described 4 cases of peanut-allergic children (aged between 12 and 15) who were able to increase their threshold to peanut after spending a period time eating boiled peanuts. Just like most patients of standard oral immunotherapy, they had to keep eating a small daily amount of boiled peanut to keep their acquired tolerance, but they were at least protected from accidental exposure to small amounts of peanut. The team pointed out that this method would be most suited to children who reacted to a type of storage protein (the 2S albumins) in the peanut, because those were the allergens that ended up in the cooking water.

In 2023, the results of an immunotherapy trial involving boiled peanut and 70 peanut-allergic Australian children between the ages of 6 and 18 were published. The children were asked to eat an increasing amount of peanuts that had been boiled for 12 hours for a period of 12 weeks, followed by a 20-week period of eating peanuts that had been boiled for two hours. This was finally followed by 20 weeks of eating roasted peanuts, gradually increasing the amount to try and reach a target of 12 peanuts a day, which they had to do for another 6 to 8 weeks. Then they were given an oral food challenge.

56 of 70 (80%) were able to reach the target amount of peanuts and passed the challenge, indicating that they had been successfully desensitised to peanut, and their skin test reactions were also significantly reduced.

The trial was not without its drawbacks, even for those who had a successful outcome; 43 children had reactions during the treatment, which corresponded to a rate of 6.58 reactions per 1000 OIT doses. Most of the reactions did not require medication, but 4 children had to use adrenaline. 3 children had to withdraw from the trial because of the adverse reactions that they had to the peanut. But, for the most part, the authors concluded that using boiled then roasted peanut may be an effective and relatively safe approach to inducing desensitisation.

The researchers did not investigate the long-term success of the treatment so it’s probable that the children, like the ones in the previous study, would have to keep eating peanut on a daily basis to remain desensitised. The search for a way to induce permanent desensitisation continues.

Flying with a peanut allergy is probably not as dangerous as you think it is.

Research has consistently shown that peanut dust settles quickly, that inhaling or touching peanut allergen does not provoke serious (if any) reactions and that surfaces that are contaminated with peanut can readily be cleaned off. And thanks to the average passenger aircraft’s environmental controls, it’s incredibly unlikely that the peanut-allergic flyer will be exposed to dangerous levels of airborne peanut allergen in the cabin. A few simple precautions should be enough to make the chance of experiencing an allergic reaction, and certainly a serious one, infinitesimally small. You can read more about that here.

Acts of intimacy can be hazardous for people with sensitive peanut allergies.

Being kissed by someone who has been eating peanuts has been reported to cause reactions in several people with peanut allergies.

In fact, these types of reactions may happen more often than you think. A 2002 survey of 379 people with life-threatening allergies to peanut, tree nuts and seeds revealed that 5.3% of them reported having had a reaction after kissing or being kissed by someone who had eaten the food that they were allergic to. Most reactions were mild, but 4 people had serious breathing problems and one child had a potentially life-threatening reaction.

Another survey of 1139 food-allergic people carried out a year later reported that 12% had had allergic symptoms after kissing or ‘close contact with’ people who had eaten the foods they were allergic to. 2 of those cases involved peanuts. All of the people in this survey were very sensitive to their triggers, with 13% reporting symptoms when they sat beside someone who was eating the food they were allergic to, and 17% experiencing symptoms if they were in the kitchen when someone was preparing that food.

The symptoms can begin just a few minutes after the kiss tend to be mild or moderate and confined to the area that’s been kissed around 70% of the time, but they can also be systemic and potentially deadly. A passionate kiss between lovers is more likely to cause a significant reaction than a peck on the cheek from a friend or a loving mother, which is more likely to cause a localised case of hives.

As an aside, although a kiss on the cheek is unlikely to cause a big reaction in a peanut-allergic child, one team of scientists has put forward the suggestion that it may be enough to sensitise an infant to peanut. They add, ‘We acknowledge that kissing is essential for a child’s social and emotional development and do not advocate avoidance of kissing but caution against high-saliva-volume kisses soon after peanut consumption in infants with eczema.’ However, there does not seem to be any other research backing up this idea (so far).

Back to the less chaste type of kisses, case reports include descriptions of peanuts eaten anytime between minutes to an hour before the harmful labial assault, including a case in which the girlfriend of a man with severe peanut allergy ate peanut 2 hours before giving him a kiss which caused his lips to swell up and his mouth to start itching. In the meantime, knowing that he had a serious allergy, she had brushed her teeth ‘intensively’, rinsed her mouth out and chewed some gum, but that clearly didn’t help.

Or maybe it did help, at least a little. In another case, which was the first report of its kind for several reasons, a meeting between 2 adolescent boys who had set up a date via a dating app ended in death because one of them, not knowing about the other one’s severe allergy, ate some peanut butter before they met up and then caused his date to have a fatal anaphylactic attack after engaging in oral sex. Unfortunately, the peanut-allergic boy was not given adrenaline quickly enough which might have helped, but there’s no way of knowing if this would have saved his life.

The problem with peanut allergens, especially when they are eaten in the form of peanut butter, are difficult to get rid of. Both hand washing and teeth cleaning can fail to get rid of all the offending peanut.

In light of the reports of potentially deadly consequences of showing affection to a severely peanut-allergic individual, an American team of researchers carried out an experiment to see how much peanut allergen remained in saliva after eating peanut butter, how long it stuck around and what. If anything, could be done about it.

30 adolescent and adult volunteers ate 2 tablespoons of commercially prepared peanut butter in a sandwich and donated salivary samples at various points during the experiment after several interventions. Interventions included brushing teeth for 2 minutes after eating the sandwich, brushing teeth and rinsing the mouth out with water, rinsing the mouth out with water without brushing teeth, waiting an hour then brushing teeth, or waiting half an hour and chewing gum for half an hour. All of the participants also gave saliva samples after eating the sandwich at various points during the day, before and after eating a full meal.

To cut a long and fairly tedious story short(ish), after eating the sandwich, 9 of 30 (30%) of the volunteers ended up with enough peanut butter in their saliva to trigger symptoms in a person with more sensitive peanut allergy. Most (26 of 30, 87%) had undetectable levels of peanut allergen one hour after eating their sandwich with no interventions. The ones who did have detectable peanut allergen had an amount that was 100-fold below the lowest dose reported to cause objective symptoms at the time of the study. There was no allergen detected in anyone’s saliva after they ate a peanut-free lunch about 3.8 hours after the allergen-laden sandwich. And the most effective intervention was the one that included waiting an hour then brushing the teeth, which got rid of 95% of the peanut allergen in 9 out of 10 people.

So the safest course of action would be to wait a few hours and eat a peanut-free meal. Brushing your teeth an hour after eating the sandwich might also be a useful intervention, but as the scientists pointed out, their study participants knew the purpose of the study and ‘may have been more detail-oriented about cleaning their mouths.’ And there is the case of the girlfriend who brushed her teeth after eating peanuts and still caused her boyfriend to get symptoms…

What this all tells us is that, if you have a severe peanut allergy, kissing and sexual contact (and sharing utensils like glasses and straws) can be perilous and so, before kissing anyone, or letting them kiss you, you should ask them what they have eaten today. Ultimately, however, the safest route to take is for the partner of the person with the severe allergy to avoid peanuts, too.

You can get a peanut allergy after an organ transplant or a blood transfusion.

The first known case of an allergy being transferred from an organ donor to a recipient happened in 1989 and involved a 35-year-old man who received a liver and a kidney from a 22-year-old man who died of peanut anaphylaxis. 3 months after getting the organs, the donor recipient develop a rash and throat swelling after eating and was subsequently diagnosed with a new peanut allergy. And thus began the reports of a long line of organ recipients developing new food allergies after organ transplants.

The organ most commonly involved is the liver. In these types of cases, peanut tends to be the 3^rd most commonly acquired food allergy (at least, in the West, it’s less common in East Asian countries) and children under the age of 1 are most at risk.

Other risk factors include having the Epstein-Barr virus in your bloodstream, a family history of atopy and having asthma and/or eczema.

Symptoms (often to multiple foods) generally manifest themselves within 18 months of the operation (with one single-centre study reporting that the risk of developing a food allergy within the first year is about 3 times higher than in subsequent years), although they can occur up to 17.6 years later.

Symptoms generally involve the skin; facial swelling and hives occur in around 4 to 5 in 10 people.  Gastrointestinal manifestations (diarrhoea, vomiting, stomach pain) also affect around half of people with LTFA, while respiratory symptoms affect about 1 in 10. Anaphylaxis affects around 16 in 100 children with LTFA, but no fatal cases have been reported so far. Although the majority (around 4 in 5) of the new food allergies are IgE-mediated, some people also get mixed or non-IgE-mediated allergies like Eosinophilic Gastrointestinal Disorders (EGIDs).

Children are much more likely to develop an allergy after a liver transplant than adults; in fact, there are case reports describing children and adults getting a liver from the same donor and the child developing a food allergy while the adult does not. Why this is so is not known, although it may be something to do with the fact that the child needs a liver transplant in the first place, or it may be because their immune system is too immature to be able to suppress the expression of newly acquired food allergies.

Or it could be something about the liver itself, as there are cases that also describe people getting different organs from the same donor and only the person getting the liver developing a new food allergy. The liver contains blood stem cells that can develop into all types of blood cells, including immune system cells that could be sensitised to the donor’s trigger allergens.

Unfortunately, once a child develops a food allergy after an organ transplant, they’re likely to keep it, although their symptoms may improve over time and, if they have developed a multiple food allergy, they may outgrow their allergy to at least some of the foods. Ultimately, around 1 in 4 may end up with an unrestricted diet.

This does not seem to be the case for adults, who do seem more likely to lose the allergy after a few months, although not always. Due to the small number of reported cases of food allergy transfer after solid organ transplant in adults, it’s difficult to say whether the allergy is more likely to be temporary or permanent.

Although less common, there are also reports of people developing new allergies to peanuts after bone marrow transplants, (including some that resolve), and lung transplants (some of which also resolve) and heart transplants, as well as multiple organ transplants (liver and kidney, pancreas and kidney).

Blood and platelet transfusions can also cause new food allergies to appear, and the development of eosinophilic gastrointestinal disorders has also been reported after cord blood transplantations (when blood stem cells are collected from umbilical cord blood and given to someone who needs a stem cell or bone marrow transplant but doesn’t have a matched donor).

Happily, this kind of allergy–called a ‘passive transfer’—is transient and tends to resolve within a few months at most, because it‘s brought on by IgE antibodies lurking in the blood of by food-allergic donors and these have a short half-life which is estimated to be several hours to a few days. In rare case, blood stem cell transfusions can cause new allergies that will probably require the patient to avoid the food allergen, however.

Finally, it’s also possible for someone who is allergic to a certain food to have a reaction to a blood transfusion, as in the case of a 6-year-old peanut-allergic boy who had an anaphylactic attack while receiving a transfusion of a blood products from a donor who had eaten several handfuls of peanuts the evening before donating their blood.

You may want to consider introducing tree nuts into your peanut-sensitised or allergic infant’s diet.

If there’s anything that nuts are known for in the world of allergy, it’s their potential to cause severe reactions and their tendency to cross-react with peanuts. So it’s not surprising that parents are often reluctant to introduce them into their infant’s diet.

But there are several good reasons why you might want to consider bucking the trend and introducing tree nuts into your child’s diet at a young age.

For a start, although many peanut-allergic children may be sensitised to tree nuts, being sensitised to a food does not mean that you will actually have allergic reactions. For example, a British study that looked at the medical records of nut-allergic children given oral challenges over a 5-year period reported that, of those with peanut allergy, only 7 of 22 (31.2 %) children with positive skin prick test to nuts actually reacted during their challenge. An American study reported that, of the 44 tree nut challenges given to people with peanut allergy who were also sensitised to tree nuts, a whopping 42 (96%) passed, although the people in this study had a relatively low rate of specific IgE to nuts which might explain the high pass rate.

At the same time, a 2020 review of the existing literature found a rate of 12% to 38% of co-existing peanut and tree nut allergies based on oral food challenges. So that’s potentially a lot of peanut-allergic people who are avoiding tree nuts unnecessarily.

And there are several good reasons to introduce your child to tree nuts. For a start, young children who are eliminating a food from their diet, especially one which is a good source of protein, tend to show signs of nutritional deficiency and compromised growth. This is especially likely to be a problem among vegetarians and vegans or children with milk or multiple food allergies who could benefit from fortified almond or hazelnut ‘milk’ drinks.

And there’s the risk that your peanut-allergic child could develop an allergy to nuts that could have been avoided. Infants with peanut allergy are apparently more likely to develop an allergy to tree nuts than to another food. And the nut-allergic seem to develop allergies to more nuts as time goes on. Experts think that this could be due to people eliminating nuts from their diets when they don’t have to, or because, like peanut, a delay in the introduction of nuts into the diet promotes the development of food allergy, so it’s possible that high-risk infants could benefit from introducing nuts into their diets when they’re about 6 months old. Trials designed to figure this out are currently underway.

Finally, there’s the fact that, although tree nut allergies can be hazardous for older people, multiple studies find that infants are actually less likely to have severe allergic reactions than older children and adults, including to peanuts. So, introducing tree nuts into your infant’s diet is actually less risky than introducing them to your child when they’re older, should they actually turn out to be allergic to some of them.

All of which is why some organisations like the British Society for Allergy and Clinical Immunology (BSACI) do not advise the complete avoidance of nuts if some nuts are known to be safe, although nuts that are known to be safe should still be avoided in restaurants due to the risk of staff misidentifying nuts or accidentally substituting other (unsafe) type of nut in a dish.

If you’re interested in introducing tree nuts into your infant’s diet, consult your allergist and they will go through the pros and cons with you. There are certain risk factors to take into account including:

• the severity of your child’s peanut allergy
• whether they have asthma or eczema
• how comfortable you are with dealing with an allergic reaction if you’re introducing nuts at home

There are also other considerations; you will also have to avoid any cross-contamination with peanuts, to introduce each nut one at a time and, if the introduction is successful, to introduce the nut(s) into their regular diet, because this is the only way to protect against allergy. Eating something new once and then eating it infrequently or never again, by contrast, is a good way of encouraging a new allergy to form.

If you have any concerns about possible reactions and you want to introduce the nuts in a safe environment, you can ask for oral testing to be performed. Of course, performing a series of oral food challenges to determine allergy versus tolerance nut by nut is time and resource intensive, and it will generally require multiple visits to an allergy centre as well as coming with a small risk of severe allergic reactions. But, finding a few nuts that your child can eat will limit their risk of nutritional deficiencies and bring some relief from dietary restrictions.

As part of the European Pronuts study, for example, nut-allergic children aged between 6 months and 16 years old were given a series of oral food challenges to different nuts which ultimately led to the children being able to introduce an average of 9 nuts into their diets. Although oral food challenges take time and effort, researchers have been able to identify ‘nut clusters’, that is, groups of nuts that seem to affect the same people in a similar way. So, for example, if you react to cashew, you’ll probably react to pistachio, and if you react to walnut, you’ll probably react to pecan, so the allergist only needs to test your reaction to 2 of those nuts.

Lab tests are also getting better and component-resolved diagnostics (CRD)—testing the blood for IgE antibodies to specific peanut allergens—can be used to determine what type of peanut allergy a person has and whether they are likely to show symptoms to certain tree nuts.

The Basophil Activation Test (BAT) is another promising diagnostic tool for nut allergy which also involves a blood test, this time to see whether or not nut allergens can provoke the basophils in your blood to release histamine. Although this test is not yet largely available in the clinical setting because it requires appropriate equipment and trained personnel, if you or your child have a history of severe allergic reactions, it certainly won’t hurt to ask your allergist about the possibility of using that kind of test to see whether or not you could introduce some tree nuts into your or their diet. Food for thought.

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